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

Hyperventilation therapy is often recommended after an episode of global cerebral ischemia (cardiac arrest), even though several workers have shown that under such circumstances the cerebral vasculature is unresponsive to changing PaCO2. However, no study has examined the effects of prolonged PaCO2 changes. We therefore studied the cerebrovascular effects of a 3-h period of continuous hypercarbia (40 to 45 torr) or hypocarbia (15 to 20 torr) in cats resuscitated from 12 min of electrically induced ventricular fibrillation. There were no differences in postresuscitation cerebral blood flow (CBF) or EEG, but intracranial pressure was lower in the hypocapnic animals. Furthermore, hypocapnic cats retained some CBF responsiveness to varying PaCO2 levels, while no such response was noted in previously hypercapnic animals. These findings suggest that some measurable changes in postarrest cerebrovascular behavior can result from prolonged hypocapnia (possibly related to tissue pH alterations). Whether such changes will have clinical utility is unclear.
Crit Care Med 1985 Sep
PMID:Cerebrovascular effects of prolonged hypocarbia and hypercarbia after experimental global ischemia in cats. 392 54

The purpose of this study was to examine regional autoregulation of blood flow in the brain during acute hypertension. In anesthetized cats severe hypertension increased blood flow more in cerebrum (159%) and cerebellum (106%) than brain stem (58%). In contrast to the heterogeneous autoregulatory response, hypocapnia produced uniform vasoconstriction in the brain. We also compared vasodilatation during severe hypertension with vasodilatation during hypercapnia. During hypercapnia, blood flow increased as much in brain stem, as in cerebrum and cerebellum. Thus regional differences in autoregulation appear to be specific for autoregulatory stimulus and are not secondary to nonspecific differences in vasoconstrictor or vasodilator capacity. To determine whether the blood-brain barrier is more susceptible to hypertensive disruption in regions with less effective autoregulation, permeability of the barrier was quantitated with 125I-albumin. Severe hypertension produced disruption of the barrier in cerebrum but not in brain stem. Thus there are parallel differences in effectiveness of autoregulation and susceptibility to disruption of the blood-brain barrier in different regions of the brain.
Am J Physiol 1985 Sep
PMID:Heterogeneity of brain blood flow and permeability during acute hypertension. 392 26

1. In anaesthetized pregnant rabbits near term, cardiac output and its distribution were measured by injection of isotope-labelled microspheres. Hypocapnia (mean arterial P(CO) (2) 18 mm Hg), induced by intermittent positive pressure hyperventilation, caused a 43% reduction in maternal placental blood flow, attributed mainly to vasoconstriction. Myometrial flow was not significantly changed.2. Moderate hypercapnia (mean arterial P(CO) (2) 46 mm Hg) caused no change in placental flow, compared with observations made while breathing air spontaneously (P(CO) (2) 31 mm Hg).3. Intravenous infusions of adrenaline or noradrenaline 1 mug/kg. min caused maternal placental vasoconstriction.4. During the especially warm summer of 1969, there was a mean 46% reduction in maternal placental blood flow in pregnant rabbits near term, breathing room air spontaneously with normal blood gas values and rectal temperatures. This was associated with an increase in the number of runts and dead foetuses.
J Physiol 1972 Sep
PMID:The effect of hyperventilation on maternal placental blood flow in pregnant rabbits. 456 82

In acute experiments on cats hypocapnia produces an appreciable diminution in the mean diameter of the capillaries and an increase in the number of the non-functioning capillaries of the brain cortex. Hypercapnia and hypoxia raise the mean diameter of the capillaries. The former leads to the opening of the non-functioning capillaries whereas the latter one does not affect this indicator. Despite the fact that the indomethacin-induced inhibition of prostaglandin biosynthesis produces no effect on the morphofunctional shifts in brain microcirculation during hypocapnia it averts the effects of hypercapnia and hypoxia on the capillary diameter. An assumption is made about the heterogeneity of receptor formations in the smooth muscles of the arterioles and precapillary sphincters responding to CO2.
Biull Eksp Biol Med 1983 Sep
PMID:[Role of endogenous prostaglandins in the mechanism of action of CO2 and O2 on the morphofunctional state of the capillary system in the cat cerebral cortex]. 641 83

