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

Abstract

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.

Effects of acute vagal nerve stimulation on the early passive electrical changes induced by myocardial ischaemia in dogs: heart rate‐mediated attenuation

“…As previously mentioned, these data strongly suggest that vagally mediated reductions in myocardial electrical impedance occurred secondary to heart rate‐dependent reductions in cardiac metabolic demand. Although these results are in agreement with previous observations on the vagal influence during ischaemia (Senges et al 1983), it should be noted that dual‐chamber pacing (right atrium and right ventricle) was used to maintain heart rate during vagal stimulation (VAG/P group). The resulting atrioventricular synchronization could alter ventricular filling (stroke volume) or sympathovagal balance (Chiladakis et al 2004), thereby confounding the response to vagal nerve stimulation.…”

“…Interestingly, and in agreement with the acute attenuation of the early ischaemic myocardial electrical impedance increase observed in the present study, vagal nerve stimulation has been shown to reduce myocardial energy demand and metabolic derangements during ischaemia (Senges et al 1983; Sammel et al 1983; Sidi et al 1995). For example, Sammel et al (1983) reported that, in addition to a potent anti‐arrhythmic effect, vagal stimulation during coronary occlusion reduced myocardial creatine kinase depletion, roughly in proportion to a reduction in the heart rate–blood pressure product.…”

“…Therefore, it is possible that increased cardiac parasympathetic activation during ischaemia may protect against arrhythmias by modulating the passive electrical properties governing electrotonic coupling in the myocardium. Since it is well known that the cardiac parasympathetic nerves have stronger atrial than ventricular actions (Takehashi et al 1985; Levy & Warner, 1994, Brack et al 2004), vagal nerve stimulation would provoke large reductions in heart rate, thereby decreasing cardiac metabolic demand during myocardial ischaemia (Senges et al 1983; Sammel et al 1983; Sidi et al 1995). As a consequence, changes in cardiac parasympathetic activity could indirectly influence the ventricular passive electrical properties early during ischaemia.…”