首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 15 毫秒
1.
Neurotoxinmicroinjected into the retrotrapezoid nucleus of anesthetized ratsdecreases phrenic activity and eliminates the response toCO2. In unanesthetized rats, suchtreatment has no effect on awake, resting breathing and decreasesCO2 sensitivity by 40% (M. Akilesh, M. Kamper, A. Li, and E. E. Nattie. J. Appl. Physiol. 82: 469-479, 1997). One important factorin explaining these disparate results is the actual size of theanatomic lesion. In the present study, we injected ibotenic acid intothe retrotrapezoid nucleus of anesthetized rats and evaluated lesionsize by using two new approaches: 1)DEAD red, a fluorescent probe that enters impaired cells through leakymembranes and binds to nucleic acids, and2) conjugation of toxin tofluorescent beads. With the use of DEAD red, the region containinglabeled dying cells was 313 ± 104 nl(n = 4), six times larger than theinitial injected volume, and the physiological effects on phrenicamplitude, the CO2 response, andblood pressure began within minutes and were substantial. Withconjugated toxin, in theory, neuronal damage would be limited to theregion of detectable fluorescence (49 ± 10 nl;n = 4). Effects on phrenicamplitude, CO2 sensitivity, andblood pressure were absent until ~2 h postinjection. Controlexperiments, with 2 h of in vitro incubation of theneurotoxin-microbead conjugate and injection of the supernatant aftercentrifugation, showed similar results that suggest release ofconjugated neurotoxin. We conclude that DEAD red provides a usefulmeans to monitor neuronal impairment in acute studies in vivo.Conjugation of neurotoxin to microbeads may be less reliable in this regard.

  相似文献   

2.
Li, Aihua, and Eugene E. Nattie. Focal centralchemoreceptor sensitivity in the RTN studied with aCO2 diffusion pipette in vivo.J. Appl. Physiol. 83(2): 420-428, 1997.We describe and use a CO2diffusion pipette to produce a quickly reversible focal acidosis in theretrotrapezoid nucleus region of the rat brain stem. No tissueinjection is made. Instead, artificial cerebrospinal fluid (aCSF)equilibrated with CO2 circulateswithin the micropipette, providing a source for continuedCO2 diffusion into the tissue fromthe pipette tip. Tissue pH electrodes show the acidosis is limited to500 µm from the tip. In controls (aCSF equilibrated with air), 1-minpipette perfusions increased tissue pH slightly and decreased phrenicnerve amplitude. In moderate- andhigh-CO2 groups (aCSF equilibratedwith 50 or 100% CO2), 1-minperfusions significantly decreased tissue pH and increased phrenicnerve amplitude in a dose-dependent manner. The responses developed andreversed within minutes. Compared with our prior use of medullary acetazolamide injections to produce a focal acidosis, in this approachthe acidosis 1) arises and reversesquickly and 2) its intensity can bevaried. This allows study of sensitivity and mechanism. We concludefrom this initial experiment that retrotrapezoid nucleus regionchemoreceptors operate within the normal physiological range ofCO2-induced tissue pH changes.

  相似文献   

3.
Important role of carotid afferents in control of breathing   总被引:5,自引:0,他引:5  
The purpose of the present study was todetermine the effect on breathing in the awake state of carotid bodydenervation (CBD) over 1-2 wk after denervation. Studies werecompleted on adult goats repeatedly before and1) for 15 days after bilateral CBD (n = 8),2) for 7 days after unilateral CBD(n = 5), and3) for 15 days after sham CBD(n = 3). Absence of ventilatorystimulation when NaCN was injected directly into a common carotidartery confirmed CBD. There was a significant(P < 0.01) hypoventilation during the breathing of room air after unilateral and bilateral CBD. Themaximum PaCO2 increase (8 Torr forunilateral and 11 Torr for bilateral) occurred ~4 days afterCBD. This maximum was transient because by 7 (unilateral)to 15 (bilateral) days after CBD, PaCO2 was only 3-4 Torr above control.CO2 sensitivity was attenuated from control by 60% on day 4 afterbilateral CBD and by 35% on day 4 after unilateral CBD. This attenuation was transient, because CO2 sensitivity returned tocontrol temporally similar to the return ofPaCO2 during the breathing of room air.During mild and moderate treadmill exercise 1-8 days afterbilateral CBD, PaCO2 was unchanged fromits elevated level at rest, but, 10-15 days after CBD,PaCO2 decreased slightly from restduring exercise. These data indicate that1) carotid afferents are animportant determinant of rest and exercise breathing and ventilatoryCO2 sensitivity, and2) apparent plasticity within theventilatory control system eventually provides compensation for chronicloss of these afferents.

