Hemodynamic and norepinephrine responses to pacing-induced heart failure in conscious sinoaortic-denervated dogs

Brändle, Marian, Kaushik P. Patel, Wei Wang, andIrving H. Zucker. Hemodynamic and norepinephrine responses topacing-induced heart failure in conscious sinoaortic-denervated dogs.J. Appl. Physiol. 81(4):1855-1862, 1996.The present study was undertaken to determinethe effects of chronic sinoaortic (baroreceptor) denervation (SAD) on the hemodynamic and sympathetic alterations thatoccur in the pacing-induced model of congestive heart failure. Twogroups of dogs were examined: intact(n = 9) and SAD(n = 9). Both groups of dogs werestudied in the control (prepace) state and each week after theinitiation of ventricular pacing at 250 beats/min. After the pacemakerwas turned off, hemodynamic and plasma norepinephrine levels returnedtoward control levels in the prepaced state and after 1 and 2 wk ofpacing. However, by 3 wk all hemodynamic and norepinephrine levelsremained relatively constant over the 10-min observation period withthe pacemaker off. With the pacemaker off, left ventricularend-diastolic pressure went from 2.7 ± 1.4 (SE) mmHg during theprepace state to 23.2 ± 2.9 mmHg in the heart failure state inintact dogs (P < 0.01). Leftventricular end-diastolic pressure increased to 27.1 ± 2.2 mmHgfrom a control level of 4.2 ± 1.9 mmHg in SAD dogs(P < 0.0003). Mean arterial pressuresignificantly decreased in intact and SAD dogs. Resting heart rate wassignificantly higher in SAD dogs and increased to 135.8 ± 8.9 beats/min in intact dogs and 136.1 ± 6.5 beats/min in SAD dogs.There were no significant differences in the hemodynamic parametersbetween intact and SAD dogs after pacing. Plasma norepinephrine wassignificantly lower in intact than in SAD dogs before pacing (197.7 ± 21.6 vs. 320.6 ± 26.6 pg/ml;P < 0.005). In the heart failurestate, plasma norepinephrine increased significantly in both intact(598.3 ± 44.2 pg/ml) and SAD (644.0 ± 64.6 pg/ml) groups. Therewere no differences in the severity or the magnitude of the developedheart failure state in SAD vs. intact dogs. We conclude from these datathat the arterial baroreflex is not the sole mechanism for the increasein sympathetic drive in heart failure.

     

Cardiovascular and humoral responses to sustained muscle metaboreflex activation in humans

Nishiyasu, Takeshi, Nobusuke Tan, Keiko Morimoto, RyokoSone, and Naotoshi Murakami. Cardiovascular and humoral responses to sustained muscle metaboreflex activation in humans.J. Appl. Physiol. 84(1): 116-122, 1998.The cardiovascular and humoral responses to sustained musclemetaboreflex activation were examined in eight male volunteers whilethey performed two 24-min exercise protocols. Each of these consistedof six 1-min bouts of isometric handgrip exercise (the left and righthands being used alternately) at 50% of maximal voluntary contraction;after each bout, there was either 3-min postexercise occlusion(occlusion protocol) or 3-min rest (control protocol). In the occlusionprotocol, mean arterial blood pressure was ~25 mmHg higher thanduring the control protocol, indicating that the muscle metaboreflexwas activated during occlusion. During the control protocol, plasmarenin activity, plasma vasopressin, and adrenocorticotropic hormonevalues were not significantly different from the values at rest. Duringthe occlusion protocol, however, plasma renin activity, plasmavasopressin, and adrenocorticotropic hormone were all significantlyincreased at 25 min. These data demonstrate that, in humans, thesustained activation of the muscle metaboreflex causes the secretion of several hormones originating from different regions.

