Glucose metabolism accelerates the decline of hypoxic vasoconstriction in rat lungs.
Isolated lungs lose the vasoconstrictor response to airway hypoxia with time of perfusion. In isolated rat lungs this loss was accelerated by the addition to perfusate of glucose or pyruvate. The addition of 3-0-methyl glucoside (a non-metabolizable glucose analog) or saline (a solvent control) did not change the rate of decline of hypoxic vasoconstriction. An inhibitor of glucose metabolism (2-deoxy-D-glucose) augmented the hypoxic pressor response. Vasoconstrictor responses to angiotensin II and KCL were not affected by any of the additions. There were no differences in perfusate osmolality among groups of lungs. These results suggest that glucose accelerated the decline of hypoxic pulmonary vasoconstriction by a metabolic, not an osmotic, effect. There may be an important link between lung glucose metabolism and the hypoxic pressor response.
D019325:3-O-Methylglucose; D000818:Animals; D003847:Deoxyglucose / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism* / Q000494:pharmacology; D007003:Hypoglycemia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D008757:Methylglucosides / Q000494:pharmacology; D011651:Pulmonary Artery / Q000503:physiopathology*; D011773:Pyruvates / Q000494:pharmacology; D051381:Rats; D012965:Sodium Chloride / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects*
D008757:Methylglucosides; D011773:Pyruvates; D019325:3-O-Methylglucose; D012965:Sodium Chloride; D003847:Deoxyglucose; D005947:Glucose