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

Cerebral blood flow (CBF) and oxygen consumption (CMRO2) were measured during acute and long-term ethanol intoxication in the rat. The purpose was to investigate whether the adaptive changes (development of tolerance) occurring in the CNS during ethanol intoxication were associated with changes in CBF and/or CMRO2. Consistent with other studies we found that acute severe ethanol intoxication (median blood alcohol concentration (BAC = 5.4 mg/ml)) caused a significant decrease in CBF and CMRO2. After 3-4 days of severe intoxication (BAC of 6.6 mg/ml) these physiological variables were less affected indicating that functional tolerance had developed: CMRO2 and CBF during acute ethanol intoxication were 9.3 ml/100 g/min and 60 ml/100 g/min respectively; after the long term intoxication period these variables reached 11.2 ml/100 g/min and 78 ml/100 g/min respectively, i.e. values not significantly lower than those of the control group. After induction of hypercapnia (PaCO2 about 80 mmHg) CBF increased by 360% in the control group; in the acutely intoxicated group CBF increased by only 127% and in the long term intoxicated group by 203% indicating that the cerebrovascular CO2-reactivity had also adapted to the ethanol intoxication. It is concluded that adaptive changes of the CNS to chronic ethanol intoxication comprise alterations in CMRO2, CBF and cerebrovascular reactivity.
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PMID:Adaptive changes in cerebral blood flow and oxygen consumption during ethanol intoxication in the rat.. 4 9

Six patients with chronic obstructive pulmonary disease (COPD) (forced expiratory volume in one second, 1.01 +/- 0.08 L [mean +/- SEM] ) were given either 1 mL of 100% alcohol per kilogram of body weight in an aqueous solution or a similar volume of water in a crossover design on consecutive days. All subjects became intoxicated and the peak alcohol concentration was 137 +/- 11 mg/dL, 40 minutes after ingestion. No significant difference was found in either PaO2 or PaCO2 between the alcohol and control period. A significant decrease in arterial pH occurred following alcohol (P less than .05), and represented a mild metabolic acidosis. Alcohol ingestion resulted in an increase in oxygen consumption (P less than .05) and carbon dioxide production (P less than .05) but no change in respiratory rate. It appears that small to moderate amounts of alcohol will not cause marked changes in oxygen tension or alveolar hypoventilation in patients with severe COPD who do not have marked hypercapnia. Nevertheless, other effects of alcohol on the cardiopulmonary system and the concomitant use of sedatives have to be considered before condoning the use of alcohol.
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PMID:Moderate alcohol dose and chronic obstructive pulmonary disease: not a cause of hypoventilation. 43 97

The ventilatory responses mediated by the central and peripheral chemoreceptors were separately assessed in eight healthy volunteers before and after the oral ingestion of ethanol in a dose of 0.75 ml/kg. No significant depression of the central response was observed, but a significant depression of the peripheral response was observed at 25 and 95 minutes after the consumption of ethanol. The peripheral chemoreceptor stimulus was the simultaneous increase of hypoxia and hypercapnia and this novel method is described.
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PMID:The effect of ethanol on the ventilatory responses mediated by the peripheral chemoreceptors in man. 65 90

Regional cerebral blood flow was measured by the 14C-ethanol technique in anesthetized rats before and after intraventricular injection of 6-hydroxydopamine. This treatment reduced the fluorescence of the central noradrenaline and dopamine nerve terminals, as well as of the perivascular nerve terminals in cerebral vessels. The administration of 6-hydroxydopamine had no significant effect on cerebral blood flow at normocapnia. The cerebrovascular reactivity to hypercapnia was significantly increased in the 6-hydroxydopamine treated animals. The results indicate an involvement of central catecholamine pathways in the cerebrovascular reactivity to hypercapnia.
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PMID:Effects of intraventricular 6-hydroxydopamine on cerebrovascular CO2 reactivity in anesthetized rats. 90 56

Brain uptake of antipyrine, water and ethanol was studied in rats under normo-, hypo- and hypercapnic conditions. Brain uptake of D- and L-lactate was studied in normal rats. The uptake was determined with the Oldendorf method, using single common carotid arterial injections of a mixture of -14C-labeled test substance and tritiated reference substance. The results demonstrate that L-lactate is taken up by the brain in significant amounts. The results also demonstrate marked differences in the uptakes of antipyrine, water and ethanol. The brain uptake of antipyrine is lower, the brain uptake of ethanol higher, than of water. The brain uptake of all 3 substances was shown not to be affected by changes in cerebral blood flow, although a decrease of brain uptake of antipyrine relative to ethanol was observed during hypo- and hypercapnia.
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PMID:Brain uptake of lactate, antipyrine, water and ethanol. 114 66

We propose a simple method that can be used to measure cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cerebral glucose consumption (CMRglu) in the conscious, freely moving rat. The method is based on the classical Kety-Schmidt approach, and uses a chronic cannula in the confluens sinuum. We tested the method by investigating the response of CBF, CMRO2, and CMRglu to hypercapnia and used the approach to investigate the effects of acute alcohol administration. Severe hypercapnia (PaCO2 approximately 80 mmHg) increased the CBF by a factor of 3.5, decreased the CMRO2 by 30%, and had no significant effect on the CMRglu. Under normocapnic conditions moderate blood alcohol levels (100-200 mg%) caused no significant effects on CBF, CMRO2, or CMRglu, but high blood alcohol levels (250-400 mg%) decreased all three parameters by approximately 25%. Under hypercapnic conditions high blood alcohol levels had no effect on CBF, CMRO2, and CMRglu.
Alcohol Clin Exp Res 1991 Oct
PMID:Cerebral blood flow and metabolic rate in the conscious, freely moving rat: the effects of hypercapnia, and acute ethanol administration. 175 6