     

Anatomic distribution of pulmonary vascular compliance

Presson, Robert G., Jr., Said H. Audi, Christopher C. Hanger, Gerald M. Zenk, Richard A. Sidner, John H. Linehan, Wiltz W. Wagner, Jr., and Christopher A. Dawson. Anatomic distribution ofpulmonary vascular compliance. J. Appl.Physiol. 84(1): 303-310, 1998.Previously, thepressure changes after arterial and venous occlusion have been used tocharacterize the longitudinal distribution of pulmonary vascularresistance with respect to vascular compliance using compartmentalmodels. However, the compartments have not been defined anatomically.Using video microscopy of the subpleural microcirculation, we havemeasured the flow changes in ~40-µm arterioles and venules aftervenous, arterial, and double occlusion maneuvers. The quasi-steadyflows through these vessels after venous occlusion permitted anestimation of the compliance in three anatomic segments: arteries >40µm, veins >40 µm, and vessels <40 µm in diameter. We foundthat ~65% of the total pulmonary vascular compliance was in vessels<40 µm, presumably mostly capillaries. The transient portions ofthe pressure and flow data after venous, arterial, and double occlusionwere consistent with most of the arterial compliance being upstreamfrom most of the arterial resistance and most of the venous compliancebeing downstream from most of the venous resistance.

     

Arterial baroreceptors control plasma vasopressin responses to graded hypotension in conscious dogs

We studied the role of cardiac and arterial baroreceptors in the reflex control of arginine vasopressin (AVP) and renin secretion during graded hypotension in conscious dogs. The dogs were prepared with Silastic cuffs on the thoracic inferior vena cava and catheters in the pericardial space. Each experiment consisted of a control period followed by four periods of inferior vena caval constriction, during which mean arterial pressure (MAP) was reduced in increments of approximately 10 mmHg. The hormonal responses were measured in five dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD+CD. The individual slopes relating MAP to plasma AVP and plasma renin activity (PRA) were used to compare the treatment effects using a 2 x 2 factorial analysis. There was a significant (P < 0.01) effect of SAD on the slope relating plasma AVP to MAP but no effect of CD and no SAD x CD interaction. In contrast, the slope relating PRA and MAP was increased (P < 0.05) by SAD but was not affected by CD. These results support the hypothesis that stimulation of AVP secretion in response to graded hypotension is primarily driven by unloading arterial baroreceptors in the dog.     

Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs

Cremona, George, Tim Higenbottam, Motoshi Takao, Edward A. Bower, and Leslie W. Hall. Nature and site of action of endogenousnitric oxide in vasculature of isolated pig lungs. J. Appl. Physiol. 82(1): 23-31, 1997.The site ofaction of endogenous and exogenous nitric oxide (NO) in isolated piglungs was investigated by using arterial, double, and venous occlusion,which allowed precapillary, postcapillary, and venous segments to bepartitioned into arterial, precapillary, postcapillary, and venoussegments. N^G-nitro-L-arginine(L-NNA;10⁵ M) increased resistancein the arterial (35 ± 6.6%, P = 0.003), precapillary (39.3 ± 5.1%,P = 0.001), and venous (18.3 ± 4.8%, P = 0.01) segments,respectively. Sodium nitroprusside(10⁵ M) and NO (80 parts/million) reversed the effects ofL-NNA. Total pulmonary vascularresistance fell with increasing flow, due to a fall in precapillaryresistance and dynamic resistance, and was significantlylower than mean total resistance.L-NNA increased the resistancesbut did not alter the pattern of the pressure-flow relationships. It isconcluded that, in isolated pig lungs, the effect of endogenous NOseems to be dependent on flow in the arterial segment and independentof flow in the precapillary segment, but variation of its release doesnot appear to be fundamental to accommodation to changes in steadyflow.

     

Cardiovascular responses during spontaneous overground locomotion in freely moving decerebrate cats

Sadamoto, Tomoko, and Kanji Matsukawa. Cardiovascularresponses during spontaneous overground locomotion in freely movingdecerebrate cats. J. Appl. Physiol.83(5): 1454-1460, 1997.To examine whether the cerebrum isessential for producing the rapid cardiovascular adjustment at thebeginning of overground locomotion, we examined heart rate (HR), meanarterial blood pressure (MAP), and integrated electromyogram (iEMG) ofthe forelimb triceps brachialis muscle in freely moving decerebratecats during locomotion. Two to four days after decerebration surgeryperformed at the level of the precollicular-premammillary body, theanimals spontaneously produced coordinated overground locomotion,supporting body weight. HR began to increase immediately before theonset of iEMG, and MAP began to rise almost simultaneously with theiEMG onset. Their increases in HR and MAP (24 ± 3 beats/min and 22 ± 4 mmHg) were sustained during locomotion. Sinoaortic denervation(SAD) did not affect the abrupt changes in HR and MAP at the beginningof locomotion (0-4 s from the onset of iEMG), whereas SAD had acontrasting effect during the subsequent period, a decrease in the HRresponse (9 ± 1 beats/min) and an increase in the MAP response (30 ± 3 mmHg). These results suggest that the cerebrum and the rostral part of the diencephalon are not essential for producing the rapid cardiovascular adjustment at the beginning of spontaneous overground locomotion. The arterial baroreflex does not contribute to this rapidadjustment but plays an important role in regulating the cardiovascularresponses during the later period of spontaneous locomotion.

