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

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 paper discusses the emergence of spontaneous hypocapnia in real aircraft flights. The flying personnel were taken under study. The hypocapnic state was diagnosed on the basis of the CO2 concentration in the alveolar air measured by a special device. In flight the CO2 concentration in the alveolar air decreased insignificantly (by 5 min Hg on the average). In emergency situations the external respiration was activated to a greater extent. It is suggested that the alveolar Pco2 level is indicative of the emotional stress.
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PMID:[Activation of external respiration and level of alveolar PCO2 in pilots in flight]. 112 4

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

This study examined the hypothesis that prevention of hypocapnia and alkalosis would ameliorate the symptoms of acute mountain sickness (AMS). Five subjects were exposed to simulated high altitude for 4 d with 3.8% CO2 added to the chamber to maintain normocapnia. Four other subjects were exposed for 4 d to hypobaric hypoxia without CO2 supplementation, and became hypocapnic. Barometric pressure was lower in the group with added CO2 so that alveolar oxygen tensions (55-60 mm Hg) would not be different. The severity of symptoms was clearly greater in normocapnic than in hypocapnic subjects. Thus, prevention of hypocapnia did not alleviate AMS symptoms. The efficacy of CO2 addition in reducing symptoms, as reported by earlier workers, was probably the result of induced hyperventilation and partial relief of hypoxia. Indeed, in the present study with two comparably hypoxic groups, CO2 addition augmented the sysptoms, possibly by causing increased cerebral vasodiladation and spinal fluid pressure.
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PMID:Acute mountain sickness: increased severity in eucapnic hypoxia. 115 91

EEG, end-tidal CO2, neck muscle EMG, eye movements, and ECG were recorded in 17 children undergoing enflurane anesthesia combined with N2O and O2. All subjects were classified in the lowest risk group and had normal pre-anesthetic EEG recordings. Eleven subjects were breathing spontaneously and six were under controlled ventilation. Thirteen subjects were hyperventilated for short periods. As previously reported for adults, various signs of increased central nervous excitability appeared. At the enflurane concentration of 4% all three cases with PaCO2 below 32 mmHg showed generalized high voltage epileptic activity of grand mal type followed by several minutes of postictal slowing. One of these subjects also showed motor manifestations of the electrographic seizure activity. At 3% enflurane, three out of eight subjects showed electrographic seizure activity of poly-spike-suppression type. One of these children also had motor manifestations during this type of seizure activity at a PaCO2 of 31 mmHg. The results indicate that electrographic seizure activity is common among children with moderate hypocapnia at enflurane concentrations of 3% or more.
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PMID:Electroencephalographic activity in children under enflurane anesthesia. 121 Oct 75

Venoconstriction occurs at high altitude. This study sought to determine whether hypoxia or hypocapnia is the cause of the venoconstriction. Five male subjects were exposed to 4,000-4,400 m (PB 440-465 mmHg) with supplemental 3.77 +/- 0.02% CO2 in a hypobaric chamber for 4 days. Similar alveolar O2 tensions were obtained in four control subjects exposed to 3,500-4,100 m (PB 455-492 mmHg) without CO2. A water-filled plethysmograph was used to determine forearm flow and venous compliance. Systemic blood pressure was measured with the cuff procedure. Catecholamines were measured in 24-h urine collections. Venous compliance fell at high altitude in both groups and was less (P less than 0.01) than control values. Forearm flow and resistance were unaltered at altitude in the group with CO2 supplementation while forearm flow decreased and resistance increased in the hypocapnic group at 72 h of exposure. Urinary catecholamines increased in the group with CO2 and remained unaltered in the hypocapnic group. It is concluded that hypoxia is responsible for decreasing venous compliance, and hypocapnia for increasing resistance and decreasing flow. Group differences observed in urinary catecholamines may be explained by differences in arterial pH.
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PMID:Sustained venoconstriction in man supplemented with CO2 at high altitude. 124 89

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

Hypobaric hypoxia causes hypocapina and alkalosis, hemoconcentration and increased hematocrit, and a decreased cardiac stroke volume. To assess the role of the hypocapnic alkalosis in causing these other changes, five men were exposed to hypobaric hypoxia at a barometric pressure (PB) of 440 torr with an alveolar O2 tension of 55 torr for 5 days with 3.77% CO2 added to the atmosphere to prevent alkalosis. They did not lose weight, and arterial CO2 tension, pH, and cardiac stroke volume were unchanged. An unchanged hematocrit implied an unchanged plasma volume. During exercise to maximum, stroke volumes equaled sea level values but arterial hypoxemia was profound, the arterial O2 tension being 39 torr. By contrast, three men at high altitude without CO2 supplementation (PB=455 torr; alveolar PO2=56 torr) had weight loss, hypocapnia, alkalosis, and decreased stroke volume. Increased hematocrits suggested decreased plasma volumes. During exercise, arterial PO2 (48 torr) was higher than in the group receiving CO2. Maximum oxygen uptakes were decreased to a similar degree in the two groups. Catecholamine excretion doubled in the group with CO2 but in the group without CO2 catechoamine excretion was unchanged. A normal pH at high altitude apparently maintained plasma volume, which, with the increased catecholamine excretion, may have prevented a decrease in stroke volume. However, the subjects with CO2 added did not have enhanced oxygen transport, because their arterial oxygenation was impaired.
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PMID:Maintained stroke volume but impaired arterial oxygenation in man at high altitude with supplemental CO2. 126 78

Brain stem respiratory neuron activity in the cat was studied in relation to efferent outflow (phrenic discharge) under the influence of several forcing inputs: 1) CO2 tension: hypocapnia produces disappearance of firing in some neurons, and conversion of respiratory-modulated to continuous (tonic) firing in others. 2) Lung inflation: during the Bruer-Hering reflex, some neurons have "classical" responses and others have "paradoxical" responses (i.e., opposite in direction to peripheral discharge). 3) Electrical stimulation: stimulus trains to the pneumotaxic center region (rostral lateral pons) produce phase-switching, whose threshold is: a) sharp (indicating action of positive-feedback mechanisms), and b) dependent on timing of stimulus delivery (indicating continuous excitability changes during each respiratory phase). Auto- and crosscorrelation analysis revealed the existence of short-term interactions between: a) medullary inspiratory (I) neurons and phrenic motoneurons; b) pairs of medullary I neurons; c) medullary I neurons and expiratory (E) neurons. A model of the respiratory oscillator is presented, in which the processes of conversion of tonic to phasic activity and switching of the respiratory phases are explained by recurrent excitatory and inhibitory loops.
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PMID:Respiratory rhythmicity in the cat. 127 48


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