Regional myocardial blood flow and coronary vascular reserve in unanesthetized ponies during pacing-induced ventricular tachycardia

Abstract

To examine the effects of tachycardia on coronary circulation, transmural distribution of myocardial blood flow (MBF, 15-μm diameter radionuclide-labeled microspheres) was studied in six healthy adult ponies at rest (heart rate = 60 ± 7 beats · min −1), during ventricular pacing at 150 and 200 beats · min −1, as well as with ventricular pacing at 250 beats · min −1 before and during maximal coronary vasodilatation (iv adenosine infusion; 4 μmole · kg −1 · min −1). Mean aortic pressure and cardiac output were unchanged from control values with ventricular pacing. Whereas ventricular pacing at 150 and 200 beats · min −1 resulted in a progressive uniform increase in transmural MBF and well-maintained endo:epi perfusion ratio, pacing at 250 beats · min −1 did not result in a further increase in MBF compared to pacing at 200 beats · min −1 and the left ventricular (LV) subendocardial:subepicardial (endo:epi) perfusion ratio was significantly less than 1.00 (0.87 ± 0.05). Blood flow to the LV papillary muscles and subendocardium was significantly less than that recorded at 200 beats · min −1. The LV endo:epi perfusion ratio with ventricular pacing at 250 beats · min −1 during adenosine infusion resulted in a decrease in mean aortic pressure (63% of control value) and a marked further reduction in blood flow to the LV papillary muscles as well as the LV subendocardium, while MBF increased dramatically in the LV subepicardium compared to values observed during ventricular pacing at 250 beats · min −1 alone. This resulted in a LV endo:epi perfusion ratio of 0.39 ± 0.09. By contrast, transmural right ventricular (RV) MBF increased significantly and the RV endo:epi perfusion ratio was well maintained. These data demonstrate that coronary vasomotion functions to maintain LV subendocardial blood flow in the pony myocardium at a heart rate of 200 beats · min −1, while at 250 beats · min −1 exhaustion of coronary vasodilator reserve in the deeper layers limits further increase in MBF.