The effects of marijuana smoke on maternal respiratory rate and gas exchange were examined in nine chronically instrumented, late gestation ewes carrying singletons. The magnitude of exposure was randomly varied producing peak plasma levels of delta-9-tetrahydrocannabinol (delta-9-THC) ranging from 0 to 161 ng/ml. delta-9-THC levels, respiratory rate and arterial blood gas tensions were monitored before and for two hours after inhalational exposure. When compared to placebo, marijuana smoke produced a dose dependent and sustained decrease in maternal respiratory rate and arterial oxygen tension without evidence of either systemic acidosis or carbon dioxide retention. A logarithmic relationship was observed between the blood level of delta-9-THC and the change in respiratory rate. The change plateaued at 30% of control at levels above 80 ng/ml. However, the relationship between the blood level of delta-9-THC and the change in arterial oxygen tension had a linear fit with a maximum decrease of 45% at a blood level of 160 ng/ml. No change was detected in minute ventilation. Fetal oxygen tension fell significantly and remained depressed after maternal values had returned to control levels. We conclude that, in this species, inhalational exposure to marijuana smoke induces a prolonged maternal ventilation/perfusion imbalance and limits fetal oxygen availability by one or more mechanisms.
Alcohol Drug Res 1987
PMID:The effects of marijuana smoke on gas exchange in ovine pregnancy. 302 63

In the human species, foetal breathing movements are detectable from the fifteenth week of gestation and their incidence increases until the start of the third trimester. Over the last 10 weeks, breathing movements are present for 30% of the time. These are contemporaneous with body and ocular movements, suggesting an association between breathing movements and paradoxical sleep, as has been seen in the foetal lamb. These phases of activity alternate with phases of foetal immobility during which breathing movements are often absent. The incidence of foetal movements rises in the late post-prandial period, under the effect of maternal hyperglycaemia. After the establishment of regular uterine contractions, foetal breathing movements disappear, perhaps under the effect of prostaglandins E2 and/or a reduction in placental blood flow. Maternal hypercapnia leads to a rise in foetal breathing movements, which corresponds in the animal to the paradoxical sleep state. In the foetal lamb, hypoxaemia is accompanied by a cessation of breathing movements coinciding with a passage to quiet sleep. It is probable that the human foetus produces a similar reaction to hypoxaemia. During quiet sleep an inhibition of the respiratory centres would exist, disappearing during paradoxical sleep. Alcohol and certain anaesthetic agents lead to an inhibition of foetal breathing movements. The effect of tobacco remains controversial. The role of foetal breathing movements in pulmonary maturation is discussed in the human species.
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PMID:[Fetal respiratory movements]. 313 63

The respiratory and psychomotor effects of a single oral dose of meptazinol (200 mg) and dextropropoxyphene (65 mg)/paracetamol (650 mg) mixture, was compared alone and in combination with ethanol (0.8 g kg-1). Peak saccade velocity following meptazinol or the dextropropoxyphene/paracetamol mixture was not significantly different from placebo. When each of the treatments was followed by ethanol administration, a significant decrease in saccade velocity (P less than 0.01) was seen. Given alone, neither of the analgesic drugs produced a significant change in the slope of the ventilatory response to hypercapnia. Ethanol did not affect the ventilatory response to hypercapnia when given alone or in combination with meptazinol, but when given with the dextropropoxyphene/paracetamol mixture, a significant reduction in the slope of the ventilatory response to hypercapnia occurred at 1.5 h (P less than 0.05) and 2 h (P less than 0.01) after administration of the analgesic drug. No pharmacokinetic interaction was demonstrated between ethanol and meptazinol or the dextropropoxyphene/paracetamol mixture in the doses used. In contrast to meptazinol, the dextropropoxyphene/paracetamol mixture interacts with ethanol on the ventilatory function.
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PMID:Comparison of the effects of therapeutic doses of meptazinol and a dextropropoxyphene/paracetamol mixture alone and in combination with ethanol on ventilatory function and saccadic eye movements. 409 95

Ethanol depresses the ventilatory responses to hypercapnia and hypoxia. We hypothesized that this ventilatory depression, like some other central nervous system effects of ethanol, might be mediated via endorphins. In a double-blind placebo-controlled study, we assessed the effect of the opiate antagonist naloxone on ventilatory responses during ethanol intoxication in 18 normal men. Standard rebreathing studies were done at baseline, after ethanol (1.5 ml/kg, p.o.), and after each of 2 intravenously administered injections. One of the injection sequences PP, NP, or PN (N = naloxone, 0.8 mg; P = placebo, 2 ml) was randomly assigned to each subject. The ventilatory responses were reduced after ethanol administration compared with those at baseline (p less than 0.05). In groups NP and PN, naloxone restored the hypercapnic response (p less than 0.05). Placebo injection did not significantly alter the response slopes. Hypoxic ventilatory responses showed the same trends but did not reach statistical significance. This study shows that naloxone reverses ethanol-induced depression of hypercapnic drive, suggesting that an opiate-mediated mechanism is responsible for this depression.
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PMID:Naloxone reverses ethanol-induced depression of hypercapnic drive. 635 14


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