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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carotid body (CB) chemosensory responses to natural and pharmacological stimuli were studied in vitro in the presence and nominal absence of CO2-HCO3- in the perfusion-superfusion media. The CBs obtained from cats (n = 10), anesthetized with sodium pentobarbitone, were simultaneously perfused and superfused with a modified Tyrode solution at 36.5 +/- 0.5 degrees C, equilibrated respectively with PO2 of 120 and less than 20 Torr. The Tyrode, nominally free of CO2-HCO3- (HEPES-NaOH, pH 7.38, 310 mOsm), was used first. Subsequently the Tyrode containing HEPES-HCO3-, equilibrated with PCO2 of 36.8 Torr (pH 7.38) was used. Chemosensory discharges were recorded from the carotid sinus nerve. Both hypoxia (PO2 = 20-25 Torr) and ischemic hypoxia stimulated the discharge in the absence and presence of CO2-HCO3-. However, the presence of CO2-HCO3- significantly raised the baseline activity, augmented the speed, sensitivity and the maximal responses to both types of hypoxia. Hypercapnic perfusate (PCO2 = 65 Torr at pH 7.17) produced a peak response equally promptly in the absence and presence of CO2-HCO3- in the ongoing perfusate but generated a larger and more sustained response. Presence of CO2-HCO3- strongly potentiated the responses to cyanide (10(-10)-10(-7) mol) but less strikingly the responses to nicotine (10(-11)-10(-8) mol). Thus, the extracellular CO2-HCO3- significantly improved the response to hypoxia but was not essential for O2 chemoreception. The underlying mechanisms of the effect of CO2-HCO3- is likely to be mediated by the Cl(-)-HCO3- anion exchanger in the pH regulation of glomus cells.
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PMID:Carotid body chemoreception in the absence and presence of CO2-HCO3-. 166 17

Carotid body chemosensory response to hypoxia is attenuated as a result of prolonged normobaric hyperoxia (NH) in the cat. The effect of NH is likely to be due to high cellular PO2 and O2-related free radicals. Accordingly, the effect would be less if O2 delivery to the chemoreceptor tissue could be compromised. The aortic bodies, which appear to have less of a circulatory O2 delivery, as suggested by their vigorous responses to a slight compromise of O2 flow compared with those of the carotid body, could provide a suitable testing material for the hypothesis. We tested the hypothesis by studying both aortic and carotid body chemoreceptors in the same cats (n = 6) which were exposed to nearly 100% O2 for about 60 h. These chemoreceptor organs were also studied in 6 control cats which were maintained in room air at sea-level. The cats were anesthetized and their carotid and aortic chemosensory fibers were identified by the usual procedure, and their responses to hypoxia and hypercapnia and to bolus injections (i.v.) of cyanide and nicotine were measured. In the NH cats, the carotid but not aortic chemosensory responses to hypoxia and cyanide were attenuated and to hypercapnia (both onset and steady state) augmented. The aortic chemoreceptors were stimulated by hypoxia, hypercapnia, cyanide and nicotine both in the NH and the control cats similarly. The results support the hypothesis that it is presumably a higher tissue blood flow and hence a higher concentration of O2-related free radicals which ultimately led to the specific attenuation of O2 chemoreception in the carotid body.
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PMID:Aortic and carotid body chemoreception in prolonged hyperoxia in the cat. 178 Jun 2

This study was aimed at determining the role of carotid bodies in the initiation and maintenance of oral breathing during nasal obstruction. We have previously shown in sheep that oral breathing during nasal obstruction was less effective in the neonate than in older lambs or adults. We considered it possible that the reduced response of the neonate was due to immaturity of carotid body chemoreceptors. Respiratory and blood gas responses to nasal obstruction were determined in 5 neonatal lambs, 6 older lambs and 6 adult ewes before and after surgically denervating the carotid bodies. Denervations were performed at 4.2 +/- 0.9 days after birth in the neonatal lambs and at 41.5 +/- 2.5 days in the older lambs. Carotid body denervation led to hypoxia, hypercapnia and acidaemia in lambs and ewes during unobstructed nasal breathing, and, in response to nasal obstruction, delayed the onset of oral breathing so that it occurred at a greater degree of hypoxia. Following carotid body denervation the degree of hypercapnia and acidaemia during nasal obstruction was greater in lambs than in ewes. We conclude that the carotid bodies in lambs and ewes play an important role in the regulation of normal blood gases and pH, and in the establishment and effectiveness of oral breathing during nasal obstruction.
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PMID:The role of carotid bodies in the establishment of oral breathing during nasal obstruction in lambs and ewes. 211 63