  相似文献   

4.
Honda, Y., H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. Effect of priorO2 breathing on ventilatoryresponse to sustained isocapnic hypoxia in adult humans.J. Appl. Physiol. 81(4):1627-1632, 1996.Sixteen healthy volunteers breathed 100%O2 or room air for 10 min in random order, then their ventilatory response to sustained normocapnic hypoxia (80% arterial O2saturation, as measured with a pulse oximeter) was studied for 20 min.In addition, to detect agents possibly responsible for the respiratorychanges, blood plasma of 10 of the 16 subjects was chemically analyzed.1) Preliminary O2 breathing uniformly andsubstantially augmented hypoxic ventilatory responses.2) However, the profile ofventilatory response in terms of relative magnitude, i.e., biphasichypoxic ventilatory depression, remained nearly unchanged.3) Augmented ventilatory incrementby prior O2 breathing wassignificantly correlated with increment in the plasma glutamine level.We conclude that preliminary O2administration enhances hypoxic ventilatory response without affectingthe biphasic response pattern and speculate that the excitatory aminoacid neurotransmitter glutamate, possibly derived from augmentedglutamine, may, at least in part, play a role in this ventilatoryenhancement.

  相似文献   

5.
Diving isknown to induce a change in the amplitude of the T wave(ATw) ofelectrocardiograms, but it is unknown whether this is linked to achange in cardiovascular performance. We analyzed ATw in guinea pigs at 10-60atm and 25-36°C, breathing 2%O2 in either helium (heliox;n = 10) or hydrogen (hydrox;n = 9) for 1 h at each pressure. Coretemperature and electrocardiograms were detected by using implantedradiotelemeters. O2 consumption rate was measured by using gas chromatography. In a previous study (S. R. Kayar and E. C. Parker. J. Appl.Physiol. 82: 988-997, 1997), we analyzed theO2 pulse, i.e., theO2 consumption rate per heartbeat, in the same animals. By multivariate regression analysis, weidentified variables that were significant toO2 pulse: body surface area,chamber temperature, core temperature, and pressure. In this study,inclusion of ATw made asignificantly better model with fewer variables. After normalizing forchamber temperature and pressure, theO2 pulse increased with increasing ATw in heliox(P = 0.001) but with decreasingATw in hydrox(P < 0.001). ThusATw is associated with thedifferences in O2 pulse foranimals breathing heliox vs. hydrox.

  相似文献   

6.
Effect of different levels of hyperoxia on breathing in healthy subjects   总被引:1,自引:0,他引:1  
Becker, Heinrich F., Olli Polo, Stephen G. McNamara, MichaelBerthon-Jones, and Colin E. Sullivan. Effect of different levelsof hyperoxia on breathing in healthy subjects. J. Appl. Physiol. 81(4): 1683-1690, 1996.Wehave recently shown that breathing 50%O2 markedly stimulates ventilationin healthy subjects if end-tidal PCO2(PETCO2) ismaintained. The aim of this study was to investigate apossible dose-dependent stimulation of ventilation byO2 and to examine possiblemechanisms of hyperoxic hyperventilation. In eight normalsubjects ventilation was measured while they were breathing 30 and 75%O2 for 30 min, withPETCO2 being held constant.Acute hypercapnic ventilatory responses were also tested in thesesubjects. The 75% O2 experimentwas repeated without controllingPETCO2 in 14 subjects, andin 6 subjects arterial blood gases were taken at baseline and at theend of the hyperoxia period. Minute ventilation(I) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75%O2 without any control onPETCO2 led toa 16% increase inI, butPETCO2 decreased by3.6 Torr (9%). There was a linear correlation(r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, withI more than doubling after 30 min of75% O2. If isocapnia is notmaintained, hyperventilation is attenuated by a decrease in arterialPCO2. There is a correlation betweenhyperoxic and hypercapnic ventilatory responses. On the basis of datafrom the literature, we concluded that the Haldane effect seems to bethe major cause of hyperventilation duringboth isocapnic and poikilocapnichyperoxia.