     

Interactive effects of K+, acid, norepinephrine, and ischemia on the heart: implications for exercise

O'Neill, Mark, Claire E. Sears, and David J. Paterson.Interactive effects of K⁺,acid, norepinephrine, and ischemia on the heart: implications forexercise. J. Appl. Physiol. 82(4):1046-1052, 1997.We tested the hypothesis that cardiac ischemiauncouples the beneficial interaction among hyperkalemia, acidosis, andraised plasma catecholamines when these chemicals are changed to mimictheir exercise levels. Potassium chloride, lactic acid, andnorepinephrine (NE) were infused intravenously for 2 min intoanesthetized, artificially ventilated, thoracotomized rabbits duringeither occlusion of the left circumflex artery (3 min;n = 10) or after a period of prolongedischemia (20 min; n = 7) that led to asmall infarction. NE (1 µg · kg¹ · min¹iv) offset the negative cardiac effects of hyperkalemia (up to 8.7 ± 0.7 mM) and acidosis (arterial pH 7.09 ± 0.03) in normal hearts. Cardiac performance was not significantly depressed by eitheracute or chronic ischemia before any infusions. However, the protectiveeffect of NE during acute ischemia or after prolonged ischemia withhyperkalemia and acidosis was substantially reduced. These results showthat cardiac ischemia attenuates the protective action of NE andincreases the depressive effects of hyperkalemia and acidosis. Whethermyocardial ischemia amplifies the cardiotoxic effects of hyperkalemiaand acidosis during vigorous exercise by attenuating the beneficialeffect of catecholamines remains to be determined.

     

Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712-717, 1997.Ten patients with preserved inotropic function having adual-chamber (right atrium and right ventricle) pacemaker placed forcomplete heart block were studied. They performed static one-leggedknee extension at 20% of their maximal voluntary contraction for 5 minduring three conditions: 1)atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HRfixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and3) HR fixed at peak exercise rate(DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode),mean arterial pressure (MAP) increased by 25 mmHg with no change instroke volume (SV) or systemic vascular resistance. During DOO-Rest andDOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of aSV-dependent increase in cardiac output (+1.3 and +1.8 l/min,respectively). The increase in SV during DOO-Rest utilized acombination of increased contractility and the Frank-Starling mechanism(end-diastolic volume 118-136 ml). However, during DOO-Ex, agreater left ventricular contractility (end-systolic volume 55-38ml) mediated the increase in SV.

     

Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange

Brimioulle, Serge, Philippe Lejeune, and Robert Naeije.Effects of hypoxic pulmonary vasoconstriction on pulmonary gasexchange. J. Appl. Physiol. 81(4):1535-1543, 1996.Several reports have suggested that hypoxicpulmonary vasoconstriction (HPV) might result in deterioration ofpulmonary gas exchange in severe hypoxia. We therefore investigated theeffects of HPV on gas exchange in normal and diseased lungs. Weincorporated a biphasic HPV stimulus-response curve observed in intactdogs (S. Brimioulle, P. Lejeune, J. L. Vachièry, M. Delcroix, R. Hallemans, and R. Naeije, J. Appl.Physiol. 77: 476-480, 1994) into a 50-compartment lung model (J. B. West, Respir.Physiol. 7: 88-110, 1969) to control the amount ofblood flow directed to each lung compartment according to the localhypoxic stimulus. The resulting model accurately reproduced the bloodgas modifications caused by HPV changes in dogs with acute lung injury.In single lung units, HPV had a moderate protective effect on alveolaroxygenation, which was maximal at near-normal alveolarPO₂ (75-80 Torr), mixed venousPO₂ (35 Torr), andPO₂ at which hemoglobin is 50%saturated (24 Torr). In simulated diseased lungs associated with40-60 Torr arterial PO₂,however, HPV increased arterial PO₂ by 15-20 Torr. We conclude that HPV can improve arterialoxygenation substantially in respiratory failure.

