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

The effects on hemoglobin oxygen transport of acute respiratory acidosis have been studied in dogs inhaling a gaseous mixture with 12% CO2 (O2 21%) for two to five hours. In a first series of experiments, it was shown that the shape of the oxyhemoglobin dissociation curve (ODC) was not modified by severe acidosis (pH congruent to 7) lasting for two and a half hours. The Hill number (N equals 2.6) did not change significantly. The aim of the second experimental series was to stuey the Bohr effect and the hemoglobin oxygen affinity (P50). The control value for the respiratory Bohr coefficient (B) was --0.54; neither after two hours (--0.52), nor after five hours of hypercapnia (--0.55) was it significantly modified. The P50 expressed at arterial pH was much increased in acidosis (congruent to 45 torr); when expressed at standard p/ 7.4, it was slightly but significantly decreased (congruent to 1 torr) at the fifth hour. At the same time there was a decrease (p smaller than 0.05) in the erythrocyte 2,3-DPG approaching 15 p. cent; on the other hand the ATP concentration did not change significantly. No significant individual correlation was found between P50(7.4), 2,3-DPG and mean hemoglobin corpuscular concentration. These results suggest that during severe respiratory acidosis neither a change in the shape of ODC, nor a change in Bohr effect do affect the hemoglobin oxygen transport. The main characteristic remains the decrease in oxygen affinity of hemoglobin, due to the erythrocyte [H+] increase induced by hypercapnia ; this phenomenon is observed as long as the 2,3-DPG decrease stays moderate.
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PMID:[Hemoglobin oxygen transport during experimental acute hypercapnia (author's transl)]. 23 80

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.
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PMID:Metabolic and respiratory responses during Helox-induced hypothermia in the white rat. 24 22

An earlier study has demonstrated that indomethacin, a prostaglandin synthesis inhibitor, blocks the cerebrovascular response to hypercapnia. This response is believed to be mediated by a lowering of pH in the cerebral interstitial fluid. Should autoregulation of cerebral blood flow (CBF) to changing perfusion pressure also be mediated by a changing interstitial pH (the "metabolic" theory), then indomethacin should impair autoregulation. This hypothesis was tested in anesthetized baboons. CBF was measured by the intracarotid 133Xe clearance technique; the preparation and the indomethacin protocol were identical to those of our previous investigation. Arterial pressure was increased by the intravenous infusion of angiotensin and decreased by controlled hemorrhage. Indomethacin was given by continuous infusion into the internal carotid artery. Although it reduced resting CBF, the cerebrovascular response to changing perfusion pressure was unchanged. Because indomethacin affects the response to changing CO2 but not that to changing perfusion pressure, the mechanisms for these two reactions presumably are different and it is improbable that changing interstitial pH is responsible for autoregulation in the cerebral circulation.
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PMID:Response of the cerebral circulation in baboons to changing perfusion pressure after indomethacin. 40 29

The activity and the isozyme B and C levels of red cell carbonic anhydrase was examined before and during CO2 inhalation in 18 patients with chronic respiratory failure. Carbonic anhydrase B and C levels did not change during 5 min breathing of high (8-9%) and low (3-5%) CO2 mixture. Carbonic anhydrase activity decreased in patients with combined hypercarbia (Paco2 greater than or equal to 45 mmHg) and hypoxemia (Pao2 less than or equal to 60 mmHg). This was accompanied by an increase in red cell K+ content, 2, 3-DPG and Hct/Hb. The activity did not change in patients with only hypoxemia. Carbonic anhydrase activity and plasma HCO-3 concentration were positively correlated (r = 0.4, P less than 0.05). A significant inverse correlation was also found between changes in red cell K+ content and those in carbonic anhydrase activity (r = - 0.42, P less than 0.05). These results indicate that 1), there is a dissociation between activity and isozyme levels in red cell carbonic anhydrase during the initial 5 min of CO2 breathing in patients with combined hypercarbia and hypoxemia, and 2), there seems a linkage exists between K+ movement across the red cell membrane and carbonic anhydrase activity.
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PMID:Effect of CO2 on carbonic anhydrase activity and isozyme levels in respiratory failure. 41 57