  相似文献   

7.
Babb, T. G. Ventilatory response to exercise insubjects breathing CO2 orHeO2.J. Appl. Physiol. 82(3): 746-754, 1997.To investigate the effects of mechanical ventilatory limitationon the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycleergometry to exhaustion once while breathing room air; once whilebreathing 3% CO2-21%O2-balanceN2; and once while breathing HeO2 (79% He and 21%O2). Minute ventilation(E) and respiratory mechanics weremeasured continuously during each 1-min increment in work rate (10 or20 W). Data were analyzed at rest, at ventilatory threshold (VTh),and at maximal exercise. When the subjects were breathing 3%CO2, there was an increase(P < 0.001) inE at rest and at VTh but not duringmaximal exercise. When the subjects were breathingHeO2,E was increased(P < 0.05) only during maximalexercise (24 ± 11%). The ventilatory response to exercise belowVTh was greater only when the subjects were breathing 3% CO2(P < 0.05). Above VTh, theventilatory response when the subjects were breathingHeO2 was greater than whenbreathing 3% CO2(P < 0.01). Flow limitation, aspercent of tidal volume, during maximal exercise was greater(P < 0.01) when the subjects werebreathing CO2 (22 ± 12%) thanwhen breathing room air (12 ± 9%) or when breathingHeO2 (10 ± 7%)(n = 7). End-expiratory lung volumeduring maximal exercise was lower when the subjects were breathingHeO2 than when breathing room airor when breathing CO2(P < 0.01). These data indicate thatolder subjects have little reserve for accommodating an increase inventilatory demand and suggest that mechanical ventilatory constraintsinfluence both the magnitude of Eduring maximal exercise and the regulation ofE and respiratory mechanics duringheavy-to-maximal exercise.

  相似文献   

8.
Thyrotropin-releasing hormone (TRH) injected into the retrotrapezoid nucleus (RTN) of anesthetized rats produces a large, prolonged stimulation of ventilatory output (C. L. Cream, A. Li, and E. E. Nattie. J. Appl. Physiol. 83: 792-799, 1997). Here we inject or dialyze TRH into the RTN of conscious rats. In 6 of 17 injections (200 nl, 3.1 +/- 1.7 mM), ventilation (VE) increased 31% by 10 min, with recovery by 60 min. With dialysis, each animal of one group (n = 5) received, in random order, 10 mM TRH, 10 mM TRHOH (a metabolite of TRH), and artificial cerebrospinal fluid (aCSF); each animal of a second group (n = 5) received aCSF and 1 mM TRH. TRHOH and aCSF had no sustained effects. TRH (1 mM) increased VE (32%, P < 0.02, by 10 min, with recovery by 60 min), O(2) consumption (VO(2); 19%, P < 0. 03), and body (rectal) temperature (T(re); 0.5 degrees C, P < 0.09). TRH (10 mM) increased VE (78%, P < 0.01, by 10 min, with no recovery at 60 min), VO(2) (48%, P < 0.01), and T(re) (1.0 degrees C, P < 0. 01). TRH also induced arousal. The tissue volume affected in dialysis, estimated by spread of dialyzed fluorescein (332.3 mol wt, mol wt of TRH = 362.4), was 1,580 +/- 256 nl for 10 mM (n = 5) and 590 +/- 128 nl for 1 mM (n = 5). We conclude that 1) the RTN is involved in the integration of VE, VO(2), T(re), and arousal and 2) TRH may establish the responsiveness of RTN neurons.  相似文献   

9.
Canet, Emmanuel, Jean-Paul Praud, and Michel A. Bureau.Periodic breathing induced on demand in awake newborn lamb. J. Appl. Physiol. 82(2): 607-612, 1997.Spontaneous periodic breathing, although a common feature infullterm and preterm human infants, is scarce in other newborn mammals.The aim of this study was to induce periodic breathing in lambs. Four10-day-old and two <48-h-old awake lambs were instrumented withjugular catheters connected to an extracorporeal membrane lung aimed atcontrolling arterial PCO2(PaCO2). ArterialPO2(PaO2) was set and maintained at thedesired level by changing inspiredO2 fraction and providingO2 through a small catheter intothe "apneic" lung. At a criticalPaO2/PaCO2combination, the four 10-day-old lambs exhibited periodic breathingthat could be initiated, terminated, and reinitiated on demand. In the2-day-old lambs with low chemoreceptor gain, periodic breathing washardly seen, regardless of the trials done to find the criticalPO2/PCO2combination. We conclude that periodic breathing can be induced inlambs and depends on criticalPaO2/PaCO2combinations and maturity of the chemoreceptors.