We tested the following hypothesis: if carotid body blood flow, and hence the relationship of the frequency of discharge in chemoreceptor afferent fibres to arterial PO2, were affected by atherosclerotic change, then a modification of the control of the respiratory and cardiovascular systems might result. Carotid body reflexes were therefore studied in conscious atherosclerotic rabbits and a control group of normal animals breathing 100% O2, three hypoxic gas mixtures to which was added sufficient CO2 to maintain the arterial PCO2 constant, and 2% and 4% CO2 in 21% O2 and N2. When breathing room air, the atherosclerotic rabbits breathed at a higher respiratory frequency and lower tidal volume than the normal animals, although there was no difference in the respiratory minute volume. The respiratory and cardiovascular responses to hyperoxia, isocapnic hypoxia and hypercapnia were essentially the same in both groups of animals. Serial sections of the carotid bodies showed pathological changes including interstitial fibrosis in the caudal part with interstitial haemorrhages. The proximal part of the ascending pharyngeal artery, the vessel supplying the organ, and its origin from the external carotid, and the arterioles in the caudal part of the carotid body were nearly always occluded to a varying extent by atheromatous plaques. The capillaries appeared normal under light microscopy. The rostral-caudal lengths of the carotid bodies were similar in the two groups. We conclude that the peripheral arterial chemoreceptor responses in atherosclerotic rabbits are relatively normal even though the arteries to, and arterioles within, the carotid body are partly occluded.
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PMID:Carotid chemoreceptor function and structure in the atherosclerotic rabbit: respiratory and cardiovascular responses to hyperoxia, hypoxia and hypercapnia. 259 Sep 27

Ventilation was measured by a plethysmographic method in awake mice before and after intraperitoneal injection of neuroleptic drugs to test the hypothesis that dopaminergic mechanisms modulate control of breathing in this species. Dose-dependent augmentation of ventilation at rest and during hypoxia, and reduced ventilation during hypercapnia was demonstrated for haloperidol, droperidol, prochlorperazine and chlorpromazine (P less than 0.05 or less for each drug). Doses of drugs causing maximal increase of the ventilatory response to hypoxia were linearly related (r = 0.98, P less than 0.001) to in vitro affinity of the drugs for dopamine receptors. Despite presumed equal dopamine-receptor blockade, the drugs had unequal effects on the ventilatory response to hypoxia. Droperidol augmented hypoxic ventilation to 290% of the control value, chlorpromazine to 250% control, prochlorperazine to 190% control and haloperidol to 120% control. These differences in efficacy were in the same order as the affinities of the drugs for alpha-adrenoceptors. The effect of combined haloperidol (90 nmol kg-1) and varying doses of phentolamine (175-900 nmol kg-1) was assessed to test the hypothesis that alpha-antagonism was a factor in determining the increase in ventilation following dopamine blockade. Phentolamine caused dose-dependent augmentation of the ventilatory effects of haloperidol (P less than 0.01) but had no ventilatory effect when given alone. Carotid body resection in anaesthetized mice abolished the stimulation of hypoxic ventilation caused by droperidol. It is concluded that dopaminergic mechanisms in the carotid body modulate ventilatory control in the awake mouse. The drugs most effective in augmenting hypoxic ventilation are those that block both dopamine and alpha-adrenoceptors.
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PMID:Ventilatory stimulation by dopamine-receptor antagonists in the mouse. 286 37

1. Carotid body blood flow (c.b.f.), the arterio-venous oxygen (A-V O(2)) difference and oxygen consumption were measured in forty-seven cats, anaesthetized with pentobarbitone, paralysed with gallamine and ventilated artificially. Carotid sinus and cervical sympathetic nerves were intact throughout.2. A system for perfusing the carotid body artificially with blood is described and evidence is given which shows that similar results were obtained whether the carotid body was naturally or artificially perfused.3. With arterial pressure, blood gas tensions and pH within physiological limits, c.b.f. varied between 33 and 68 mul./min, average 41.5; A-V O(2) difference between 0.21 and 0.46 ml./100 ml., average 0.34, and calculated oxygen consumption between 0.115 and 0.195 mul. O(2)/min, average 0.147.4. With constant mean arterial pressure, hypoxia (30-40 mm Hg P(a, O2)) or hypercapnia (> 50 mm Hg P(a, CO2)) resulted in a small increase of c.b.f., up to 14 mul./min above control; an average fall of A-V O(2) difference by 49% of control and an average fall of oxygen consumption by 36% of control.5. Carotid body blood flow fell linearly with mean arterial pressure over the range 100-170 mm Hg, the slope of the curve varying between 0.78 and 1.22 mul. min(-1). mm Hg(-1). M.A.P. A-V O(2) difference was unaffected so that oxygen consumption fell in proportion to c.b.f.6. It is concluded that the unique response of the carotid body to these stimuli is a fall in oxygen consumption and that this bears a closer relation to the known pattern of chemoreceptor discharge than do changes in total blood flow.
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PMID:The effect of hypoxia, hypercapnia and hypotension upon carotid body blood flow and oxygen consumption in the cat. 549 34