Steady-state responses to hyperoxic hypercapnia and eucapnic hypoxia were measured both as minute ventilation (VE) and as inspiratory mouth occlusion pressure (P0.1) with and without 25 cm H2O/I/s added resistance (R). Reduction in slope of the ventilatory response to CO2 with R was highly significant in all 3 subjects whereas the response to hypoxia was barely significantly reduced in 1 subject and not significantly decreased in two. Although P0.1 was higher with than without R under all conditions, the slope of the P0.1 response to CO2 with R was not increased in two subjects and only slightly increased in the third. The slope of the P0.1 response to hypoxia was significantly greater in all subjects with R. Expiratory reserve volume was increased with R but the change was the same with hypoxia and hypercapnia. We conclude that ventilation is better maintained with resistive loading during hypoxia than during hypercapnia and that this results from a greater force output of inspiratory muscles as reflected by a higher P0.1. This suggests a greater neural output to these muscles.
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PMID:Ventilatory and occlusion pressure response to CO2 and hypoxia with resistive loads. 42 14

1. Mongrel dogs were anaesthetized with chloralose, paralysed, ventilated and vagotomized and given a beta-blocking drug, sotalol, in sufficient doses to block the effects of 5 microgram of adrenaline. 2. Changes in inspired CO2 concentration were produced, causing increases of arterial PCO2 up to 120 mmHg. The effects on myocardial blood flow were measured with radioactive microspheres. Coronary sinus and arterial blood was sampled. 3. In the absence of beta-blockade, an increase in arterial PCO2 produced variable effects. In some dogs coronary blood flow increased, while in others there was no change. There was a mean increase in coronary blood flow at arterial PCO2 values above 85 mmHg which was abolished by beta-blockade. 4. In the presence of beta-blockade, an increase of arterial PCO2 produced depression of left ventricular performance, i.e. a fall of maximum rate of rise of left ventricular pressure and a rise of left ventricular end-diastolic pressure. 5. In the presence of beta-blockade, there were no consistent changes in myocardial blood flow, left ventricular pressure or cardiac output. 6. In the absence of beta-blockade, coronary arterial minus venous ocygen content was reduced by hypercapnia. In the presence of beta-blockade, the changes were small and not statistically significant. The direct coronary vasodilator effect was therfore negligible. 7. It is concluded that the previously reported hypercapnic vasodilatation was mainly an effect of sympatho-adrenergic stimulation by hypercapnia. 8. In the presence of beta-blockade, coronary sinus PO2 increased markedly, with little change in coronary sinus oxygen content; this was consistent with a shift to the right of the oxy-haemoglobin dissociation curve. Under circumstances of hypercapnia, a rise in coronary sinus (and presumably tissue) PO2 failed to produce vasoconstriction. 9. It is argued that the vasodilator effect of hydrogen ions and the vasoconstrictor effect of oxygen probably cancel one another when the arterial PCO2 is raised.
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PMID:The effect of carbon dioxide upon myocardial contractile performance, blood flow and oxygen consumption. 43 Mar 87

1. A combination of bilateral lesions within the nucleus parabrachialis medialis complex (n.p.b.m.) and bilateral vagotomy typically resulted in an apneustic respiratory pattern in decerebrate and paralysed cats. Integrated efferent phrenic nerve activity was recorded as an index of the respiratory rhythm.2. Changes in components of this apneustic breathing cycle were evaluated in response to steady-state hypercapnia and hypoxia. The components evaluated were (a) the period of phrenic discharge (inspiratory time, T(I)), (b) the period of no detectable phrenic activity (expiratory time, T(E)), (c) the total duration of the apneustic respiratory cycle (T(TOT), the sum of T(I) and T(E)), and (d) the average height of the integrated phrenic nerve activity (apneustic depth).3. Elevations of P(A, CO2) from values below 45 torr to 50-60 torr, under both hyperoxic and normoxic conditions, resulted in significant elevations of T(I), T(E), T(TOT) and depth. Further P(A, CO2) elevations to approximately 70 torr caused no change, or frequently, a decrease in T(I), T(E) and T(TOT); the apneustic depth increased in most animals.4. Diminutions in P(A, O2) from normoxic to hypoxic levels at isocapnia typically caused an increase in apneustic depth and, concomitantly, significant decreases in T(I), T(E) and T(TOT).5. Pharmacological stimulation of the carotid chemoreceptors by intracarotid administration of 1.0-20 mug NaCN produced a premature onset of phrenic nerve activity if delivered during the expiratory period. Such NaCN administrations, delivered during the inspiratory phase, resulted in an augmentation of the integrated phrenic discharge and a premature termination of phrenic activity. Carotid sinus nerve section eliminated the response to NaCN administration.6. In experimental animals having bilateral carotid sinus nerve section, normoxic hypercapnia caused similar changes in the apneustic breathing pattern to those recorded in cats having intact carotid chemoreceptors. However, isocapnic hypoxia induced time-dependent changes in the pattern of phrenic discharge including diminutions in depth, an onset of gasping-type activity, or expiratory apnea.7. In a few animals, bilateral n.p.b.m. lesions and bilateral vagotomy resulted in expiratory apnea which was continuous as long as ventilation with air was maintained. This expiratory apnea was replaced by an apneustic breathing pattern following diminutions of P(A, O2) below 90 torr. This establishment of an apneustic breathing pattern by hypoxia was observed both in animals having intact, as well as sectioned, carotid sinus nerves. This expiratory apnea could also be terminated by a single apneustic inspiration following general somatic stimulation or, in cats having intact carotid chemoreceptors, following intracarotid NaCN administration.8. It is concluded that hypercapnia and hypoxia produce differential alterations of the apneustic breathing pattern in decerebrate cats. Further, the hypoxia-induced changes are considered to represent the net result of carotid chemoreceptor stimulation and brain stem depression. The results of this study are considered in the context of proposed mechanisms for phase-switching of the respiratory cycle.
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PMID:Differential alteration by hypercapnia and hypoxia of the apneustic respiratory pattern in decerebrate cats. 43 Apr 30