The effect of sleep state on ventilatory rhythmicity following graded hypocapnia was determined in two normal subjects and one patient with a chronic tracheostomy. Passive positive-pressure hyperventilation (PHV) was performed for 3 min awake and during nonrapid-eye-movement (NREM) sleep with hyperoxia [fractional inspired O2 concentration (FIO2) = 0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no immediate posthyperventilation apnea was noted following abrupt cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep levels and 1-2 Torr below the waking level. In hypoxia, PETCO2 increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr below NREM sleep levels and 1-2 Torr above awake levels. Apnea duration (5-45 s) was significantly correlated to the magnitude of hypocapnia (range 27-41 Torr). PHV caused no apnea when isocapnia was maintained via increased inspired CO2. Prolonged hypoxia caused periodic breathing, and the abrupt transition from short-term hypoxic-induced hyperventilation to acute hyperoxia caused apnea during NREM sleep when PETCO2 was lowered to or below the subject's apneic threshold as predetermined (passively) by PHV. We concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].
J Appl Physiol Respir Environ Exerc Physiol 1983 Sep
PMID:Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation. 641 11

The ventilation and carbon dioxide elimination of each lung, and pulmonary arterial pressure, were studied in 17 patients during the early phases of anaesthesia for pulmonary surgery. The patients were ventilated mechanically to moderate hypocapnia. Expired tidal volume and carbon dioxide elimination rate of the lung to be operated on, and of the other lung, were similar in the supine position. There was a significant (P less than 0.01) increase in ventilation and a decrease in end-tidal PCO2 of the upper lung after turning the patient on to the side. Simultaneously, the physiological deadspace fraction of tidal volume (VD/VT) increased from 42 to 45% (P less than 0.05). Mean pulmonary arterial pressure (MPAP) increased slightly as surgery on the chest wall commenced. A concomitant increase of carbon dioxide elimination from the upper lung occurred also, although the distribution of ventilation, between the lungs, was unchanged in comparison with the conditions during undisturbed anaesthesia. Individual changes in MPAP (delta MPAP) and corresponding changes in VD/VT (delta (VD/VT)) were negatively correlated (r = -0.68, P less than 0.01). The regression equation was delta (VD/VT) (%) = 0.7 - 0.83 X delta MPAP (mmHg). It was concluded that variations in pulmonary arterial pressure during surgical stimulation may significantly affect the pattern of carbon dioxide elimination in the lungs. However, there was no evidence that these effects were important clinically.
Br J Anaesth 1984 Sep
PMID:Carbon dioxide elimination from each lung during endobronchial anaesthesia. Effects of posture and pulmonary arterial pressure. 643 15

Topical application of sodium arachidonate (50-200 micrograms/ml) or bradykinin (0.1-10 micrograms/ml) on the brain surface of anesthetized cats caused dose-dependent cerebral arteriolar dilation. This dilation was blocked by 67-100% in the presence of superoxide dismutase and catalase. These enzymes did not affect the changes in arteriolar diameter caused by alterations in arterial blood PCO2, or the arteriolar dilation from topical acetylcholine. Enzymes inactivated by heat had no effect on the vasodilation from arachidonate or bradykinin. Superoxide dismutase alone or catalase alone reduced the dilation during application of 200 micrograms/ml of arachidonate for 15 minutes; they also completely prevented the residual dilation seen 1 hour after washout, as well as the reduction in the vasoconstrictive effects of arterial hypocapnia observed at this time. The results show that superoxide anion radical and hydrogen peroxide, or radicals derived from them, such as the hydroxyl radical, are mediators of the cerebral arteriolar dilation from sodium arachidonate or bradykinin. These radicals are not the endothelium-derived relaxant factor released by acetylcholine. The presence of both superoxide anion radical and hydrogen peroxide is required for the production of the vascular damage seen during prolonged application of high concentrations of sodium arachidonate.
Circ Res 1984 Sep
PMID:Oxygen radicals mediate the cerebral arteriolar dilation from arachidonate and bradykinin in cats. 643 60