     

Suppressive action of endogenous adenosine on ovine fetal nonshivering thermogenesis

Ball, Karen T., Tania R. Gunn, Peter D. Gluckman, and GordonG. Power. Suppressive action of endogenous adenosine on ovinefetal nonshivering thermogenesis. J. Appl.Physiol. 81(6): 2393-2398, 1996.Nonshiveringthermogenesis is not initiated when the fetal sheep is cooled in uterobut appears to require the removal of an inhibitor of placental originat birth. To test whether adenosine is such an inhibitor, we examinedthe effect of the adenosine antagonist theophylline on the initiationof nonshivering thermogenesis during sequential cooling, ventilation, and umbilical cord occlusion in utero. Theophylline (18 mg/kg bolus and0.6 mg ^· kg^{1 ·} min¹thereafter) was infused for 90 min before and 90 min after cord occlusion. Theophylline enhanced the nonshivering thermogenic freefatty acid (FFA) and glycerol responses before cord occlusion, raisingFFA concentrations 99% to 415 ± 60 µeq/l(P < 0.01) and glycerol levels 87%to 526 ± 135 µmol/l (P < 0.05). These FFA (P < 0.001) andglycerol (P < 0.05) concentrationswere significantly greater than the corresponding period during thebirth-simulation control. Umbilical cord occlusion did not alter FFAlevels but induced a 41% rise in glycerol concentrations to 774 ± 203 µmol/l (P < 0.05). Theincreases in nonshivering thermogenic indexes after the administrationof the adenosine-receptor antagonist suggest that the quiescent stateof ovine fetal brown adipose tissue may result, in part, from the tonicinhibitory actions of adenosine and that a decrease in adenosineconcentrations enhances nonshivering thermogenesis. However, thefurther rise after umbilical cord occlusion suggests that at least oneother inhibitor of placental origin inhibits nonshivering thermogenesisbefore birth.

     

Neuromuscular fatigue after maximal stretch-shortening cycle exercise

Strojnik, V., and P. V. Komi. Neuromuscular fatigueafter maximal stretch-shortening cycle exercise. J. Appl. Physiol. 84(1): 344-350, 1998.To examinesome possible sites of fatigue during short-lasting maximally intensivestretch-shortening cycle exercise, drop jumps on an inclined sledgeapparatus were analyzed. Twelve healthy volunteers performed jumpsuntil they were unable to maintain jumping height >90% of theirmaximum. After the workout, the increases in the blood lactateconcentration and serum creatine kinase activation were statisticallysignificant (P < 0.001 and P < 0.05, respectively) but rathersmall in physiological terms. The major changes after the workout wereas follows: the single twitch was characterized by smaller peak torque(P < 0.05) and shorter time to peak(P < 0.05) and half-relaxation time(P < 0.01). The double-twitch torqueremained at the same level (P > 0.05), but with a steeper maximal slope of torque rise(P < 0.05); during 20- and 100-Hzstimulation the torque declined (both P < 0.01) and the maximal voluntarytorque changed nonsignificantly but with a smaller maximal slope oftorque rise (P < 0.01) and a higheractivation level (P < 0.05),accompanied by an increased electromyogram amplitude. These findingsindicate that the muscle response after the short-lasting consecutivemaximum jumps on the sledge apparatus may involve two distinctmechanisms acting in opposite directions:1) The contractile mechanism seemsto be potentiated through a shorterCa²⁺ transient and fastercross-bridge cycling, as implied by twitch changes.2) High-frequency action potentialpropagation shows an impairment, which is suggested as the possibledominant reason for fatigue in exercise of this type.

     

Greater airway narrowing in immature than in mature rabbits during methacholine challenge

Shen, X., V. Bhargava, G. R. Wodicka, C. M. Doerschuk, S. J. Gunst, and R. S. Tepper. Greater airway narrowing in immature thanin mature rabbits during methacholine challenge. J. Appl. Physiol. 81(6): 2637-2643, 1996.It hasbeen demonstrated that methacholine (MCh) challenge produces a greaterincrease in lung resistance in immature than in mature rabbits (R. S. Tepper, X. Shen, E. Bakan, and S. J. Gunst.J. Appl. Physiol. 79: 1190-1198, 1995). To determine whether this maturational difference in the response to MCh was primarily related to changes in airway resistance (Raw) or changes in tissue resistance, we assessed airway narrowing in1-, 2-, and 6-mo-old rabbits during intravenous MCh challenge (0.01-5.0 mg/kg). Airway narrowing was determined frommeasurements of Raw in vivo and from morphometric measurements on lungsections obtained after rapidly freezing the lung after the MChchallenge. The fold increase in Raw was significantly greater for 1- and 2-mo-old animals than for 6-mo-old animals. Similarly, the degree of airway narrowing assessed morphometrically was significantly greaterfor 1- and 2-mo-old animals than for 6-mo-old animals. The foldincrease in Raw was highly correlated with the degree of airwaynarrowing assessed morphometrically(r² = 0.82, P < 0.001). We conclude that thematurational difference in the effect of MCh on lung resistance isprimarily caused by greater airway narrowing in the immature rabbits.