The effect of carbon dioxide on oxygen dioxide tension in the endolymph was determined by the micropolarographic technique. Different concentrations (5% and 10% CO2) and different exposure times (3, 5, and 20 minutes) were investigated. The highest levels of PO2 in the endolymph (101.7, 93.9 and 69.5 mm Hg) were accomplished by respiration of 10% CO2, 90% O2, for 20, 5 and 3 minutes consecutively. The lowest PO2 increase, 50.7 mm Hg was observed after breathing 5% CO2, 90% O2 for 20 minutes. Extreme hypercapnia caused an increase of endocochlear potentials (EP) in all groups. In the second group EP increased from +79.3 to +84.9 and in all groups they had returned to the pretreatment level after CO2 discontinuation. These results support the theory that carbonic anhydrase participates in the generation of EP. At the same time that EP increased, cochlear microphonics declined and opposite after the breathing mixture was discontinued. The results permit the conclusion that high levels of PO2 in endolymph is achievable even with short periods of respiration with high CO2 mixture, and suggest the role of carbonic anhydrase during EP generation.
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PMID:Variation of endocochlear PO2 and cochlear potentials by breathing carbon dioxide. 44 16

Ventilatory responses of unanesthetized turtles to changes in the intrapulmonary CO2 content of a vascularly isolated and an intact lung were measured during spontaneous breathing. The hyperpnea associated with inhalation of CO2 by the vascularly isolated lung was 19% of that associated with inhalation of CO2 by the intact lung. Transection of the vagus nerve supplying the isolated lung abolished this response. We conclude that both inhibition of pulmonary stretch receptor discharge with increasing levels of FICO2 and a functional increase in central inspiratory volume threshold during hypercapnia contribute to tidal volume increases following CO2 inhalation in normal animals. The major component of the ventilatory response of intact turtles to increasing levels of FICO2, however, was an increase in respiratory frequency. When CO2 was inspired only by the vascularly isolated lung the increase in respiratory frequency was only 21% of that recorded when the same levels of CO2 were inspired by the intact lung. Thus the ventilatory response of turtles to increasing levels of FICO2 is primarily dependent upon concomitant hypercapnia.
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PMID:Pulmonary receptor chemosensitivity and the ventilatory response to inhaled CO2 in the turtle. 45 69

Pyrenebutyric acid (PBA), the intracellular fluorescent indicator, was used to measure the partial pressure of oxygen (PO2) in the exposed cerebral cortex of anesthetized cats at hyperbaric pressures up to 4 ATA. The validity of the PBA method for determining cortical PO2 was confirmed by demonstrating a precise linear relationship between Pao2 and the reciprocal of the fluorescence of PBA in the brain as the cat was ventilated with sequentially greater oxygen pressures while holding the Paco2 nearly constant. Increments in the Paco2 while the Pao2 was maintained at a high (about 2,000 Torr) level resulted in stepwise greater oxygen tensions in the brain until an oxygenation end point was reached with a Paco2 averaging near 122 Torr. Greater amounts of CO2 did not bring the mean PO2 of the brain, 1,017 Torr, closer to 2,000 Torr. During normocapnia the cortical PO2 was greater than the PO2 of cerebral venous blood collected from the superior sagittal sinus; however, in hypercapnia (PaCO greater than 45 Torr), the PO2 of the sinus blood exceeded the value determined in the cortex. This latter observation is taken as evidence for convective shunting of cerebral arterial blood to venous circulation when hypercapnia is present.
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PMID:Oxygen tensions measured in cat cerebral cortex under hyperbaric conditions. 45 30


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