Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Effects of changes in PaCO2 on pulmonary input impedance. 111 Feb 43

Forty-seven patients undergoing elective/emergency surgery were investigated for the recovery pattern by numerically scoring the state of consciousness, skeletomuscular tone, respiration and blood pressure after the neuromuscular transmission at the level of thenar muscles returned to normalcy. Anaesthesia in them consisted of thiopentone induction and passive ventilation with nitrous oxide and oxygen mixtures (4 1/2:2 1/2 1) with consequent changes in PaCO-2 (22.0 to 90 mm Hg) after using 0.43 to 0.68 mg/kg d-tubocurarine or 2.3 to 3.8 mg/kg gallamine. In this series twelve patients were selected at random and biological assay of cerebrospinal fluid in them for curare/gallamine after 15 min anaesthesia and in the recovery phase was carried out on frog rectus muscle. All the patients recovered satisfactorily and did not present clinical signs of depression of central nervous system, even though all of them showed the presence of curare (ranging from 0.05 to 0.33 mug/ml) and gallamine (from 0.1 to 0.75 mug/ml) in the cerebrospinal fluid. This study therefore indicates that thiopentone, nitrous oxide and relaxant type of anaesthesia does not cause clinical syndrome of post-operative paralysis even when mild to moderate degree of hypocapnia is present and even when such a technique of anaesthesia is administered in poor-risk patients with associated changes in acid-base balance, electrolytes etc. Significant quantities of skeleto-muscular relaxant drug (used during the technique) when found in cerebrospinal fluid after the technique of anaesthesia need not induce post-operative paralysis in man.
 ...
PMID:Role of thiopentone, nitrous oxide and relaxant anaesthesia in causing the syndrome of post-operative paralysis in man. 112 16

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.
 ...
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.
 ...
PMID:Acute mountain sickness: increased severity in eucapnic hypoxia. 115 91

Exercise-induced bronchospasm (EIB) in some cases of asthma is related to hypocapnia, hypoxemia, and acidosis, but studies have shown that children do not develop as abnormal PCO2, PO2, or pH levels with the induction of EIB. Gradient changes of alveolar-arterial oxygen differences reveal ventilation perfusion abnormalities existing at the onset of exercise in those patients who do develop EIB.
 ...
PMID:Blood gas in exercise-induced bronchospasm: a review. 118 78

In eleven intact mechanically ventilated dogs anaesthetized with pentobarbitone, mean arterial pressure was reduced to 55% of the control value by ventilating with 1-1.5% halothane. At normocapnia this resulted in decreases in myocardial blood-flow and oxygen consumption to 47% and 55% of their respective control values and an increase in myocardial vascular resistance to 123% of control value. When hypocapnia (mean PaCO2=26 mm Hg) was superimposed on hypotension, myocardial blood-flow was further decreased to 38% of control value whereas oxygen consumption did not alter significantly. When halothane was discontinued, allowing recovery from hypotension, the rate of recovery of myocardial blood-flow and cardiac output was much slower than that of arterial pressure.
 ...
PMID:The combined effect of halothane-induced hypotension and hypocapnia on canine myocardial blood-flow and oxygen consumption. 120 Nov 59

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.
 ...
PMID:A method for determining blood flow and oxygen consumption in the rat brain. 125 48

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.
 ...
PMID:Maintained stroke volume but impaired arterial oxygenation in man at high altitude with supplemental CO2. 126 78

Ketanserin, a 5HT2- and alpha 1-receptor antagonist, decreases blood pressure by decreasing systemic vascular resistance without causing reflex cardiac stimulation, while cardiac output remains unchanged. To date, little is known about the effects of ketanserin on cerebral haemodynamics and cerebral metabolism. According to a recently published study, ketanserin seems not to impair cerebral blood flow autoregulation in man. The present study was designed to investigate the influence of ketanserin on cerebral circulation and metabolism, and the cerebrovascular response to CO2 in man. METHODS. Twenty male patients between 44 and 67 years of age who were scheduled for coronary artery bypass surgery were randomly allocated to one of two groups. In group 1 measurements were performed after induction of anaesthesia during normocapnia (p(a) CO2 approximately 40 mm Hg) and hypocapnia (p(a) CO2 approximately 30 mm Hg). Then, ketanserin was given at a bolus dose of 0.3 mg.kg-1 followed by an infusion of 0.06 mg.kg-1.h-1 and measurements were repeated under hypocapnic and normocapnic conditions. Patients of group 2 were hyperventilated at first, then normoventilated. Afterwards, ketanserin was administered at the above-mentioned dose and measurements were again performed during normocapnia and hypocapnia. Cerebral blood flow (CBF) was measured using the argon wash-in technique. Cerebral venous blood was obtained from a catheter in the superior bulb of the right internal jugular vein. Cerebral perfusion pressure (CPP) was calculated by subtracting jugular bulb pressure from mean arterial pressure and cerebral vascular resistance (CVR) by dividing CPP by CBF. Cerebral metabolic rates of oxygen, glucose, and lactate were calculated by multiplying the arterial-cerebral venous oxygen and substrate differences by CBF. RESULTS AND DISCUSSION. Ketanserin decreased CPP by 16% to about 60 mm Hg. Cerebral blood flow remained unchanged as a result of an insignificant decline in CVR. Hyperventilation increased CVR by 32%, while CBF decreased by 27% to the same value that had been obtained during hypocapnia without ketanserin. The percentage changes in CBF per mm Hg change in CO2 were 1.45%/mm Hg (group 1 and 2.91%/mm Hg (group 2), respectively, without ketanserin and 1.98%/mm Hg and 2.22%/mm Hg with ketanserin. As CO2-responsiveness with ketanserin was higher in group 1 but lower in group 2 than without ketanserin, the direction in which ventilation was changed rather than ketanserin was responsible for these changes in CO2-responsiveness. Neither during normocapnia nor during hypocapnia did ketanserin have any effects on cerebral metabolic activity. Thus, it can be concluded that ketanserin does not impair CBF regulation and metabolism and that cerebral vascular responsiveness to hypocapnia is preserved.
 ...
PMID:[Cerebral effects of ketanserin. The influence on hemodynamics and brain metabolism]. 144 11

The oxygen-binding properties of Hb molecule are unchanged in the third trimester of normal pregnancy and in pregnancy complicated by slight iron-deficiency anemia. Hb affinity to oxygen in whole blood is formed under the effect of the three main ligands H+, CO2, and 2,3-DPH. The development of hypocapnia in pregnant women results in elevation of pH values, reduction of pCO2, increase of intraerythrocytic 2,3-DPH concentration by 15-18%. Variously directed effects of H+, CO2, and 2,3-DPH on Hb affinity to O2 result in normal P50 values and therefore the Hb-O2 dissociation curve is not shifted to the right. Thus, in pregnant women with alkalosis 2,3-DPH effect on Hb affinity to oxygen completely eliminates H+ and CO2 effects but not compensates for Hb deficiency in the blood.
 ...
PMID:[Status of the oxygen transport system of hemoglobin in physiological pregnancy and pregnancy complicated by iron deficiency anemia]. 147 17


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>