Neural mechanism underlying tachycardia induced by nonhypotensive a-v shunt.
The mechanism underlying tachycardia resulting from nonhypotensive arteriovenous shunt (shunt open plus infusion of blood to compensate for the fall in mean arterial pressure resulting from opening of a shunt) was investigated in anesthetized, artificially ventilated dogs. In dogs with intact autonomic innervation, dogs with beta-adrenergic blockage (BB), and dogs with BB plus spinal section at C7 (BBSS), opening of the shunt resulted in tachycardia (P less than 0.01 for all comparisons), which was, however, not significantly different on comparison among groups (P greater than 0.40 for all comparisons). This shows that afferent and efferent sympathetic-mediated reflexes do not play a significant role in this tachycardia response. Additionally, the tachycardia response was significant in dogs with BBSS plus right or left vagotomy, but it was completely abolished in dogs with BBSS plus bilateral vagotomy. This suggests that in dogs with blockade of sympathetic afferent and efferent pathways, tachycardia resulting from nonhypotensive arteriovenous shunt may be due to a cardioacceleratory reflex with its ascending and its descending pathways in each vagus nerve.
D000818:Animals; D001166:Arteriovenous Shunt, Surgical; D004285:Dogs; D005260:Female; D006321:Heart / Q000294:innervation; D006339:Heart Rate; D007796:Laminectomy; D008297:Male; D011311:Pressoreceptors / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D012018:Reflex; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology*
D011433:Propranolol