     

Role of endogenous female hormones in hypoxic chemosensitivity

Tatsumi, Koichiro, Cheryl K. Pickett, Christopher R. Jacoby,John V. Weil, and Lorna G. Moore. Role of endogenous female hormones in hypoxic chemosensitivity. J. Appl.Physiol. 83(5): 1706-1710, 1997.Effective alveolar ventilation and hypoxicventilatory response (HVR) are higher in females than in males andafter endogenous or exogenous elevation of progesterone and estrogen.The contribution of normal physiological levels of ovarian hormones toresting ventilation and ventilatory control and whether their site(s) of action is central and/or peripheral are unclear.Accordingly, we examined resting ventilation, HVR, and hypercapnicventilatory responses (HCVR) before and 3 wk after ovariectomy in fivefemale cats. We also compared carotid sinus nerve (CSN) and centralnervous system translation responses to hypoxia in 6 ovariectomized and 24 intact female animals. Ovariectomy decreased serum progesterone butdid not change resting ventilation, end-tidalPCO₂, or HCVR (allP = NS). Ovariectomy reduced theHVR shape parameter A in the awake(38.9 ± 5.5 and 21.2 ± 3.0 before and after ovariectomy, respectively, P < 0.05) andanesthetized conditions. The CSN response to hypoxia was lower inovariectomized than in intact animals (shape parameterA = 22.6 ± 2.5 and 54.3 ± 3.5 in ovariectomized and intact animals, respectively,P < 0.05), but central nervous system translation of CSN activity into ventilation was similar inovariectomized and intact animals. We concluded that ovariectomy decreased ventilatory and CSN responsiveness to hypoxia, suggesting that the presence of physiological levels of ovarian hormones influences hypoxic chemosensitivity by acting primarily at peripheral sites.

     

Prior eccentric contractions impair maximal insulin action on muscle glucose uptake in the conscious rat

Asp, Sven, Allan Watkinson, Nicholas D. Oakes, and Edward W. Kraegen. Prior eccentric contractions impair maximal insulin action on muscle glucose uptake in the conscious rat.J. Appl. Physiol. 82(4):1327-1332, 1997.Our aim was to examine the effect of prioreccentric contractions on insulin action locally in muscle in theintact conscious rat. Anesthetized rats performed one-leg eccentriccontractions through the use of calf muscle electrical stimulationfollowed by stretch of the active muscles. Two days later, basal andeuglycemic clamp studies were conducted with the rats in the awakefasted state. Muscle glucose metabolism was estimated from2-[¹⁴C(U)]deoxy-D-glucoseandD-[3-³H]glucose administration, and comparisons were made between the eccentrically stimulated and nonstimulated (control) calfmuscles. At midphysiological insulin levels, effects ofprior eccentric exercise on muscle glucose uptake were notstatistically significant. Maximal insulin stimulation revealed reducedincremental glucose uptake above basal(P < 0.05 in the red gastrocnemius;P < 0.1 in the white gastrocnemiusand soleus) and impaired net glycogen synthesis in all eccentricallystimulated muscles (P < 0.05). Weconclude that prior eccentric contractions impair maximal insulin action (responsiveness) on local muscle glucose uptake and glycogen synthesis in the conscious rat.

