Background Co2nduction velocity is known to be an important determinant of the electrical stability of the heart. Slowing of conduction velocity is implicated in the genesis of re-entrant cardiac arrhythmia and there is substantial interest in the pathological causes of slowed conduction. Despite this, current understanding of the basic physiological mechanisms regulating conduction velocity is poor. It is unclear whether the sympathetic nervous system directly regulates the conduction of electrical impulses within the ventricular myocardium. Interpretation of existing studies, largely performed in vivo, are complicated by non-cardiac effects of catecholamine infusion. To address this, we have examined the effects of bilateral sympathetic nerve stimulation (SNS) on conduction velocity in then ventricles of isolated guinea pig hearts.
Objective To determine the effects of SNS on conduction velocity in the guinea pig heart.
Methods High resolution spatiotemporal optical mapping was conducted in electrically paced hearts before and during bilateral SNS. Hearts were mechanically uncoupled using blebbistatin (15micromol/L) and stained with commonly used potentiometric dyes (Rh-237 or Di-8-ANEPPS). A region of interest (ROI) spanning from the apex to the mid-wall of the left ventricle was analysed. Pacing stimuli were applied at the epicardial apex and an activation map was generated. This activation map was then used to calculate conduction velocity using the multi-vector method.
Results Figure 1 presents data on the regulation of ventricular conduction velocity by SNS in the isolated innervated guinea pig heart. A typical analysis is shown in figure 1A, which shows a change in conduction velocity from 78 to 89 cm/s with SNS and a reduction in the total activation time within the selected ROI from 8.9 to 8.3 ms. This effect was reproducibly seen in hearts stained with Rh-237, as shown in Figure 1B, where conduction velocity is consistently increased by SNS in a rate-independent manner (mean increase of 7.9±0.4%). Comparable data for hearts stained with Di-8-ANEPPS are presented in figure 1C, which shows no observable effect of SNS. Summary data in figure 1D illustrate that Di-8-ANEPPS not only abolishes the response to SNS, but also significantly slows conduction velocity in comparison to Rh-237 stained hearts. Further analysis demonstrated similar changes in heart rate, action potential shortening and heterogeneity of action potential duration with SNS in Rh-237 and Di-8-ANEPPS stained hearts. Thus, the effects of Di-8-ANEPPS on the regulation of conduction velocity by SNS are not due to general inhibition of the actions of the sympathetic nervous system. Rather, Di-8-ANEPPS appears to interfere with the normal physiological regulation of ventricular conduction velocity.
Conclusions SNS directly regulates conduction velocity in the ventricular myocardium of the guinea pig heart, but Di-8-ANEPPS inhibits this response.
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