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1.
Hyde Richard W.; Geigel Edgar J.; Olszowka Albert J.; Krasney John A.; Forster Robert E. II; Utell Mark J.; Frampton Mark W. 《Journal of applied physiology》1997,82(4):1290-1296
Hyde, Richard W., Edgar J. Geigel, Albert J. Olszowka, JohnA. Krasney, Robert E. Forster II, Mark J. Utell, and Mark W. Frampton.Determination of production of nitric oxide by the lower airwaysof humanstheory. J. Appl. Physiol.82(4): 1290-1296, 1997.Exercise and inflammatory lung disorderssuch as asthma and acute lung injury increase exhaled nitric oxide(NO). This finding is interpreted as a rise in production of NO by thelungs (NO)but fails to take into account the diffusing capacity for NO(DNO) that carries NO into thepulmonary capillary blood. We have derived equations to measureNO from thefollowing rates, which determine NO tension in the lungs(PL) at any moment from 1) production(NO);2) diffusion, whereDNO(PL) = rate of removal by lung capillary blood; and3) ventilation, whereA(PL)/(PB 47) = the rate of NO removal by alveolar ventilation(A) and PB is barometric pressure. During open-circuit breathingwhen PL is not in equilibrium,d/dtPL[VL/(PB 47)] (where VL is volumeof NO in the lower airways) = NO DNO(PL) A(PL)/(PB 47). When PL reaches asteady state so that d/dt = 0 andA iseliminated by rebreathing or breath holding, then PL = NO/DNO.PL can be interpreted as NOproduction per unit of DNO. Thisequation predicts that diseases that diminishDNO but do not alterNO willincrease expired NO levels. These equations permit precise measurementsof NO thatcan be applied to determining factors controlling NO production by thelungs. 相似文献
2.
Padilla Jaime; Garcia-Villalon Angel Luis; Fernandez Nuria; Monge Luis; Gomez Bernardino; Dieguez Godofredo 《Journal of applied physiology》1998,85(6):2205-2212
To analyze the effect of hyperthermia on thevascular response, the isometric response of isolated rabbit femoralartery segments was recorded at 37°C and hyperthermia (41 and44°C). Contraction to potassium (5 × 103-5 × 102 M) was significantlygreater at 41 and 44 than at 37°C and increased by inhibition ofnitric oxide (NO) synthesis withN-nitro-L-arginine(L-NNA;104 M) or endotheliumremoval at 37°C but not at 41 or 44°C. Norepinephrine (109-104M) produced a concentration-dependent contraction greater at 41 or 44 than at 37°C and not modified by endothelium removal orL-NNA at either temperature.Phenylephrine(109-104M) produced a contraction increased by warming to 44°C but not to41°C. The specific2-adrenoceptor agonist BHT-920produced a weak contraction, reduced by the1-adrenoceptor antagonist prazosin (106 M) andincreased at 44°C but not at 41°C. The concentration-dependent contraction to endothelin-1 (ET-1;1011-107M) was increased by warming to 41 and 44°C and by endothelium removal or L-NNA at 37°C butnot at 41 or 44°C. Response to ET-1 was reduced by endothelinETA-receptor antagonist BQ-123(105 M) andETB-receptor antagonist BQ-788(105 M). In arteriesprecontracted with ET-1(108-3 × 108 M), relaxation tosodium nitroprusside(108-104M) was increased at 41 and 44°C vs. at 37°C, but that of ACh (108-104M) or adenosine(108-104M) was not different at all temperatures studied. Relaxation to ACh,but not adenosine, was reduced similarly byL-NNA at all temperaturesstudied. These results suggest hyperthermia in muscular arteries mayinhibit production of, and increase dilatation to, NO, resulting inunchanged relaxation to ACh and increased constriction to KCl and ET-1,and may increase constriction to stimulation of1-adrenoceptors byNO-independent mechanisms. 相似文献
3.
Susceptibility to periodic breathing with assisted ventilation during sleep in normal subjects 总被引:6,自引:0,他引:6
Meza Sonia; Mendez Manuel; Ostrowski Michele; Younes Magdy 《Journal of applied physiology》1998,85(5):1929-1940
Assisted ventilation with pressure support (PSV)or proportional assist (PAV) ventilation has the potential to produceperiodic breathing (PB) during sleep. We hypothesized that PB willdevelop when PSV level exceeds the product of spontaneous tidal volume (VT) and elastance(VTsp · E)but that the actual level at which PB will develop[PSV(PB)] will be influenced by thePCO2 (difference between eupneicPCO2 andCO2 apneic threshold) and by RR[response of respiratory rate (RR) to PSV]. We also wishedto determine the PAV level at which PB develops to assess inherentventilatory stability in normal subjects. Twelve normal subjectsunderwent polysomnography while connected to a PSV/PAV ventilatorprototype. Level of assist with either mode was increased in smallsteps (2-5 min each) until PB developed or the subject awakened.End-tidal PCO2,VT, RR, and airway pressure (Paw) were continuously monitored, and the pressure generated byrespiratory muscle (Pmus) was calculated. The pressure amplification factor (PAF) at the highest PAV level was calculated from[(Paw + Pmus)/Pmus], where Paw is peak Paw continuous positive airway pressure. PB with central apneas developedin 11 of 12 subjects on PSV. PCO2ranged from 1.5 to 5.8 Torr. Changes in RR with PSV were small andbidirectional (+1.1 to 3.5min1). With use ofstepwise regression, PSV(PB) was significantly correlated withVTsp(P = 0.001), E(P = 0.00009),PCO2 (P = 0.007), and RR(P = 0.006). The final regressionmodel was as follows: PSV(PB) = 11.1 VTsp + 0.3E 0.4 PCO2 0.34 RR 3.4 (r = 0.98). PBdeveloped in five subjects on PAV at amplification factors of1.5-3.4. It failed to occur in seven subjects, despite PAF of upto 7.6. We conclude that 1) aPCO2 apneic threshold exists duringsleep at 1.5-5.8 Torr below eupneicPCO2,2) the development of PB during PSVis entirely predictable during sleep, and3) the inherent susceptibility to PBvaries considerably among normal subjects. 相似文献
4.
