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

The effects of halothane, enflurane, and methoxyflurane on hypocapnic bronchoconstriction (increased airway resistance and decreased compliance of the lung) were studied in vivo in the isolated left lower lobe of the canine lung. Hypocapnic bronchoconstriction, induced by altering the concentration of CO2 in gas ventilating the lobe, was repeated in the presence and absence of various concentrations of anesthetic gases (halothane: 0.5, 1.0, and 3.0 per cent; enflurane: 1.0, 3.0, and 5.0 per cent; methoxyflurane: 0.25, 0.50, and 1.0 per cent). In the higher concentrations, all three drugs blocked the bronchoconstrictor effect produced when the inspired CO2 was decreased from 5 to 0 per cent. In lower concentrations, halothane was the most effective blocking drug. Propranolol did not affect the ability of the three anesthetics to block hypocapnic bronchoconstriction, nor did the beta-receptor blocking drug sotalol affect the blocking effects of halothane. The ability of these anesthetics to block hypocapnic bronchoconstriction probably is mediated not through an adrenergic mechanism but by one that is nonspecific. (Key words: Lung, bronchoconstriction; Carbon dioxide, hypocarbia; Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Anesthetics, volatile, methoxyflurane.)
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PMID:Hypocapnic bronchoconstriction and inhalation anesthetics. 24 37

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