     

Neuromuscular factors contributing to in vivo eccentric moment generation

Webber, Sandra, and Dean Kriellaars. Neuromuscularfactors contributing to in vivo eccentric moment generation.J. Appl. Physiol. 83(1): 40-45, 1997.Muscle series elasticity and its contribution to eccentricmoment generation was examined in humans. While subjects [male,n = 30; age 26.3 ± 4.8 (SD) yr; body mass 78.8 ± 13.1 kg] performed an isometric contractionof the knee extensors at 60° of knee flexion, a quick stretch was imposed with a 12°-step displacement at 100°/s. The test wasperformed at 10 isometric activation levels ranging from 1.7 to 95.2%of maximal voluntary contraction (MVC). A strong linear relationship was observed between the peak imposed eccentric moment derived fromquick stretch and the isometric activation level(y = 1.44x + 7.08; r = 0.99). This increase in theeccentric moment is consistent with an actomyosin-dependent elasticitylocated in series with the contractile element of muscle. Byextrapolating the linear relationship to 100% MVC, the predictedmaximum eccentric moment was found to be 151% MVC, consistent with invitro data. A maximal voluntary, knee extensor strength test was alsoperformed (5-95°, 3 repetitions, ±50, 100, 150, 200, and250°/s). The predicted maximum eccentric moment was 206% of theangle- and velocity-matched, maximal voluntary eccentric moments. Thiswas attributed to a potent neural regulatory mechanism that limits therecruitment and/or discharge of motor units during maximalvoluntary eccentric contractions.

     

Reflex tracheal smooth muscle contraction and bronchial vasodilation evoked by airway cooling in dogs

Pisarri, Thomas E., and Gordon G. Giesbrecht. Reflextracheal smooth muscle contraction and bronchial vasodilation evoked byairway cooling in dogs. J. Appl.Physiol. 82(5): 1566-1572, 1997.Coolingintrathoracic airways by filling the pulmonary circulation with coldblood alters pulmonary mechanoreceptor discharge. To determine whetherthis initiates reflex changes that could contribute to airwayobstruction, we measured changes in tracheal smooth muscle tension andbronchial arterial flow evoked by cooling. In ninechloralose-anesthetized open-chest dogs, the right pulmonary artery wascannulated and perfused; the left lung, ventilated separately, providedgas exchange. With the right lung phasically ventilated, filling theright pulmonary circulation with 5°C blood increased smooth muscletension in an innervated upper tracheal segment by 23 ± 6 (SE) gfrom a baseline of 75 g. Contraction began within 10 s of injection andwas maximal at ~30s. The response was abolished by cervical vagotomy.Bronchial arterial flow increased from 8 ± 1 to 13 ± 2 ml/min, withlittle effect on arterial blood pressure. The time course wassimilar to that of the tracheal response. This response was greatlyattenuated after cervical vagotomy. Blood at 20°C also increasedtracheal smooth muscle tension and bronchial flow, whereas 37°Cblood had little effect. The results suggest that alteration ofairway mechanoreceptor discharge by cooling can initiate reflexes thatcontribute to airway obstruction.

     

Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip

Mostoufi-Moab, Sogol, Eric J. Widmaier, Jacob A. Cornett,Kristen Gray, and Lawrence I. Sinoway. Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip. J. Appl. Physiol. 84(1): 277-283, 1998.We examined the effects of unilateral, nondominant forearmtraining (4 wk) on blood pressure and forearm metabolites duringischemic and nonischemic rhythmic handgrip (30 1-s contractions/min at25% maximal voluntary contraction). Contractions were performed by 10 subjects with the forearm enclosed in a pressurized Plexiglas tank toinduce ischemic conditions. Training increased the endurance time inthe nondominant arm by 102% (protocol1). In protocol 2,tank pressure was increased in increments of 10 mmHg/min to +50 mmHg.Training raised the positive-pressure threshold necessary to engage thepressor response. In protocol 3,handgrip was performed at +50 mmHg and venous blood samples wereanalyzed. Training attenuated mean arterial pressure (109 ± 5 and98 ± 4 mmHg pre- and posttraining, respectively, P < 0.01), venous lactate (2.9 ± 0.4 and 1.8 ± 0.3 mmol/l pre- and posttraining, respectively,P < 0.01), and the pH response (7.21 ± 0.02 and 7.25 ± 0.01, pre- and posttraining, respectively, P < 0.01). However, deep venousO₂ saturation was unchanged.Training increased the positive-pressure threshold for metaboreceptorengagement, reduced metabolite concentrations, and reduced meanarterial pressure during ischemic exercise.