Mazzeo Robert S.; Carroll Joy D.; Butterfield Gail. E.; Braun Barry; Rock Paul B.; Wolfel Eugene E.; Zamudio Stacy; Moore Lorna G. 《Journal of applied physiology》2001,90(1):121-126
We have previouslydocumented the importance of the sympathetic nervous system inacclimatizing to high altitude in men. The purpose ofthis investigation was to determine the extent to which -adrenergicblockade affects the sympathoadrenal responses to exercise during acutehigh-altitude exposure in women. Twelve eumenorrheic women (24.7 ± 1.3 yr, 70.6 ± 2.6 kg) were studied at sea level and onday 2 of high-altitude exposure (4,300-m hypobaric chamber)in either their follicular or luteal phase. Subjects performed twograded-exercise tests at sea level (on separate days) on a bicycleergometer after 3 days of taking either a placebo or an -blocker (3 mg/day prazosin). Subjects also performed two similar exercise testswhile at altitude. Effectiveness of blockade was determined byphenylephrine challenge. At sea level, plasma norepinephrine levelsduring exercise were 48% greater when subjects were -blockedcompared with their placebo trial. This difference was only 25% whensubjects were studied at altitude. Plasma norepinephrine values weresignificantly elevated at altitude compared with sea level but to agreater extent for the placebo (59%) vs. blocked (35%) trial. Amore dramatic effect of both altitude (104% placebo vs. 95%blocked) and blockade (50% sea level vs. 44% altitude) wasobserved for plasma epinephrine levels during exercise. No phasedifferences were observed across any condition studied. It wasconcluded that -adrenergic blockade 1) resulted in acompensatory sympathoadrenal response during exercise at sea level andaltitude, and 2) this effect was more pronounced for plasma epinephrine. 相似文献
5.
Combined heart rate and activity improve estimates of oxygen consumption and carbon dioxide production rates 总被引:1,自引:0,他引:1
Moon, Jon K., and Nancy F. Butte. Combined heart rateand activity improve estimates of oxygen consumption and carbon dioxideproduction rates. J. Appl. Physiol.81(4): 1754-1761, 1996.Oxygen consumption(O2) andcarbon dioxide production (CO2) rates were measuredby electronically recording heart rate (HR) and physical activity (PA).Mean daily O2 andCO2 measurements by HR andPA were validated in adults (n = 10 women and 10 men) with room calorimeters. Thirteen linear and nonlinear functions of HR alone and HR combined with PA were tested as models of24-h O2 andCO2. Mean sleepO2 andCO2 were similar to basalmetabolic rates and were accurately estimated from HR alone[respective mean errors were 0.2 ± 0.8 (SD) and0.4 ± 0.6%]. The range of prediction errorsfor 24-h O2 andCO2 was smallestfor a model that used PA to assign HR for each minute to separateactive and inactive curves(O2, 3.3 ± 3.5%; CO2, 4.6 ± 3%). There were no significant correlations betweenO2 orCO2 errors and subject age,weight, fat mass, ratio of daily to basal energy expenditure rate, orfitness. O2,CO2, and energy expenditurerecorded for 3 free-living days were 5.6 ± 0.9 ml · min1 · kg1,4.7 ± 0.8 ml · min1 · kg1,and 7.8 ± 1.6 kJ/min, respectively. Combined HR and PA measured 24-h O2 andCO2 with a precisionsimilar to alternative methods. 相似文献
6.
