| Abstrakt: |
Recently, the 1adrenoceptor was shown to mediate direct coronary vasodilation independent of metabolic demand in canine arrested heart preparation. To investigate the 1adrenoceptormediated direct vasodilation in a beating heart preparation, we compared coronary blood flow CBF and coronary sinus oxygen tension PO2in anesthetized openchest dogs using a 1selective agonist, T0509. T0509 0.0050.05 gkg intravenously, i.v. increased the maximal rate of increase in left ventricular pressure LV dpdtmaxand heart rate HR to an extent similar to that induced by isoproterenol ISO without decreasing diastolic blood pressure DBP. A 1adrenoceptor antagonist, —bisoprolol 10 gkg, but not a 2adrenoceptor antagonist, ICI 118,551 30 gkg, inhibited the T0509induced increase in LV dpdtmaxand HR. Thus, T0509 showed selective 1stimulation at the doses used. T0509 also caused 1selective relaxation in isolated coronary arteries. ISO increased both CBF and PO2. The early phase of the increase in CBF and the concurrent increase in PO2were inhibited by ICI 118,551, whereas the late phase of the increase in CBF was inhibited by —bisoprolol. T0509 increased CBF, and this increase was inhibited by —bisoprolol. A slight but significant increase in PO2induced by T0509 was not altered by these doses of the antagonists. Our results indicate that the T0509induced increase in CBF is due mainly to an indirect effect on myocardial 1adrenoceptors. 1Adrenoceptormediated direct vasodilation could not be demonstrated clearly in the beating heart, even when a combination of T0509 and a selective 2adrenoceptor antagonist was used. |
