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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The respiratory frequency, tidal volume and ventilization responses of 20 conscious cats to hypoxia, at controlled levels of alveolar CO2, revealed a characteristic steady state response in the majority of animals which indicated a negative interaction of stimuli on tidal volume and minute volume of ventilation, but a positive interaction on frequency. Another series of studies, conducted on seven conscious cats, sought to identify hypoxic response thresholds and depression thresholds, by determining responses over a wide range of hypoxic stimulus intensities, and at different controlled alveolar PCO2. Response threshold was at about 65 torr PAO2. Under eucapnic conditions, ventilation began to fail at PAO2 about 30 torr due to failure of tidal volume. The frequency continued to increase even in the lowest range of PAO2. With hypocapnia no failure of ventilation, frequency, or tidal volume was seen even at the lowest PAO2, but with hypercapnia, the tidal volume began to fail at PAO2 about 50 torr. The minute volume however, continued to increase into the lowest range of PAO2, because the frequency continued to respond at a rate greater than the tidal volume was failing. The results are discussed in terms of interactive depression manifest through the coupled responses of peripheral and central mechanisms.
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PMID:Hypoxia and carbon dioxide as separate and interactive depressants of ventilation. 101 31

The haemodynamic responses to hypocapnia and hypercapnia have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia (1% halothane in oxygen) and under nitrous oxide anaesthesia (30% oxygen in nitrous oxide). In the absence of significant variations of either myocardial contractility or left ventricular end-diastolic pressure, the changes of stroke volume and cardiac output (diminution because of hypocapnia, augmentation because of hypercapnia) were determined by alterations of systemic vascular resistance (augmentation because of hypocapnia, diminution because of hypercapnia).
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PMID:Effect of CO2 on myocardial contractility and aortic input impedance during anaesthesia. 109 15

Pulmonary arterial input impedance spectra were computed in goats in whom the appropriate pressure and flow transducers had been chronically implanted. In response to either hypocapnia or hypercapnia, under anesthesia (1% halothane in a 70% nitrous oxide--30% oxygen mixture) there were no significant modifications of impedance at zero frequency; no consistent or significant changes in the impedance moduli at frequencies between 2 and 14 Hz were observed; the position of the first impedance minimum or the subsequent maximum was not modified; however, pulmonary vascular resistance increased significantly with hypercapnia. Although the load opposing right ventricular ejection was not modified by variation of Paco2, right ventricular work was reduced in response to hypocapnia and augmented in response to hypercapnia.
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PMID:Effects of changes in PaCO2 on pulmonary input impedance. 111 Feb 43

Total cerebral blood flow and oxidative cerebral metabolism were measured at normal pCO2, hypocapnia and hypercapnia in 15 unconscious patients in the acute phase after head trauma. In the basal position (normal CO2) measurements were within normal limits and did not correspond to the severity of the clinical picture. But on altering arterial pCO2 there were market changes in oxidative cerebral metabolism, which suggests an abnormal cerebral regulatory mechanism. Measurement of the same functions 14 days later indicated, on the one hand, persistence of changes, but, on the other, a return to normal of previously markedly elevated cerebral glucose uptake. Comparing cerebral blood flow and metabolism between patients who survived and those who died in the acute phase after brain damage, there were no significant differences.
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PMID:[Changes in cerebral blood flow and oxidative cerebral metabolism after extensive acute head trauma (author's transl)]. 112 47

The effects of changes in airway CO2 partial pressure (PAco2) and arterial CO2 partial pressure (Paco2) on lung mechanics were studied in dogs by utilizing unilateral pulmonary artery occlusion and a tracheal divider which allowed separate variation of PAco2 and Paco2. When Paco2 was held at a reasonably normal level, lower than normal PAco2 levels resulted in large compliance decreases, alteration of the complete static pressure-volume curves, and increases in resistance. Invreases in PAco2 to hypercapnic levels did not produce changes. When PAco2 was held at a reasonably normal level, changes in Paco2 levels were positively and directly related to resistance with small and inconsistent effects on compliance and on complete static pressure-volume curves. A combination of low PAco2 and high Paco2 produced large increases in resistance, alterations of the static pressure-volume curve, and decreases in compliance. Vagotomy during the combined stimulus resulted in only a decrease in resistance without change in lung elastic properties. The results suggest that the mechanical effects of airway hypocapnia and systemic hypercapnia are additive. However, small airways effects of low PAco2 appear to be maximal and uninfluenced by the vagally mediated response to Paco2 increases.
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PMID:Effects of airway versus arterial CO2 changes on lung mechanics in dogs. 114 Oct 90