Yan, Sheng, Pawel Sliwinski, and Peter T. Macklem.Association of chest wall motion and tidal volume responses during CO2 rebreathing.J. Appl. Physiol. 81(4):1528-1534, 1996.The purpose of this study is to investigate theeffect of chest wall configuration at end expiration on tidal volume(VT) response duringCO2 rebreathing. In a group of 11 healthy male subjects, the changes in end-expiratory andend-inspiratory volume of the rib cage (Vrc,E andVrc,I, respectively) and abdomen (Vab,E and Vab,I, respectively) measured by linearizedmagnetometers were expressed as a function of end-tidalPCO2(PETCO2). The changes inend-expiratory and end-inspiratory volumes of the chest wall(Vcw,E and Vcw,I,respectively) were calculated as the sum of the respectiverib cage and abdominal volumes. The magnetometer coils were placed atthe level of the nipples and 1-2 cm above the umbilicus andcalibrated during quiet breathing against theVT measured from apneumotachograph. TheVrc,E/PETCO2 slope was quite variable among subjects. It was significantly positive (P < 0.05) in fivesubjects, significantly negative in four subjects(P < 0.05), and not different fromzero in the remaining two subjects. TheVab,E/PETCO2slope was significantly negative in all subjects(P < 0.05) with a much smallerintersubject variation, probably suggesting a relatively more uniformrecruitment of abdominal expiratory muscles and a variable recruitmentof rib cage muscles during CO2rebreathing in different subjects. As a group, the meanVrc,E/PETCO2,Vab,E/PETCO2, andVcw,E/PETCO2slopes were 0.010 ± 0.034, 0.030 ± 0.007, and0.020 ± 0.032 l / Torr, respectively;only theVab,E/PETCO2 slope was significantly different from zero. More interestingly, theindividualVT/PETCO2slope was negatively associated with theVrc,E/PETCO2(r = 0.68,P = 0.021) and Vcw,E/PETCO2slopes (r = 0.63,P = 0.037) but was not associated withtheVab,E/PETCO2slope (r = 0.40, P = 0.223). There was no correlation oftheVrc,E/PETCO2 andVcw,E/PETCO2slopes with age, body size, forced expiratory volume in 1 s, orexpiratory time. The groupVab,I/PETCO2 slope (0.004 ± 0.014 l / Torr) was not significantlydifferent from zero despite theVT nearly being tripled at theend of CO2 rebreathing. Inconclusion, the individual VTresponse to CO2, althoughindependent of Vab,E, is a function ofVrc,E to the extent that as theVrc,E/PETCO2slope increases (more positive) among subjects, theVT response toCO2 decreases. These results maybe explained on the basis of the respiratory muscle actions andinteractions on the rib cage. 相似文献
7.
Treppo Steven; Mijailovich Srboljub M.; Venegas Jose G. 《Journal of applied physiology》1997,82(4):1163-1176
Treppo, Steven, Srboljub M. Mijailovich, and José G. Venegas. Contributions of pulmonary perfusion and ventilation toheterogeneity in A/measured by PET. J. Appl. Physiol. 82(4): 1163-1176, 1997. To estimate the contributions of the heterogeneity in regionalperfusion () and alveolar ventilation(A) to that of ventilation-perfusionratio (A/), we haverefined positron emission tomography (PET) techniques to image localdistributions of andA per unit of gas volume content(s and sA,respectively) and VA/ indogs. sA was assessed in two ways:1) the washout of 13NN tracer after equilibrationby rebreathing (sAi), and2) the ratio of an apneic image after a bolus intravenousinfusion of 13NN-saline solution to an image collectedduring a steady-state intravenous infusion of the same solution(sAp).sAp was systematically higher than sAi in allanimals, and there was a high spatial correlation betweens andsAp in both body positions(mean correlation was 0.69 prone and 0.81 supine) suggesting thatventilation to well-perfused units was higher than to those poorlyperfused. In the prone position, the spatial distributions ofs, sAp, and A/ were fairlyuniform with no significant gravitational gradients; however, in thesupine position, these variables were significantly more heterogeneous,mostly because of significant gravitational gradients (15, 5.5, and10%/cm, respectively) accounting for 73, 33, and 66% of thecorresponding coefficient of variation (CV)2 values. Weconclude that, in the prone position, gravitational forces in blood andlung tissues are largely balanced out by dorsoventral differences inlung structure. In the supine position, effects of gravity andstructure become additive, resulting in substantial gravitationalgradients in s andsAp, with the higherheterogeneity inA/ caused by agravitational gradient in s, only partially compensated by that in sA. 相似文献
8.
Worsnop Christopher; Kay Amanda; Pierce Robert; Kim Young; Trinder John 《Journal of applied physiology》1998,85(3):908-920
Ventilationdecreases at sleep onset. This change is initiated abruptly at -electroencephalographic transitions. The aim of this study was todetermine the contributions of reduced activity in respiratory pumpmuscles and upper airway dilator muscles to this change. Surfaceelectromyograms over the diaphragm (Di) and intercostal muscles andfine-wire intramuscular electrodes in genioglossus (GG) and tensorpalatini (TP) muscles were recorded in nine healthy young men. It wasshown that phasic Di and both phasic and tonic TP activities were lowerduring than during activity. Breath-by-breath analysis of thechanges at - transitions during the sleep-onset period showed anumber of changes. At - transitions, phasic activity of Di,intercostal, and GG muscles fell and rose again, and phasic and tonicactivities of TP fell and remained at low levels during . With astate transition from to , the phasic and tonic activities ofthe Di, GG, and TP increased dramatically. It is now clear that thefall in ventilation that occurs with sleep is related to a fall inactivities of both upper airway dilator muscles and respiratory pumpmuscles. 相似文献
9.