Ventilatory regulation of intact, unrestrained lugworms Arenicola marina living in glass-tube artificial burrows was examined for values of inspired seawater PO2, PIO2, from 20 to 700 torr, at constant ambient pH and PCO2 values. The water ventilation rate and the respiratory characteristics of the ventilated seawater were measured. The water convection requirement and the corresponding specific rates of O2 uptake and CO2 production were calculated. The mean ventilatory water flow was a complex function of PIO2: decrease in hyperoxia, increase in hypoxia, decrease in extreme hypoxia. Compared to the normoxic responses, hyperoxia led to a hypercapnia (and acidosis) and moderate hypoxia to a hypocapnia (and alkalosis) in the expired water, variations which presumably reflect blood acid-base balance changes. Thus, as in other water breathers, the regulation of the organism's oxygenation may override the regulation of its acid-base balance. The lugworm's oxygen exchanger is highly efficient. However, below a critical partial pressure, PIO2 ca 120 torr, values of O2 consumption and ventilation decreased. A second critical O2 partial pressure appeared at PIO2 values between 80 and 40 torr; a 'switch-on' of anaerobic metabolism. These phenomena may be viewed as features of an adaptative respiratory strategy selected for in relation with the lugworm's particular peristaltic ventilatory mechanism and its intertidal mode of life.
Respir Physiol 1984 Sep
PMID:Ventilation and respiratory gas exchanges of the lugworm Arenicola marina (L.) as functions of ambient PO2 (20-700 torr). 644 Dec 15

Acute respiratory alkalosis (blood pH, 7.60; arterial PCO2, 15 mmHg (1 mmHg = 133.322 Pa); plasma bicarbonate, 14 mM) was induced in nine anesthetized dogs by increasing their respiratory rate and depth. Renal glutamine extraction and ammonia production expressed per 100 mL of glomerular filtration rate did not change during acute hypocapnia, whereas arterial glutamine concentration decreased significantly from 0.47 to 0.36 mM. Hypocapnia did not change plasma potassium concentration and its urinary excretion. Acute hypocapnia increased lactate extraction and pyruvate production, whereas citrate extraction and glutamate and alanine production did not change. Citraturia remained minimal. Renal cortical glutamine concentration fell from 0.64 to 0.38 mM during hypocapnia while alpha-ketoglutarate, glutamate, malate, oxaloacetate, and citrate did not change. Lactate concentration rose from 1.1 to 2.0 mM. Glutamine concentration in the liver and muscle decreased following acute hypocapnia. Our data are compatible with the hypothesis that an acute respiratory alkalosis might not result in any change in the hydrogen ion concentration and (or) gradient between the mitochondrial matrix and the cytosol. Consequently, renal glutamine extraction and ammonia production are not reduced, renal cortical concentrations of relevant metabolites in the ammoniagenic pathway are not changed, and renal handling of citrate remains unaffected.
Can J Physiol Pharmacol 1984 Sep
PMID:Renal metabolism and ammoniagenesis during acute respiratory alkalosis in the dog. 649 24

In order to study the effects of PaCO2 and PaO2 on the laryngeal closure reflex, changes in laryngeal resistance of the isolated cat larynx were measured before and during the stimulation of the superior laryngeal nerve (SLN) at various levels of PaCO2 and PaO2. The results showed that laryngeal resistance before SLN stimulation [LR (baseline)] increased slightly during hypocapnia. SLN stimulation produced laryngospasm which was defined as a sharp rise in the laryngeal resistance. Hypercapnia alone and hypoxia alone increased ventilation but decreased the degree and duration of laryngospasm due to SLN stimulation. On the other hand, hypocapnia augmented and prolonged the duration of this laryngospasm. These results suggest that PaCO2 and PaO2 regulate the laryngeal closure reflex in a way such that the degree of laryngospasm changes in inverse proportion to the activity of the respiratory center.
Anesthesiology 1981 Sep
PMID:Modification of laryngospasm in response to changes in PaCO2 and PaO2 in the cat. 679 29


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