| Abstrakt: |
To test the hypothesis that adenosine is required to mediate the sustained increase in myocardial flow evoked by isoproterenol haemodynamic indices, myocardial blood flow (microspheres), and regional myocardial oxygen consumption were measured in eight closed chest, sedated pigs (a) at control, (b) after isoproterenol (6.9(2.8) ng·kg−1·min−l (mean (SD)) infused into the left anterior descending coronary artery, (c) repeat control, and (d) after a simultaneous infusion of the same dose of isoproterenol and adenosine deaminase (10 U·kg−1·min−1). Data were acquired at one and 10 minutes after each infusion and compared with control measurements. Heart rate was held constant by atrial pacing. Peak left ventricular dP/dt (mm Hg·s−1) increased significantly (control 2190(32) mean (SD)) at both one (2900(302)) and 10 minutes (3010(391)) of isoproterenol infusion alone. At one minute of simultaneous infusion there was no change (control 1970(447)) in left ventricular dP/dt (2290(521)), although dP/dt was significantly increased at 10 minutes of simultaneous infusion (2790(483)). Transmural flow (ml·min−1·g−1) increased significantly (control 1.49(0.46)) in the distal left anterior descending zone at one (1.94(0.48)) and 10 minutes (2.07(0.27)) of isoproterenol infusion alone. In contrast, flow failed to increase (control 1.65(0.27)) during the first minute of simultaneous infusion (1.73(0.38)), although it did increase significantly by 10 minutes (1.91(0.21). Finally, although myocardial oxygen consumption (ml·min−1·100 g−1) increased significantly (control 16.4(4.7)) at both one (20.1(4.7)) and 10 minutes (19.4(3.6)) of isoproterenol infusion alone, it failed to increase (control 18.2(3.8)) at one (19.3(4.6)) and 10 minutes (19.1(3.8)) of simultaneous infusion.The data indicate that destruction of interstitial adenosine by adenosine deaminase initially impairs the ability of the myocardium to adjust to an abrupt increase in myocardial oxygen demand induced by isoproterenol. Within 10 minutes, however, the absence of adenosine is compensated for by some other mediator(s) and so flow increases despite the destruction of the nucleoside. Accordingly, adenosine appears to play a role in mediating the immediate but not the sustained flow response to isoproterenol. [ABSTRACT FROM PUBLISHER] |