Hasday Jeffrey D.; Bannerman Douglas; Sakarya Sirhan; Cross Alan S.; Singh Ishwar S.; Howard Deborah; Drysdale Beth-Ellen; Goldblum Simeon E. 《Journal of applied physiology》2001,90(1):90-98
Fever is an important regulator ofinflammation that modifies expression and bioactivity of cytokines,including tumor necrosis factor (TNF)-. Pulmonary vascularendothelium is an important target of TNF- during the systemicinflammatory response. In this study, we analyzed the effect of afebrile range temperature (39.5°C) on TNF--stimulatedchanges in endothelial barrier function, capacity for neutrophilbinding and transendothelial migration (TEM), and cytokine secretion inhuman pulmonary artery endothelial cells (EC). Permeability for[14C]BSA tracer was increased by treatment with TNF-,and this effect was augmented by incubating EC at 39.5°C. Treating ECwith 2.5 U/ml TNF- stimulated an increase in subsequent neutrophiladherence and TEM. Incubating EC at 39.5°C caused a 30% increase inTEM but did not modify the enhancement of neutrophil adherence or TEMby TNF- treatment. Analysis of cytokine expression in EC culturesexposed to TNF- at either 37° or 39.5°C revealed three patternsof temperature and TNF- responsiveness. Granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL)-8 were notdetectable in untreated EC but were increased after TNF- exposure,and this increase was enhanced at 39.5°C. IL-6 expression was alsoincreased with TNF- exposure, but IL-6 expression was lower in39.5°C EC cultures. Transforming growth factor-1 was constitutively expressed, and its expression was not influenced eitherby TNF- or exposure to 39.5°C. These data demonstrate thatclinically relevant shifts in body temperature might cause importantchanges in the effects of proinflammatory cytokines on the endothelium. 相似文献
10.
Effects of head-down-tilt bed rest on cerebral hemodynamics during orthostatic stress 总被引:4,自引:0,他引:4
Zhang Rong; Zuckerman Julie H.; Pawelczyk James A.; Levine Benjamin D. 《Journal of applied physiology》1997,83(6):2139-2145
Zhang, Rong, Julie H. Zuckerman, James A. Pawelczyk, andBenjamin D. Levine. Effects of head-down-tilt bed rest on cerebralhemodynamics during orthostatic stress. J. Appl.Physiol. 83(6): 2139-2145, 1997.Our aim was todetermine whether the adaptation to simulated microgravity (µG)impairs regulation of cerebral blood flow (CBF) during orthostaticstress and contributes to orthostatic intolerance. Twelvehealthy subjects (aged 24 ± 5 yr) underwent 2 wk of 6°head-down-tilt (HDT) bed rest to simulate hemodynamic changes thatoccur when humans are exposed to µG. CBF velocity in the middlecerebral artery (transcranial Doppler), blood pressure, cardiac output(acetylene rebreathing), and forearm blood flow were measured at eachlevel of a ramped protocol of lower body negative pressure (LBNP;15, 30, and 40 mmHg × 5 min, 50 mmHg × 3 min, then 10 mmHg every 3 min to presyncope) beforeand after bed rest. Orthostatic tolerance was assessed by using thecumulative stress index (CSI; mmHg × minutes) for the LBNPprotocol. After bed rest, each individual's orthostatic tolerance wasreduced, with the group CSI decreased by 24% associated with greaterdecreases in cardiac output and greater increases in systemic vascularresistance at each level of LBNP. Before bed rest, mean CBF velocitydecreased by 14, 10, and 45% at 40 mmHg, 50 mmHg, andmaximal LBNP, respectively. After bed rest, mean velocity decreased by16% at 30 mmHg and by 21, 35, and 39% at 40 mmHg,50 mmHg, and maximal LBNP, respectively. Compared with pre-bedrest, post-bed-rest mean velocity was less by 11, 10, and 21% at30, 40, and 50 mmHg, respectively. However, therewas no significant difference at maximal LBNP. We conclude thatcerebral autoregulation during orthostatic stress is impaired byadaptation to simulated µG as evidenced by an earlier and greater fall in CBF velocity during LBNP. We speculate that impairment ofcerebral autoregulation may contribute to the reduced orthostatic tolerance after bed rest. 相似文献
11.
