Effects of acute vagally-mediated bradycardia on systemic hemodynamics and coronary blood flow before and after coronary stenosis.

The effects of short episodes (1 min) of vagally-mediated bradycardia were studied in 9 anesthetized dogs utilizing vagal stimulation and slow atrial pacing (120 and 80 beats/min) before and after graded coronary constriction of the left anterior descending (LAD) and the left circumflex (CCA). In the presence of 90% LAD stenosis, bradycardia tended to restore both the elevated total LAD coronary vascular resistance (CVR-LAD) and the reduced, total CVR-CCA towards control levels obtained at corresponding slow rates in the absence of coronary stenosis; as a result, LAD coronary flow (F-LAD) was relatively less reduced and the accessory rise of F-CCA disappeared. In the presence of combination of 90% LAD plus 70% CCA stenosis, the effects of bradycardia on total CVR-LAD and F-LAD were similar to those obtained with single 90% LAD stenosis, but the accessory flow through the CCA was abolished resulting in no significant difference of the rate-dependent alterations of total CVR-CCA and F-CCA as compared with those observed in the absence of coronary stenosis. In the presence of single or combined coronary stenosis, bradycardia restored the depressed aortic pressure and cardiac output towards control values obtained at comparable slow rates before coronary stenosis. The results support the concept that in the presence of 90% LAD stenosis vagally-mediated bradycardia 1) decreases the tension-time index (myocardial nutritional demand) shifting cardiac performance to less expensive "flow work" and 2) facilitates antegrade flow through the highly stenotic LAD thereby inhibiting accessory flow through the nonstenotic CCA.

Effect of brief periods of paced ventricular tachycardia on coronary blood flow in dogs before and after graded coronary stenosis.

The effect of short bouts (1 min) of electrically induced ventricular tachycardias (VT) of increasing rates (160-240/min) was studied in 8 anesthetized dogs before and after graded constrictions of the left anterior descending (LAD) and the circumflex (CCA) coronary arteries. In the absence of coronary stenosis, paroxysmal VT caused a significant decrease in tension-time index (TTI), coronary blood flow (CBF) and coronary vascular resistance (CVR). Single and combined coronary stenosis caused relatively small alterations of the VT-induced depression of the systemic hemodynamics but reversed the effect of paroxysmal VT on the CVR. In the presence of single 90% LAD stenosis, VT resulted in an increase in CVR-LAD and a decrease in F-LAD associated with a fall in CVR-CCA and a rise in F-CCA. Combination of 90% LAD plus 70% CCA stenosis abolished the compensatory fall of CVR-CCA resulting in a pronounced reduction of F-CCA during VT. The results support the concept that in the presence of severe coronary stenosis brief paroxysmal ventricular tachycardias do increase myocardial nutritional demand but rather decrease nutritional supply.