  相似文献   

10.
Nattie, Eugene E., and Aihua Li. Centralchemoreception in the region of the ventral respiratory group in therat. J. Appl. Physiol. 81(5):1987-1995, 1996.We injected acetazolamide (AZ; 5 × 106 M, 1 nl) into theregion of the ventral respiratory group (VRG) of anesthetized paralyzedventilated rats. Control injections (mock cerebrospinal fluid,n = 6, or the inactive AZ analogue 2-acetylamino-1,3,4-thiadiazole-5-sulfon-t-butylamide,n = 6) did not increase the integratedphrenic neurogram [phrenic nerve amplitude (PNA)]. The AZinjections produced a focal region of tissue acidosis with a radius < 300-400 µm and are used as a probe for sites of centralchemosensitivity. Injection location is determined by anatomicanalysis. Of 22 VRG injections of AZ, 14 increased the amplitude of thePNA over 15-90 min; 8 had no effect. In 17 cases, we measuredmedullary tissue pH at the injection center and/or at a distantsite and reaffirmed the size of the acidotic region produced by suchsmall AZ injections. Of injections with pH electrodes within300-400 µm of the injection center, all responders showed anacid pH; three nonresponders showed an acid pH, and one an alkaline pH.In a subgroup of five rats, at VRG sites with known respiratory effectsidentified by prior glutamate injection (10 nl, 100 mM), all subsequentAZ injections produced a PNA response. Simultaneous measurement of PNAand tissue pH responses at the injection center of eight rats did notshow a uniform correlation in time; initially, both changed with asimilar time course, but PNA recovered more quickly. We conclude that1) the region of the VRG containssites of ventilatory chemoreception,2) ineffective AZ injections doproduce a tissue acidosis but at sites with minimal impact onbreathing, and 3) tissuepH does not uniquely represent the chemoreceptor stimulus.

  相似文献   

11.
We sought to determine whether chronic exposure tointermittent hypoxia (CIH) increases sympathetic responsiveness tosubsequent chemoreflex stimulation. Sprague-Dawley rats were exposed to30 days of CIH: exposure chamber%O2 [fractionalconcentration of chamber O2(FcO2)]nadir 6.5-7% with return to 21% each minute for 8 h/day duringthe diurnal sleep period (Exp group). Sham controls (SC group) weresimilarly handled but kept at 21%FcO2 andcompared with unhandled controls (UC group). Rats were then anesthetized with urethan, and preganglionic cervical sympathetic activity (CSA), diaphragm electromyogram, arterial pressure, and electrocardiogram were recorded while the rats were spontaneously breathing 100% O2, room air, 10%O2, 12%CO2, and 10%O2-12%CO2. CSA and heart rate were alsorecorded during phenylephrine infusion to assess baroreceptor function.Mean arterial pressure was significantly greater in Exp than in SC andUC rats during all conditions (P < 0.05). A vasopressor response to 10%O2-12%CO2 was observed only in Exp rats.CSA was greater in Exp than in SC and UC rats during 10%O2, 12%CO2, and 10%O2-12%CO2 but not during room-air exposure. A significant increase in CSA compared with room air wasnoted during 10% O2, 12%CO2, and 10%O2-12%CO2 in Exp but not in SC or UCrats. No differences in baroreceptor function were observed amonggroups. We conclude that CIH leads to increased sympatheticresponsiveness to chemoreflex stimulation.

  相似文献   

12.
Crawford, Paul, Peter A. Good, Eric Gutierrez, Joshua H. Feinberg, John P. Boehmer, David H. Silber, and Lawrence I. Sinoway. Effects of supplemental oxygen on forearm vasodilation in humans.J. Appl. Physiol. 82(5):1601-1606, 1997.Supplemental O2 reduces cardiac output andraises systemic vascular resistance in congestive heart failure. Inthis study, 100% O2 was given tonormal subjects and peak forearm flow was measured. Inexperiment 1, 100%O2 reduced blood flow andincreased resistance after 10 min of forearm ischemia (flow 56.7 ± 7.9 vs. 47.8 ± 6.7 ml · min1 · 100 ml1;P < 0.02; vascular resistance 1.7 ± 0.2 vs. 2.4 ± 0.4 mmHg · min · 100 ml · ml1;P < 0.03). Inexperiment 2, lower body negativepressure (LBNP; 30 mmHg) and venous congestion (VC) simulatedthe high sympathetic tone and edema of congestive heart failure.Postischemic forearm flow and resistance were measured under fourconditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100%O2+LBNP+VC. LBNP and VC did notlower peak flow. However, O2raised minimal resistance (2.3 ± 0.4 RA; 2.8 ± 0.5 O2+LBNP+VC,P < 0.04). When O2 alone(experiment 1) was compared withO2+LBNP+VC(experiment 2), no effect of LBNP+VCon peak flow or minimum resistance was noted, although the return rateof flow and resistance toward baseline was increased.O2 reduces peak forearm flow evenin the presence of LBNP and VC.