Liposome encapsulation attenuates hemoglobin-induced vasoconstriction in rabbit arterial segments 总被引:2,自引:0,他引:2
Rudolph Alan S.; Sulpizio Anthony; Hieble Paul; Macdonald Victor; Chavez Mark; Feuerstein Giora 《Journal of applied physiology》1997,82(6):1826-1835
Rudolph, Alan S., Anthony Sulpizio, Paul Hieble, VictorMacdonald, Mark Chavez, and Giora Feuerstein. Liposomeencapsulation attenuates hemoglobin-induced vasoconstriction in rabbitarterial segments. J. Appl. Physiol.82(6): 1826-1835, 1997.Free hemoglobin (Hb) induces a potentvasoconstrictor response that may limit its therapeutic application asa red blood cell replacement. We have investigated whetherencapsulation of stroma-free Hb (SFHb) or cross-linked Hb (-Hb)in liposomes modulates Hb vasoactivity in isolated blood vessels.Relaxation of rabbit thoracic vessels was measured before and afterexposure to acellular SFHb, -Hb, and liposome-encapsulated SFHbor -Hb. SFHb and -Hb caused significant inhibition ofcarbachol-induced relaxation at 0.5 mg/dl, whereas encapsulationinhibited vessel relaxation at 30- to 60-fold higher Hb concentrations.The contractile response of rabbit ear arterial segments to electricalstimulation in the presence of acellular -Hb resulted in a 150%increase (EC150) in contractileamplitude at 0.23 mg/dl, whereas theEC150 for encapsulated -Hbwas 13.7 mg/dl. Mechanistic studies of the vasoconstrictor activity ofHb demonstrated that acellular -Hb had no effect onnorepinephrine release in the rabbit ear artery. In addition, neitheracellular nor encapsulated -Hb preparations inhibited endothelialnitric oxide (NO) synthase activity isolated from bovine pulmonaryartery. However, inhibition of vessel relaxation by acellular orencapsulated -Hb was reversed by the NO donor S-nitrosylpenacillamine, implicatingHb-NO binding as a possible mechanism for the vasoconstrictor response.In vitro stopped-flow kinetic studies of Hb-NO binding showed similarrates of reaction for conversion of oxyhemoglobin to methemoglobin(metHb; <2 ms), followed by rapid conversion of metHb to NO-Hb (300 ms) for both acellular and encapsulated -Hb, demonstrating thatliposome encapsulation does not retard NO-Hb binding. The attenuatedvasoactivity of encapsulated Hb may, therefore, result from the limitedaccess of encapsulated Hb to NO imposed by the physical size of theliposome and reduced penetration of Hb across the vascular endothelium. 相似文献
12.
Shimazu Takeshi; Yukioka Tetsuo; Ikeuchi Hisashi; Mason Arthur D. Jr.; Wagner Peter D.; Pruitt Basil A. Jr. 《Journal of applied physiology》1996,81(5):2250-2259
Shimazu, Takeshi, Tetsuo Yukioka, Hisashi Ikeuchi, Arthur D. Mason, Jr., Peter D. Wagner, and Basil A. Pruitt, Jr.Ventilation-perfusion alterations after smoke inhalation injury inan ovine model. J. Appl. Physiol.81(5): 2250-2259, 1996.To study the pathophysiological mechanismof progressive hypoxemia after smoke inhalation injury, alterations inventilation-perfusion ratio(A/)were studied in an ovine model by using the multiple inert gaselimination technique. Because ethane was detected in expired gas ofsome sheep, we replaced ethane with krypton, which was a uniqueapplication of the multiple inert gas elimination technique when one ofthe experimental gases is present in the inspirate. Severity-related changes were studied 24 h after injury in control and mild, moderate, and severe inhalation injury groups. Time-related changes were studiedin controls and sheep with moderate injury at 6, 12, 24, and 72 h.Arterial PO2 decreased progressivelywith severity of injury as well as with time. In smoke-exposed animals,blood flow was recruited to lowA/compartment (0 < A/ < 0.1; 17.6 ± 10.6% of cardiac output, 24 h,moderate injury) from normal A/compartment (0.1 < A/ < 10). However, increases in true shunt(A/ = 0; 5.6 ± 2.5%, 24 h, moderate injury) and dead space were notconsistent findings. TheA/patterns suggest the primary change in smoke inhalation injury to be adisturbance of ventilation. 相似文献
13.
Dishart Michael K.; Schlichtig Robert; Tonnessen Tor Inge; Rozenfeld Ranna A.; Simplaceanu Elena; Williams Donald; Gayowski Timothy J.P. 《Journal of applied physiology》1998,84(3):791-797
Dysoxia canbe defined as ATP flux decreasing in proportion toO2 availability with preserved ATPdemand. Hepatic venous -hydroxybutyrate-to-acetoacetate ratio(-OHB/AcAc) estimates liver mitochondrial NADH/NAD and may detectthe onset of dysoxia. During partial dysoxia (as opposed to anoxia),however, flow may be adequate in some liver regions, diluting effluentfrom dysoxic regions, thereby rendering venous -OHB/AcAc unreliable.To address this concern, we estimated tissue ATP whilegradually reducing liver blood flow of swine to zero in a nuclearmagnetic resonance spectrometer. ATP flux decreasing withO2 availability was taken asO2 uptake(O2) decreasing inproportion to O2 delivery(O2);and preserved ATP demand was taken as increasingPi/ATP.O2, tissuePi/ATP, and venous -OHB/AcAcwere plotted againstO2to identify critical inflection points. Tissue dysoxia required meanO2for the group to be critical for bothO2 and forPi/ATP. CriticalO2values for O2 andPi/ATP of 4.07 ± 1.07 and 2.39 ± 1.18 (SE) ml · 100 g1 · min1,respectively, were not statistically significantly different but notclearly the same, suggesting the possibility that dysoxia might havecommenced after O2 begandecreasing, i.e., that there could have been"O2 conformity." CriticalO2for venous -OHB/AcAc was 2.44 ± 0.46 ml · 100 g1 · min1(P = NS), nearly the same as that forPi/ATP, supporting venous -OHB/AcAc as a detector of dysoxia. All issues considered, tissue mitochondrial redox state seems to be an appropriate detector ofdysoxia in liver. 相似文献
14.
