Minimal alpha 1- and alpha 2-adrenoceptor-mediated coronary vasoconstriction in the anaesthetized swine.

alpha-Adrenoceptor-mediated coronary vasoconstriction contributes to the initiation and aggravation of experimental and clinical myocardial ischaemia. However, the extent of alpha 1- and alpha 2-adrenoceptor-mediated constriction has not been characterized in the porcine coronary circulation despite the frequent use of this experimental model. Fifteen swine were anaesthetized with either alpha-chloralose, enflurane or isoflurane to determine the amount of alpha-adrenoceptor-mediated coronary constriction elicited by either the selective alpha 1-adrenoceptor agonist methoxamine or the selective alpha 2-adrenoceptor agonist azepexole. The left anterior descending coronary artery was cannulated and perfused by an external pump delivering constant blood flow from the carotid artery. Following bilateral cervical vagotomy and beta-adrenoceptor blockade with propranolol (2 mg kg-1), graded dosages of either one of the alpha-adrenoceptor agonists (9-45 micrograms kg-1 min-1) were infused into the coronary perfusion line while coronary arterial pressure (CAP) was measured through a distal side arm of the cannula to detect changes in coronary vascular resistance. Infusion of the alpha-adrenoceptor agonists was terminated when systemic arterial pressure increased. Sonomicrometers were used to measure anterior left ventricular wall thickening for the assessment of regional contractile function. During methoxamine infusion, no increase in vascular resistance was observed during alpha-chloralose, enflurane or isoflurane anaesthesia, whereas the infusion of azepexole increased CAP from 103 +/- 31 mmHg to 120 +/- 35 mmHg (alpha-chloralose), from 101 +/- 16 mmHg to 122 +/- 11 mmHg (enflurane) and from 84 +/- 20 mmHg to 94 +/- 19 mmHg (isoflurane), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)