     

Ultrasound Doppler estimates of femoral artery blood flow during dynamic knee extensor exercise in humans

Rådegran, G. Ultrasound Dopplerestimates of femoral artery blood flow during dynamic knee extensorexercise in humans. J. Appl. Physiol.83(4): 1383-1388, 1997.Ultrasound Doppler has been used tomeasure arterial inflow to a human limb during intermittent staticcontractions. The technique, however, has neither been thoroughlyvalidated nor used during dynamic exercise. In this study, the inherentproblems of the technique have been addressed, and the accuracy wasimproved by storing the velocity tracings continuously and calculatingthe flow in relation to the muscle contraction-relaxation phases. Thefemoral arterial diameter measurements were reproducible with a meancoefficient of variation within the subjects of 1.2 ± 0.2%. Thediameter was the same whether the probe was fixed or repositioned atrest (10.8 ± 0.2 mm) or measured during dynamic exercise. The bloodvelocity was sampled over the width of the diameter and the parabolicvelocity profile, since sampling in the center resulted in anoverestimation by 22.6 ± 9.1% (P < 0.02). The femoral arterial Doppler blood flow increased linearly(r = 0.997, P < 0.001) with increasing load [Doppler blood flow = 0.080 · load (W) + 1.446 l/min] and was correlated positively with simultaneousthermodilution venous outflow measurements(r = 0.996, P < 0.001). The two techniques werelinearly related (Doppler = thermodilution · 0.985 + 0.071 l/min; r = 0.996, P < 0.001), with a coefficient ofvariation of ~6% for both methods.

     

Changes in regional lung mechanics and ventilation distribution after unilateral pulmonary artery occlusion

Simon, Brett A., Koichi Tsuzaki, and Jose G. Venegas.Changes in regional lung mechanics and ventilation distribution after unilateral pulmonary artery occlusion. J. Appl.Physiol. 82(3): 882-891, 1997.Regionalpneumoconstriction induced by alveolar hypocapnia is an importanthomeostatic mechanism for optimization of ventilation-perfusionmatching. We used positron imaging of ¹³NN-equilibrated lungs to measurethe distribution of regional tidal volume(VT), lung volume(VL), and lung impedance(Z) before and after left (L)pulmonary artery occlusion (PAO) in eight anesthetized, open-chestdogs. Measurements were made during eucapnic sinusoidal ventilation at0.2 Hz with 4-cmH₂O positive end expiratory pressure. Right(R) and L lung impedances(ZRandZL)were determined from carinal pressure and positron imaging of dynamicregional VL. LPAO caused anincrease in|ZL|relative to|ZR|,resulting in a shift in VT awayfrom the PAO side, with a L/R|Z| ratio changing from 1.20 ± 0.07 (mean ± SE) to 2.79 ± 0.85 after LPAO(P < 0.05). Although mean L lungVL decreased slightly, theVL normalized parametersspecific admittance and specific compliance both significantly decreased with PAO. Lung recoil pressure at 50% totallung capacity also increased after PAO. We conclude that PAO results inan increase in regional lung Z thatshifts ventilation away from the affected area at normal breathingfrequencies and that this effect is not due to a change inVL but reflects mechanicalconstriction at the tissue level.

     

Sidestream smoke exposure enhances rapidly adapting receptor responses to substance P in young guinea pigs

Bonham, A. C., K. S. Kott, and J. P. Joad. Sidestreamsmoke exposure enhances rapidly adapting receptor responses to substance P in young guinea pigs. J. Appl.Physiol. 81(4): 1715-1722, 1996.We determinedthe effect of sidestream tobacco smoke (SS) exposure on responses oflung rapidly adapting receptors (RARs), peak tracheal pressure (Ptr),and arterial blood pressure (ABP) to substance P in young guinea pigs.Guinea pigs were exposed to SS or filtered air fromday 8 to days41-45 of life. They were then anesthetized andgiven three doses of intravenous substance P (1.56-4.94 nmol/kg).SS exposure augmented substance P-evoked increases in RAR activity(P = 0.029 by analysis of variance) but not substance P-evoked increases in peak Ptr or decreases in ABP.Neurokinin 1-receptor blockade (CP-96345, 400 nmol/kg) attenuatedsubstance P-evoked increases in RAR activity(P = 0.001) and ABP(P = 0.009) but not in peak Ptr(P = 0.06). Thus chronic exposure toSS in young guinea pigs exaggerates RAR responsiveness to substance P. The findings may help explain the increased incidence of airwayhyperresponsiveness and cough in children chronically exposed toenvironmental tobacco smoke.