Wolfel Eugene E.; Selland Mark A.; Cymerman A.; Brooks George A.; Butterfield Gail E.; Mazzeo Robert S.; Grover Robert F.; Reeves John T. 《Journal of applied physiology》1998,85(3):1092-1102
Wholebody O2 uptake (O2)during maximal and submaximal exercise has been shown to be preservedin the setting of -adrenergic blockade at high altitude, despitemarked reductions in heart rate during exercise. An increase in strokevolume at high altitude has been suggested as the mechanism thatpreserves systemic O2 delivery (blood flow × arterialO2 content) and thereby maintains O2 at sea-level values. To test thishypothesis, we studied the effects of nonselective -adrenergicblockade on submaximal exercise performance in 11 normal men(26 ± 1 yr) at sea level and on arrival and after 21 days at 4,300 m. Six subjects received propranolol (240 mg/day), and five subjectsreceived placebo. At sea level, during submaximal exercise, cardiacoutput and O2 delivery were significantly lower inpropranolol- than in placebo-treated subjects. Increases instroke volume and O2 extraction were responsible for themaintenance of O2. At 4,300 m,-adrenergic blockade had no significant effect onO2, ventilation, alveolarPO2, and arterial blood gases duringsubmaximal exercise. Despite increases in stroke volume, cardiac outputand thereby O2 delivery were still reduced inpropranolol-treated subjects compared with subjects treated withplacebo. Further reductions in already low levels of mixed venousO2 saturation were responsible for the maintenance ofO2 on arrival and after 21 days at4,300 m in propranolol-treated subjects. Despite similarworkloads and O2,propranolol-treated subjects exercised at greater perceived intensitythan subjects given placebo at 4,300 m. The values for mixed venousO2 saturation during submaximal exercise inpropranolol-treated subjects at 4,300 m approached thosereported at simulated altitudes >8,000 m. Thus -adrenergicblockade at 4,300 m results in significant reduction in O2delivery during submaximal exercise due to incomplete compensation bystroke volume for the reduction in exercise heart rate. Total bodyO2 is maintained at a constant levelby an interaction between mixed venous O2 saturation, thearterial O2-carrying capacity, and hemodynamics duringexercise with acute and chronic hypoxia. 相似文献
15.
Greater rate of decline in maximal aerobic capacity with age in physically active vs. sedentary healthy women 总被引:8,自引:0,他引:8
Tanaka Hirofumi; Desouza Christopher A.; Jones Pamela P.; Stevenson Edith T.; Davy Kevin P.; Seals Douglas R. 《Journal of applied physiology》1997,83(6):1947-1953
Tanaka, Hirofumi, Christopher A. DeSouza, Pamela P. Jones,Edith T. Stevenson, Kevin P. Davy, and Douglas R. Seals. Greater rate of decline in maximal aerobic capacity with age in physically active vs. sedentary healthy women. J. Appl.Physiol. 83(6): 1947-1953, 1997.Using ameta-analytic approach, we recently reported that the rate of declinein maximal oxygen uptake(O2 max) with age inhealthy women is greatest in the most physically active and smallest inthe least active when expressed in milliliters per kilogram per minuteper decade. We tested this hypothesis prospectively underwell-controlled laboratory conditions by studying 156 healthy, nonobesewomen (age 20-75 yr): 84 endurance-trained runners (ET) and 72 sedentary subjects (S). ET were matched across the age range forage-adjusted 10-km running performance. Body mass was positivelyrelated with age in S but not in ET. Fat-free mass was not differentwith age in ET or S. Maximal respiratory exchange ratio and rating ofperceived exertion were similar across age in ET and S, suggestingequivalent voluntary maximal efforts. There was a significant butmodest decline in running mileage, frequency, and speed with advancingage in ET.O2 max(ml · kg1 · min1)was inversely related to age (P < 0.001) in ET (r = 0.82) and S(r = 0.71) and was higher atany age in ET. Consistent with our meta-analysic findings,the absolute rate of decline inO2 max was greater inET (5.7ml · kg1 · min1 · decade1)compared with S (3.2 ml · kg1 · min1 · decade1;P < 0.01), but the relative (%)rate of decline was similar (9.7 vs 9.1%/decade; notsignificant). The greater absolute rate of decline inO2 max in ET comparedwith S was not associated with a greater rate of decline in maximalheart rate (5.6 vs. 6.2beats · min1 · decade1),nor was it related to training factors. The present cross-sectional findings provide additional evidence that the absolute, but not therelative, rate of decline in maximal aerobic capacity with age may begreater in highly physically active women compared with theirsedentary healthy peers. This difference does not appear to be relatedto age-associated changes in maximal heart rate, bodycomposition, or training factors. 相似文献
16.