  相似文献   

13.
Albert, T. S. E., V. L. Tucker, and E. M. Renkin. Acutealveolar hypoxia increases blood-to-tissue albumin transport: role ofatrial natriuretic peptide. J. Appl.Physiol. 82(1): 111-117, 1997.Plasmaimmunoreactive atrial natriuretic peptide (irANP) and blood-to-tissueclearance of 131I-labeled ratserum albumin (CRSA) wereexamined in anesthetized rats during hypoxic ventilation(n = 5-7/group). Hypoxia (10 min) increased irANP from 211 ± 29 (room air) to 229 ± 28 (15%O2, not significant), 911 ± 205 (10% O2), and 4,374 ± 961 pg/ml (8% O2),respectively. Graded increases inCRSA were significant at 8%O2 in fat (3.6-fold), ileum(2.2-fold), abdominal muscles (2.0-fold), kidney (1.8-fold), andjejunum (1.4-fold). CRSA wasdecreased in back skin and testes; heart, brain, and lungs wereunaffected. The increases in CRSAwere related to irANP and not to arterial PO2. Circulating plasma volume wasnegatively correlated with whole bodyCRSA. Graded increases inextravascular water content (EVW) were found in the kidney, left heart,and cerebrum and were positively related toCRSA in the kidney. EVW decreased in gastrointestinal tissues; the magnitude was inversely related toCRSA. We conclude that ANP-inducedprotein extravasation contributes to plasma volume contraction duringacute hypoxia.

  相似文献   

14.
Kayar, Susan R., and Erich C. Parker. Oxygen pulse inguinea pigs in hyperbaric helium and hydrogen. J. Appl. Physiol. 82(3): 988-997, 1997.We analyzedO2 pulse, the total volume of O2 consumed per heart beat, inguinea pigs at pressures from 10 to 60 atmospheres. Animals were placedin a hyperbaric chamber and breathed 2%O2 in either helium (heliox) orhydrogen (hydrox). Oxygen consumption rate(O2) was measured by gaschromatographic analysis. Core temperature and heart rate were measuredby using surgically implanted radiotelemeters. TheO2 was modulated over afourfold range by varying chamber temperature from 25 to 36°C. There was a direct correlation betweenO2 and heartrate, which was significantly different for animals in heliox vs.hydrox (P = 0.003). By usingmultivariate regression analysis, we identified variables that weresignificant to O2 pulse: bodysurface area, chamber temperature, core temperature, and pressure.After normalizing for all nonpressure variables, the residualO2 pulse was found to decreasesignificantly (P = 0.02) with pressurefor animals in heliox but did not decrease significantly(P = 0.38) with pressure for animalsin hydrox over the range of pressures studied. This amounted to aroughly 25% lower O2 pulse fornormothermic animals in 60 atmospheres heliox vs. hydrox. These resultssuggest that reduction of cardiovascular efficiency in a hyperbaricenvironment can be mitigated by the choice of breathing gas.

  相似文献   

15.
Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. DouglasBradley. Effects of inhaledCO2 and added dead space on idiopathic central sleep apnea. J. Appl.Physiol. 82(3): 918-926, 1997.We hypothesizedthat reductions in arterial PCO2 (PaCO2) below the apnea threshold play akey role in the pathogenesis of idiopathic central sleep apnea syndrome(ICSAS). If so, we reasoned that raisingPaCO2 would abolish apneas in thesepatients. Accordingly, patients with ICSAS were studied overnight onfour occasions during which the fraction of end-tidalCO2 and transcutaneous PCO2 were measured: during room airbreathing (N1), alternating room airand CO2 breathing(N2),CO2 breathing all night(N3), and addition of dead space viaa face mask all night (N4).Central apneas were invariably preceded by reductions infraction of end-tidal CO2. Bothadministration of a CO2-enrichedgas mixture and addition of dead space induced 1- to 3-Torr increasesin transcutaneous PCO2, whichvirtually eliminated apneas and hypopneas; they decreased from43.7 ± 7.3 apneas and hypopneas/h onN1 to 5.8 ± 0.9 apneas andhypopneas/h during N3(P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep duringCO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients werebreathing through added dead space duringN4 (P < 0.005). Because raisingPaCO2 through two different meansvirtually eliminated central sleep apneas, we conclude that centralapneas during sleep in ICSA are due to reductions inPaCO2 below the apnea threshold.