Carotid body chemoreceptor responses to sudden changes in pETCO2 (end-tidal tracheal CO2 partial pressure) and paCO2 (arterial CO2 partial pressure) from one stable state to another at a constant level of PETO2 (end-tidal tracheal O2 partial pressure) and paO2 (arterial O2 partial pressure) were studied in 18 anesthetized cats. Chemoreceptor activity was recorded from single or pauci-fiber filaments of a cut sinus nerve. During a hypercapnic stimulus by CO2 inhalation the discharge rate rapidly increased to a peak and then adapted to a lower level in 20-30 s showing an overshoot in the response. Likewise, withdrawal of the hypercapnic stimulus was followed by an undershoot in chemoreceptor activity. Hypoxia decreased the latency of the response and increased the overshoot and stable state responses to hypercapnia. The responses to step paCO2 increases by blood perfusion were qualitatively similar but the latency and time to peak amplitude were shorter and the peak amplitude was larger at any given perfusate pO2. The stable state responses to a given paCO2 achieved by CO2 inhalation or by blood perfusion were similar. The transient overshoot and undershoot in the activity produced by the increase and decrease in paCO2 were blocked by acetazolamide, a carbonic anhydrase inhibitor. The results are best explained by postulating that in the carotid body tissue, H+ is generated from CO2 in one compartment in the presence of carbonic anhydrase and is transported to another containing the receptor site in a pO2 dependent way--a high pO2 attenuating and a low pO2 augmenting it.
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PMID:Adaptive response of carotid body chemoreceptors to CO2. 680 May 65

Carotid body chemoreceptor afferent discharge was recorded in the sinus nerve of sheep fetuses within a few days of term, exteriorized from ewes given pentobarbitone anaesthesia, and in six newborn lambs, 7-21 h old. Chemoreceptor discharge, defined as such since it was irregular, had no relation to the heart beat and was excited by hypoxia, hypercapnia, H+ and NaCN, was recorded in only 8 out of 20 fetuses. It was abundant in both the newborn lambs and also in fetus carotid bodies studied in vitro. Although electrical stimulation of the sympathetic fibres to the carotid body excited the fetal chemoreceptors and caused a fall in carotid body blood flow, the fetal chemoreceptors still responded to natural stimuli and drugs in both fetus and lamb after the sympathetic pathway had been cut. Further, there appeared to be clear dissociation of chemoreceptor and sympathetic activation shortly after birth. These results confirm and extend earlier studies and they suggest that, although the sympathetic pathway may contribute to chemoreceptor activation at birth, other, possibly more important, factors must be involved. These are discussed.
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PMID:The role of sympathetic nerves in the activation of the carotid body chemoreceptors at birth in the sheep. 725 96

Golden-mantled ground squirrels exhibited a strong hypoxic ventilatory response but a blunted hypercapnic ventilatory response and showed no interactive effects when both stimuli were presented together. They exhibited a resting hypoxic ventilatory drive which was eliminated by carotid body denervation. Carotid denervation also shifted the threshold of the hypoxic ventilatory response but had no effect on the slope of either the hypoxic or hypercapnic ventilatory responses. Chronic exposure (2-12 months) to hypoxic-hypercapnic conditions (16% O2, 4% CO2) resulted in a sustained increase in ventilation. Initial increases in both tidal volume (VT) and breathing frequency (fR) were followed by a subsequent further increase in VT and concomitant decrease in fR (acclimation) which had little overall effect on ventilation (VE) but further increased calculated alveolar ventilation (VA). Respiratory sensitivity to hypoxia and hypercapnia were unaltered under these conditions. On acute return to breathing room air, VE remained elevated (approximately 35%) compared to control animals suggesting that deacclimation takes time. Carotid body denervation in these animals had similar effects to those seen in control animals suggesting that acclimation did not involve changes in carotid body input.
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PMID:Ventilatory responses to acute and chronic hypoxic hypercapnia in the ground squirrel. 781 46

We investigated in conscious rats the characteristics and modes of action of CO2 on thermoregulation and ventilatory control during cold stress. In a group of 10 rats studied intact and after carotid body denervation, measurements of metabolic rate (VO2), ventilation (V), shivering, and colonic temperature (Tc) were made at controlled ambient temperatures (Ta) of 25, 20, 15, 10, and 5 degrees C. Animals were exposed on different days to 1) normoxia, 2) normoxia and 4% CO2, 3) 12% hypoxia, or 4) 10.8% hypoxia and 4% CO2. The following results were obtained. 1) During CO2 exposure in normoxia or hypoxia, VO2 is increased at Ta of 25 degrees C and decreased for lower Ta. These effects are partly mediated by carotid body afferents. 2) Shivering and nonshivering thermogenesis and therefore Tc regulation are affected by CO2 exposure as shown by relationships between VO2-Tc and VO2-shivering intensity. 3) V is controlled by PO2 and PCO2 directly through their peripheral and central actions but also indirectly through their effects on VO2. Our conclusions are as follows. 1) Control of Tc is markedly dependent on PCO2 level. Carotid body afferents play a role, but direct central effects acting on the different sources of thermogenesis and possibly on thermolysis are most prominent. 2) As far as control of V is concerned, during hypercapnia in normoxia or hypoxia, several analogies may be formed between exposure to cold and muscular exercise, both of which increase VO2 and V, suggesting common integrative mechanisms at the central nervous system level.
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PMID:Ventilatory and metabolic responses to cold and CO2 in intact and carotid body-denervated awake rats. 812 76


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