Blood volume and cardiac index in rats after exchange transfusion with hemoglobin-based oxygen carriers 总被引:3,自引:0,他引:3
Migita Russell; Gonzales Armando; Gonzales Maria L.; Vandegriff Kim D.; Winslow Robert M. 《Journal of applied physiology》1997,82(6):1995-2002
Migita, Russell, Armando Gonzales, Maria L. Gonzales, Kim D. Vandegriff, and Robert M. Winslow. Blood volume and cardiac indexin rats after exchange transfusion with hemoglobin-based oxygencarriers. J. Appl. Physiol. 82(6):1995-2002, 1997.We have measured plasma volume and cardiac indexin rats after 50% isovolemic exchange transfusion with humanhemoglobin cross-linked between the -chains withbis(3,5-dibromosalicyl)fumarate (Hb) and with bovine hemoglobinmodified with polyethylene glycol (PEGHb). Hb and PEGHb differ incolloid osmotic pressure (23.4 and 118.0 Torr, respectively), oxygenaffinity (oxygen half-saturation pressure of hemoglobin = 30.0 and 10.2 Torr, respectively), viscosity (1.00 and 3.39 cP, respectively), andmolecular weight (64,400 and 105,000, respectively). Plasma volume wasmeasured by Evans blue dye dilution modified for interference by plasmahemoglobin. Blood volumes in PEGHb-treated animals were significantlyelevated (74.0 ± 3.5 ml/kg) compared with animals treated withHb (49.0 ± 1.2 ml/kg) or Ringer lactate (48.0 ± 2.0 ml/kg) or with controls (58.2 ± 1.9 ml/kg). Heart rate reductionafter Hb exchange is opposite to that expected with blood volumecontraction, suggesting that Hb may have a direct myocardialdepressant action. The apparently slow elimination of PEGHb during the2 h after its injection is a consequence of plasma volume expansion:when absolute hemoglobin (concentration × plasma volume) iscompared for PEGHb and Hb, no difference in their eliminationrates is found. These studies emphasize the need to understand bloodvolume regulation when the effects of cell-free hemoglobin onhemodynamic measurements are evaluated. 相似文献
17.
Hardarson Thorir; Skarphedinsson Jon O.; Sveinsson Torarinn 《Journal of applied physiology》1998,84(2):411-416
Hardarson, Thorir, Jon O. Skarphedinsson, and TorarinnSveinsson. Importance of the lactate anion in control ofbreathing. J. Appl. Physiol. 84(2):411-416, 1998.The purpose of this study was to examine theeffects of raising the arterialLa andK+ levels on minute ventilation(E) in rats. EitherLa or KCl solutions wereinfused in anesthetized spontaneously breathing Wistar rats to raisethe respective ion arterial concentration ([La] and[K+]) gradually tolevels similar to those observed during strenuous exercise.E, blood pressure, and heart rate wererecorded continuously, and arterial[La],[K+], pH, and bloodgases were repeatedly measured from blood samples. To prevent changesin pH during the Lainfusions, a solution of sodium lactate and lactic acid was used. Raising [La] to13.2 ± 0.6 (SE) mM induced a 47.0 ± 4.0% increase inE without any concomitant changes ineither pH or PCO2. Raising[K+] to 7.8 ± 0.11 mM resulted in a 20.3 ± 5.28% increase inE without changes in pH. Thus ourresults show that Laitself, apart from lactic acidosis, may be important in increasing E during strenuous exercise, and weconfirm earlier results regarding the role of arterial[K+] in the control ofE during exercise. 相似文献
18.
Scheuermann Barry W.; Kowalchuk John M.; Paterson Donald H.; Cunningham David A. 《Journal of applied physiology》1998,85(4):1384-1393
Inhibition of carbonic anhydrase (CA) isassociated with a lower plasma lactate concentration([La]pl)during fatiguing exercise. We hypothesized that a lower[La]plmay be associated with faster O2uptake (O2) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz,10 mg/kg body wt iv). On 6 separate days, each subject performed 6-minstep transitions in work rate from 0 to 100 W (below ventilatory threshold,<ET)or to a O2 corresponding to~50% of the difference between the work rate atET and peakO2(>ET).Gas exchange was measured breath by breath. Trials were interpolated at1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (<ET) or athree-component exponential model(>ET).Arterialized venous blood was sampled from a dorsal hand vein andanalyzed for[La]pl.MRT was similar during Con (31.2 ± 2.6 and 32.7 ± 1.2 s for onand off, respectively) and Acz (30.9 ± 3.0 and 31.4 ± 1.5 s for on and off, respectively) for work rates<ET. Atwork rates >ET, MRTwas similar between Con (69.1 ± 6.1 and 50.4 ± 3.5 s for on andoff, respectively) and Acz (69.7 ± 5.9 and 53.8 ± 3.8 s for on and off, respectively). On- and off-MRTs were slower for>ET thanfor <ETexercise.[La]plincreased above 0-W cycling values during<ET and>ET exercise but was lower at the end of the transition during Acz (1.4 ± 0.2 and 7.1 ± 0.5 mmol/l for<ET and>ET,respectively) than during Con (2.0 ± 0.2 and 9.8 ± 0.9 mmol/lfor <ETand >ET,respectively). CA inhibition does not affectO2 utilization at the onset of<ET or>ETexercise, suggesting that the contribution of oxidative phosphorylationto the energy demand is not affected by acute CA inhibition with Acz. 相似文献
19.