  相似文献   

16.
Forster, H. V., L. G. Pan, T. F. Lowry, T. Feroah, W. M. Gershan, A. A. Whaley, M. M. Forster, and B. Sprtel. Breathing ofawake goats during prolonged dysfunction of caudal M ventrolateral medullary neurons. J. Appl. Physiol.84(1): 129-140, 1998.Cooling the caudal M ventrolateralmedullary (VLM) surface for 30 s results in a sustained apnea inanesthetized goats but only a 30% decrease in breathing in awakegoats. The purpose of the present study was to determine, in the awakestate, the effect of prolonged (minutes, hours) caudal M neuronaldysfunction on eupneic breathing andCO2 sensitivity. Dysfunction wascreated by ejecting excitatory amino acid receptor antagonists or aneurotoxin on the VLM surface through guide tubes chronically implantedbilaterally on a 10- to 12-mm2portion of the caudal M VLM surface of 12 goats. Unilateral and bilateral ejections (1 µl) of selective antagonists forN-methyl-D-aspartic acid ornon-N-methyl-D-asparticacid receptors had no significant effect on eupneic breathing orCO2 sensitivity. Unilateralejection of a nonselective excitatory amino acid receptor antagonistgenerally had no effect on eupneic breathing orCO2 sensitivity. However, bilateral ejection of this antagonist resulted in a significant 2-Torrhypoventilation during eupnea and a significant reduction inCO2 sensitivity to 60 ± 9% ofcontrol. Unilateral ejection of the neurotoxin kainic acid initiallystimulated breathing; however, breathing then returned to near controlwith no incidence of apnea. After the kainic acid ejection,CO2 sensitivity was reducedsignificantly to 60 ± 7% of control. We conclude that in the awakestate a prolonged dysfunction of caudal M VLM neurons results incompensation by other mechanisms (e.g., carotid chemoreceptors, wakefulness) to maintain near-normal eupneic breathing, butcompensation is more limited for maintainingCO2 sensitivity.

  相似文献   

17.
Bairam, A., P. De Grandpré, C. Dauphin, and F. Marchal. Effects of caffeine on carotid sinus nervechemosensory discharge in kittens and cats. J. Appl.Physiol. 82(2): 413-418, 1997.Caffeine (C)decreases apneic episodes in premature infants and is thought tostimulate breathing mainly by a central mechanism. While the methylxanthines theophylline and aminophylline are known to alter thecarotid chemoreceptor activity, there are little data on C. The aim ofthe study was to examine the effects of C on the carotid sinus nervedischarge (CSND) in developing animals. Nine kittens 17-21 daysold and six adult cats that were anesthetized and artificially ventilated were studied. They received four consecutive doses of C,each of 10 mg/kg, administered at intervals of 20 min either asintravenous bolus injection (6 kittens, 3 cats) or continuous infusion(3 kittens, 3 cats). Bolus injections of C invariably induced a promptbut transient increase in the CSND from 4.1 ± 0.6 to 8.1 ± 1.0 (SE) impulses/s in kittens (P = 0.01)and from 3.9 ± 0.1 to 7.9 to 1.0 impulses/s in cats (after thefirst injection). This response was associated with a significantdecrease in arterial blood pressure. Continuous infusion of C did notinduce any early change in either CSND or blood pressure in kittens orcats. Fifteen minutes after C injection or infusion was begun, CSNDvalues in air, 8% O2-balanceN2, or 100%O2 were not significantlydifferent from control. Haloperidol administered at theend of the experiment in four cats and four kittens significantlyincreased CSND and did not suppress the early response to C injection.It is concluded that caffeine administered by bolus in the kitteninduces a transient stimulation of the CSND that is associated with adecrease in the arterial blood pressure and is independent of thedopaminergic mechanisms in the carotid body. The lack of sustainedeffect implies the main mechanism to the ventilatory stimulation by Cmust be central.

