Enhancement of beta-adrenoceptor function after reperfusion following cardioplegic arrest in rat hearts.

We investigated alterations in a beta-adrenoceptor (BAR) system after reperfusion following hypothermic ischemia induced by a high-potassium (18 meq/liter) cardioplegic solution in isolated rat hearts. Materials were divided into two groups: the reperfusion group (Gr-R, n = 5) with 40 min reperfusion following 40 min cardioplegic arrest (10 degrees C) and the control group (Gr-C, n = 5) with no ischemia as time-matched perfused control. BAR and adenylate cyclase activities in crude membrane fractions were compared. Results showed that basal, NaF-, and forskolin-stimulated adenylate cyclase activity did not differ between the two groups. The maximal enzyme activity in the presence of 10(-4) M (-)-isoproterenol was higher in Gr-R than in Gr-C, while the net activity stimulated by (-)-isoproterenol was 74% higher in Gr-R than in Gr-C. The [125I]Iodocyanopindolol [( 125I]CYP) binding assay showed that BAR density was 14% higher in Gr-R than in Gr-C, while the affinity was not significantly different. The IC50 values of (-)-isoproterenol for [125I]CYP binding were lower in Gr-R than in Gr-C and the proportion of high-affinity binding sites was higher in Gr-R than in Gr-C. These data showed that 40 min reperfusion following hypothermic cardioplegic arrest (40 min) resulted in significant increases in myocardial BAR density and maximal (-)-isoproterenol-stimulated adenylate cyclase activity, and enhancement of BAR affinity for beta-adrenergic agonists due to the increase in the proportion of high-affinity binding sites.