Intracerebroventricular (i.c.v.) administration of ouabain to chloralose-anesthetized, vagotomized cats elicited a dose-related increase in blood pressure and heart rate followed by ventricular arrhythmias; these effects were attributable to a sympathoadrenal discharge triggered fromthe centeral nerouv system. In presence of an effective vascular α-blockade with an i.v. α-blocker, the vasopressor response to i.c.v. ouabain was reverse toa vasodepressor one; this is reminiscent of the ‘vasomotor reversal phenomenon of Dale’. On the other hand, in the presence of an effective β-blockade with an i.v. β-blocker the vasopressor response was augmented. The vascular response to i.lc.v. oubain is thus the net effect mediated by both α- and β-2-receptors and the blockade of one unmasks the other. The pre-existing α-blockade prevented the appearance of arrhythmias after i.c.v. auabain. This may have been due to the ability of the α-blocker to prevent the rise in BP, however, a direct antiarrhythmic effect on the heart may also have been involved. The pre-existing β-blockade failed to significantly affect the tachycardia and the incidence of arrhythmias. This suggests that adrenergic neurogenic arrhythmias differ from the arrhythmias induced by exogenously administered catecholamines, since the latter are completely antagonized by β-blockers wehreas the former and less readily antagonized. Further, the ability of a β-blocker to inhibit the isoprenaline-induced tachycardia (as a test of β-blockade) may not accurately reflect the ability to antagonized the cardiac effects evoked by a strong and diffused sympathetic stimulation. Futhermore, it appears that the blockade of cardiac β-receptors is not equivalent to surgical sympathetic denervation of the heart and that the arrhythmogenic stimuli originating in the central nervous system may travel to the heart through pathways resistant to conventionally employed antagonists such as β-blockers.
- Neurogenic arrhytmias
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