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

The authors examine the respiratory tests performed during a two years-period in 676 pneumoconiotic miners. Spirography was normal in 8% of the cases; a mixed ventilatory impairment, with an obstructive prevalence of variable extent, was present in 2/3 of the cases. Pharmacodynamic tests in 353 subjects showed a frequent non-specific bronchial sensitivity (34.2% of the whole group). Hypoxaemia (PaO2 below 75 mmHg) with normo- or hypocapnia was observed in 379 patients; hypercapnia was relatively uncommon (9.9%) and occurred mainly in bronchitic patients. The breath holding CO lung transfer test was very often disturbed, as the diffusing capacity (DLCO) was below the predicted value in about 80% of the population. Radiofunctional comparisons were carried out in an homogeneous group of 212 subjects. The data clearly demonstrate that functional abnormalities were not exclusively seen in extensive radiological forms. As far as it goes beyond a simple ventilatory study, the measurement of the breath holding lung transfer factor for CO has proved to be a valuable element in the functional statement of anthracosilicosis. The polymorphism of the pulmonary repercussions of dust exposure explains individual differences between the results of the main investigations, and this emphasizes the need for a series of diversified tests.
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PMID:[Respiratory parameters in pneumoconiotic miners in the north French coal district (author's transl)]. 121 56

Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) were measured in rats under nitrous oxide anaesthesia, using a 133Xenon modification of the Kety and Schmidt inert gas technique with sampling of cerebral venous blood from the retroglenoid vein. Extracerebral contamination of the venous blood sampled was studied by comparing the rates at which the activity of 133Xenon decreased in blood and tissues. Contamination was avoided by gentle compression of the contralateral retroglenoid vein during sampling. CBF and CMRo2 of the rat brain were 80+/-2 and 7.6+/-0.2 ml-(100g)-1-min-1, respectively. These values are about 25% lower than those previously obtained for cerebral cortical tissue under similar conditions. Induced hypercapnia (Paco2 about 70 mm Hg) or hypocapnia (Paco2 15-20 mm Hg) gave rise to expected changes in CBF but did not alter CMRo2. The CMRo2 of the rat brain is at least twice that of the human brain. This species difference, which is similar to that previously reported for the oxygen uptake of cerebral tissue in vitro, probably reflects on inverse relationship between brain weight and neuronal packing density.
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PMID:A method for determining blood flow and oxygen consumption in the rat brain. 125 48

The cerebrovascular response to hypercapnia and hyperventilation was studied in normal and jaundiced baboons by the intracarotid 133Xe injection technique. The baboons with bile duct ligation were found to have decreased CBF at all levels of PaCO2. This difference between normal and jaundiced baboons was 13% at normocapnia rising to 33% with hypercapnia and 37% with hypocapnia. The CBF values all were increased toward normal by use of an alpha-adrenoreceptor blockade (phentolamine). It is suggested that the obstructive jaundice potentiated an inherent vasoconstrictor alpha-adrenergic mechanism to oppose the effects of CO2. Also, alteration of the PaCO2 may have produced its effects on the cerebral vessels by altering this adrenergic mechanism.
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PMID:Abnormal cerebrovascular response to altered PaCO2 in baboons with obstructive jaundice. 126 12

1. Four human subjects exercised in hypoxia (end-tidal partial pressure of O2 (P(ET),O2) ca 55 Torr; heart rate ca 100-130 beats min-1), and the contribution to the respiratory drive of the peripheral and central chemoreflex pathways have been separated on the basis of the latencies and the time courses of the responses to sudden changes of stimulus. 2. The subjects were exposed to repeated end-tidal step changes in PCO2 of ca 3-3.5 Torr (at nearly constant P(ET),O2) and PO2 (between ca 55 and 230 Torr) at three regions along the expiratory ventilation VE-P(ET),CO2 response line (hypocapnia, eucapnia, hypercapnia). The dynamics of the ventilatory responses were calculated using a two-compartment non-linear least-squares optimization method. 3. The component of the response attributable to the peripheral chemoreflex loop may in some subjects contribute up to 75% of the ventilatory drive during mild hypocapnic hypoxic exercise and ca 72% of the total gain following steps of P(ET),CO2 during hypoxic exercise. These data support the notion that the effectiveness of the peripheral chemoreceptor pathway is enhanced in moderate exercise. 4. During hypoxic exercise, the time delays and time constants attributed to the peripheral chemoreflex pathways (ca 3.5 and 9 s respectively) and to the central chemoreflex pathways (ca 9.5 and 47 s respectively) are some of the shortest reported. 5. The dynamics of the peripheral and central chemoreflex pathways appeared to be largely independent of each other. 6. There was a notable absence of systematic change of inspiratory and expiratory durations during the step-induced transients.
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PMID:Dynamics of the ventilatory response in man to step changes of end-tidal carbon dioxide and of hypoxia during exercise. 129 45


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