Acute hyperglycaemia does not alter coronary vascular function in isolated, perfused rat hearts

Abstract

The purpose of this study was to evaluate the hypothesis that acute hyperglycaemia in hearts of rats without diabetes alters coronary vascular responses to nitric oxide (NO), adenosine (ADO) and phenylephrine (PHE). Coronary function was studied in isolated, Langendorff-perfused, non-beating rat hearts that were perfused with an oxygenated Krebs-Henseleit solution containing 40 mM KCl to arrest the hearts. Changes in coronary vascular resistance were assessed by measuring changes in coronary perfusion pressure under constant flow conditions. Coronary responses to ADO, sodium nitroprusside (SNP), PHE and L-NAME (inhibitor of NO synthase) were studied either under normoglycaemic conditions (100 mg/dl d-glucose) or after 60 min of hyperglycaemic perfusion (500 mg/dl d-glucose). d-mannitol was used as a hyperosmotic control. Hyperglycaemia did not alter vasodilator responses to ADO or SNP in the presence or absence of L-NAME. Furthermore, hyperglycaemia, compared with normoglycaemia, did not alter vasoconstrictor responses induced by L-NAME or PHE. Sixty minutes of exposure to 500 mg/dl of d-glucose in an isolated, non-beating, buffer-perfused rat heart did not significantly affect coronary vascular smooth muscle vasodilator responses to NO and ADO or alter alpha(1)-adrenoceptor-mediated vasoconstrictor responses to PHE. Furthermore, an unchanged vasoconstrictor response to L-NAME suggests that acute hyperglycaemia did not alter NO bioavailability.