Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effect of a single oral dose of propranolol on the ventilatory response to hypercapnia has been studied in five healthy subjects. 2. Propranolol produced a small but significant reduction in the slope of the ventilation/end-tidal PCO2 regression line. 3. Propranolol did not significantly change vital capacity or forced expiratory volume in 1 s.
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PMID:Effect of propranolol on the ventilatory response to hypercapnia in man. 51 56

In pentobarbital-anesthetized cats, over arterial paCO2 values of 20-60 mm Hg, cerebral blood flow (CBF, Xenon) and cardiac output (CO, thermal dilution) show positively inflicted curves with slopes significantly greater than zero. To examine the role of the locus coeruleus (LC) in these responses, bilateral stereotactic thermo-coagulation lesions of the LC were made. The effect of lesions confirmed to involve the LC bilaterally (n = 10), were compared with the effects of misdirected lesions placed in the cerebellum and lateral to the LC (n = 10) and sham lesions (n = 10). Ten days after the lesioning procedure, the animals were re-anesthetized with pentobarbital and paCO2 response curves were determined for CBF and CO prior to and following intravenous administration of propranolol (1 mg/kg, i.v.). The results obtained with the sham-operated animals and the animals with lesions outside of the LC were indistinguishable. Bilateral LC lesions had no significant effect on normocapnic CBF as compared to control animals. They did, however, significantly reduce the slope of the CBF paCO2 response curve. Propranolol produced a significant reduction in CBF in lesioned and non-lesioned animals measured at all levels of pCO2 and did not alter the slope of the pCO2 response curve for any group as compared to predrug values. Bilateral lesions of the LC did not significantly alter either normocapnic CO or the slope of the CO-paCO2 relationship, but did reduce the elevation in mean arterial blood pressure otherwise observed during hypercarbia. Measurement of norepinephrine levels in cortex indicate a close correlation between the ability of the lesion to reduce norepinephrine content and produce the observed physiological effects. The results of these experiments suggest that the hypercapnic response of CBF, but not CO to arterial paCO2 is modulated by systems which traverse the dorsal brainstem. The role of the locus coeruleus-catecholamine cell bodies in this effect, however, must be considered speculative until further transmitter-selective interventions are carried out.
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PMID:Effect in cat of locus coeruleus lesions on the response of cerebral blood flow and cardiac output to altered paCO2. 300 58

Rats were anesthetized with urethane (1.5 g/kg i.p.) paralyzed with gallamine (3 mg/kg, i.v.), artificially ventilated and the vagi, carotid sinus and aortic nerves were cut. PaCO2 levels of 16.4 +/- 0.8, 23.3 +/- 1.6, 32.3 +/- 1.8 and 51.9 +/- 2.2 mm Hg were obtained by hyperventilation in 0%, 3%, 5% and 8% CO2 in O2, respectively. Radioactive microspheres labelled with 57Co or 113Sn were injected into the left ventricle and cardiac output and regional blood flows were determined by the 'arterial reference sample' method. Increasing PaCO2 induced an increase in systemic arterial pressure which was predominantly due to a significant increase in total peripheral resistance, while the increase in cardiac output was much less pronounced and no changes in heart rate were observed. The effect of increasing PaCO2 on regional vascular resistance (VR) was not uniformly distributed. CO2 induced a dilatation in the cerebral, bronchial and hepatic artery vascular beds. Coronary VR was not affected while vasoconstriction was induced by CO2 in the other vascular territories. This vasoconstriction was most significant in skeletal muscle, skin, pancreas, large intestine and kidneys. In most of these territories the vasoconstrictor effect of CO2 was observed at PaCO2 levels above 23.3 mm Hg, while between 16.4 and 23.3 mm Hg there was either no change or a decrease in VR. Propranolol and phentolamine (1 mg/kg and 10 mg/kg, i.v., respectively), which caused a 78% +/- 2% adrenergic blockade, significantly reduced the CO2 pressor and vasoconstrictor effects. Our experiments show that, after peripheral chemoreceptor denervation in the rat: (a) there is a direct relationship between PaCO2 and VR mediated by the sympathetic nervous system over the whole range of PaCO2 values from hypocapnia to hypercapnia, and (b) the various vascular territories contribute to a different extent to the CO2-induced changes in total peripheral resistance.
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PMID:Regional hemodynamic effects of changes in PaCO2 in the vagotomized, sino-aortic de-afferented rat. 392 91

The effect of beta-adrenoceptor antagonists on the respiratory response to carbon dioxide rebreathing was studied in eight normal subjects. Propranolol, atenolol, metoprolol, and placebo were given in random, double-blind fashion. Subjects were studied before each treatment period, after one dose, and after eight days of treatment with each drug. A rebreathing method was used to produce progressive hypercapnia and the respiratory response was assessed by measuring minute ventilation and maximum rate of change of inspiratory mouth pressure. Beta-blockade was assessed by the reduction in heart rate during steady state exercise on a cycle ergometer. There was no change in the respiratory response to carbon dioxide after a single dose or eight days treatment of any drug. All three active drugs produced a significant reduction in exercise heart rate. The forced expiratory volume in one second was not altered by any of the drugs.
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PMID:Effect of acute and chronic beta-blockade on carbon dioxide sensitivity in normal man. 678 64

The effects of intravenous injections of isoproterenol (0.5-2 microgram) on the responses of carotid body chemoreceptor afferents and on integrated phrenic activity were investigated in twelve anesthetized and three decerebrate, unanesthetized cats. All animals were paralyzed and artificially ventilated. Isoproterenol stimulated carotid chemoreceptor activity and this stimulation was augmented by both hypoxia and hypercapnia. Following an injection of isoproterenol, the ratio of the minute phrenic activity relative to mean carotid chemoreceptor activity was increased. Thus, the stimulation of inspiratory phrenic output exceeded the stimulation of the chemoreceptor afferent input, and the peripheral chemoreflex activity does not account for the entire ventilatory response. To distinguish between a direct effect of isoproterenol and a possible secondary effect mediated via an increased venous return and an increased PaCO2, the latencies of the response of carotid chemoreceptors to both isoproterenol and hypercapnia were compared before and after carbonic anhydrase inhibition by acetazolamide. After acetazolamide, the latency of the response to hypercapnia increased from 3.5 sec to 8 sec whereas the latency of response to isoproterenol increased less, from 4.7 sec to 6.3 sec. Thus, isoproterenol stimulation was not mediated by CO2-H+. Propanolol, which blocked the systemic vascular effect, only partially blocked the chemoreceptor stimulation caused by isoproterenol, indicting that the effect of isoproterenol on chemoreceptor activity was not due to systemic cardiovascular changes.
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PMID:Augmentation of carotid body chemoreceptor responses by isoproterenol in the cat. 726 23