Khimenko Pavel L.; Bagby G. J.; Fuseler J.; Taylor Aubrey E. 《Journal of applied physiology》1998,85(6):2005-2011
The effects ofboth recombinant rat tumor necrosis factor- (TNF-) and ananti-TNF- antibody were studied in isolated buffer-perfused ratlungs subjected to either 45 min of nonventilated[ischemia-reperfusion (I/R)] or air-ventilated(/R) ischemia followed by 90 min of reperfusion and ventilation. In the I/R group, the vascularpermeability, as measured by the filtration coefficient(Kfc),increased three- and fivefold above baseline after 30 and 90 min ofreperfusion, respectively (P < 0.001). Over the same time intervals, theKfc for the/R group increased five- and tenfold above baseline values, respectively (P < 0.001).TNF- measured in the perfusates of both ischemic modelssignificantly increased after 30 min of reperfusion. Recombinant ratTNF- (50,000 U), placed into perfusate after baseline measurements,produced no measurable change in microvascular permeability in controllungs perfused over the same time period (135 min), but I/R injury wassignificantly enhanced in the presence of TNF-. An anti-TNF-antibody (10 mg/rat) injected intraperitoneally into rats 2 h beforethe lung was isolated prevented the microvascular damage in lungsexposed to both I/R and /R (P < 0.001). These results indicatethat TNF- is an essential component at the cascade of events thatcause lung endothelial injury in short-term I/R and/R models of lung ischemia. 相似文献
20.
Magnitude and time course of hemodynamic responses to Mueller maneuvers in patients with congestive heart failure 总被引:2,自引:0,他引:2
Hall Michael J.; Ando Shin-Ichi; Floras John S.; Bradley T. Douglas 《Journal of applied physiology》1998,85(4):1476-1484
To simulate theimmediate hemodynamic effect of negative intrathoracic pressure duringobstructive apneas in congestive heart failure (CHF), without inducingconfounding factors such as hypoxia and arousals from sleep, eightawake patients performed, at random, 15-s Mueller maneuvers (MM) attarget intrathoracic pressures of 20 (MM 20) and40 cmH2O (MM 40),confirmed by esophageal pressure, and 15-s breath holds, as apneic timecontrols. Compared with quiet breathing, at baseline, before theseinterventions, the immediate effects [first 5 cardiac cycles(SD), P values refer to MM 40compared with breath holds] of apnea, MM 20, and MM 40 were, for left ventricular (LV) systolic transmural pressure (Ptm), 1.0 ± 1.9, 7.2 ± 3.5, and 11.3 ± 6.8 mmHg(P < 0.01); for systolic bloodpressure (SBP), 2.9 ± 2.6, 5.5 ± 3.4, and 12.1 ± 6.8 mmHg (P < 0.01); and forstroke volume (SV) index, 0.4 ± 2.8, 4.1 ± 2.8, and6.9 ± 2.3 ml/m2(P < 0.001), respectively.Corresponding values over the last five cardiac cycles were for LVPtm6.4 ± 4.4, 5.4 ± 6.6, and 4.5 ± 9.1 mmHg (P < 0.01); for SBP6.9 ± 4.2, 8.2 ± 7.7, and 24.2 ± 6.9 mmHg (P < 0.01); and for SVindex 0.4 ± 2.1, 5.2 ± 2.8, and 9.2 ± 4.8 ml/m2(P < 0.001), respectively.Thus, in CHF patients, the initial hemodynamic response to thegeneration of negative intrathoracic pressure includes an immediateincrease in LV afterload and an abrupt fall in SV. The magnitude ofresponse is proportional to the intensity of the MM stimulus. By theend of a 15-s MM 40, LVPtm falls below baseline values, yet SVand SBP do not recover. Thus, when 40cmH2O intrathoracic pressure issustained, additional mechanisms, such as a drop in LV preload due toventricular interaction, are engaged, further reducing SV. The neteffect of MM 40 was a 33% reduction in SV index (from 27 to 18 ml/min2), and a 21% reductionin SBP (from 121 to 96 mmHg). Obstructive apneas can have adverseeffects on systemic and, possibly, coronary perfusion in CHF throughdynamic mechanisms that are both stimulus and timedependent. 相似文献