  相似文献   

18.
Cerniglia, George J., David F. Wilson, Marek Pawlowski,Sergei Vinogradov, and John Biaglow. Intravascular oxygendistribution in subcutaneous 9L tumors and radiation sensitivity.J. Appl. Physiol. 82(6):1939-1945, 1997.Phosphorescence quenching was evaluated as atechnique for measuring PO2 in tumors and for determining the effect of increasedPO2 on sensitivity of the tumors toradiation. Suspensions of cultured 9L cells or small pieces of solidtumors from 9L cells were injected subcutaneously on the hindquarter ofrats, and tumors were grown to between 0.2 and 1.0 cm in diameter.Oxygen-dependent quenching of the phosphorescence of intravenouslyinjected Pd-meso-tetra-(4-carboxyphenyl) porphine was used to image thein vivo distribution of PO2 in thevasculature of small tumors and surrounding tissue. Maps (512 × 480 pixels) of tissue oxygen distribution showed that thePO2 within 9L tumors was low(2-12 Torr) relative to the surrounding muscle tissue (20-40Torr). When the rats were given 100% oxygen or carbogen (95%O2-5%CO2) to breathe, thePO2 in the tumors increasedsignificantly. This increase was variable among tumors and was greaterwith carbogen compared with 100% oxygen. Based on irradiation andregrowth studies, carbogen breathing increased the sensitivity of thetumors to radiation. This is consistent with the measured increase inPO2 in the tumor vasculature. It isconcluded that phosphorescence quenching can be used for noninvasivedetermination of the oxygenation of tumors. This method for oxygenmeasurements has great potential for clinical application in tumoridentification and therapy.

  相似文献   

19.
Glia are thoughtto be important in brain extracellular fluid ion and pH regulation, buttheir role in brain stem sites that sense pH and stimulate breathing isunknown. Using a diffusion pipette, we administered the glial toxin,fluorocitrate (FC; 1 mM) into one such brain stem region, theretrotrapezoid nucleus (RTN) for 45-60 min. This dose and timeperiod were chosen so that the effects of FC would be largelyreversible. Within minutes, tissue pH decreased, and respiratory outputincreased. Both recovered almost completely after cessation of FCadministration. The response to systemicCO2 stimulation was unaffected byFC treatment compared with that following control diffusion. Anatomicanalysis showed, at the center of FC administration, some small (meandiameter = 5.1 µm) cells that stained for DEAD Red, a marker foraltered cell membrane permeability, and some fragmented glia (glialfibrillary acidic protein immunohistochemistry). The average RTN tissuevolume that contained such DEAD Red-positive cells was 271 nl, ~23%of the volume of one RTN region. Reversible disruption of glia in theRTN, a region known to contain central chemoreception, results in anacidic local pH and in stimulation of respiratory output.

  相似文献   

20.
Gelfand, R., C. J. Lambertsen, J. M. Clark, and E. Hopkin.Hypoxic ventilatory sensitivity in men is not reduced by prolongedhyperoxia (Predictive Studies V and VI). J. Appl.Physiol. 84(1): 292-302, 1998.Potential adverseeffects on the O2-sensing functionof the carotid body when its cells are exposed to toxic O2 pressures were assessed duringinvestigations of human organ tolerance to prolonged continuous andintermittent hyperoxia (Predictive Studies V and VI). Isocapnic hypoxicventilatory responses (HVR) were determined at 1.0 ATA before and aftersevere hyperoxic exposures: 1)continuous O2 breathing at 1.5, 2.0, and 2.5 ATA for 17.7, 9.0, and 5.7 h and2) intermittentO2 breathing at 2.0 ATA (30 minO2-30 min normoxia) for 14.3 O2 h within 30-h total time. Postexposure curvature of HVR hyperbolas was not reduced compared withpreexposure controls. The hyperbolas were temporarily elevated tohigher ventilations than controls due to increments in respiratory frequency that were proportional toO2 exposure time, notO2 pressure. In humans, prolongedhyperoxia does not attenuate the hypoxia-sensing function of theperipheral chemoreceptors, even after exposures that approach limits ofhuman pulmonary and central nervous system O2 tolerance. Current applicationsof hyperoxia in hyperbaric O2therapy and in subsea- and aerospace-related operations are guided byand are well within these exposure limits.

  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号