Vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.
Testing for the susceptibility for vasodepressor reaction in humans involves the combination of restriction of venous return by passive upright tilting and the administration of isoproterenol. To explore the basis of the vasodepressor test in humans, the present experiment examined whether a reduced cardiac volume coupled with adrenergic stimulation causes a vasodepressor reaction in rats. Vasodepressor reaction was defined as paradoxical heart rate slowing in conjunction with hypotension during inferior vena caval occlusion. Inferior vena caval occlusion was performed for 60 s and the maximum changes in R-R were measured during seven states as follows. (A) Under control conditions inferior vena caval occlusion alone accelerated the rate in 32 of 32 rats (delta R-R, -13.9 +/- 1.7 ms, p less than 0.001). (B) When inferior vena caval occlusion was performed during an infusion of isoproterenol (0.5-1.0 micrograms.min-1), a vasodepressor reaction was observed in all rats as the heart rate slowed (delta R-R, +138.1 +/- 14.8 ms, p less than 0.001). The vasodepressor reaction was further examined during isoproterenol and inferior vena caval occlusion under five additional states. (C) After atropine the vasodepressor reaction was unchanged (delta R-R, +132.7 +/- 24.8 ms, p less than 0.001). (D) After bilateral vagotomy the paradoxical slowing was eliminated. (E) After intrapericardial lidocaine the paradoxic slowing was eliminated. (F) After bilateral stellectomy nonsignificant slowing was still present, but this was markedly reduced when compared with B (p less than 0.001). (G) Following chronic chemical sympathetic denervation with 6-hydroxydopamine the paradoxic bradycardia was eliminated.


CONCLUSIONS
(1) Reduced cardiac volume combined with adrenergic stimulation can stimulate a vasodepressor reaction; (2) the vasodepressor reaction requires signalling by the afferent but not efferent vagal fibers; (3) the bradycardia is mainly due to withdrawal of sympathetic efferent tone.
Waxman
M B
MB
Department of Medicine, University of Toronto, Ont., Canada.
Asta
J A
JA
Cameron
D A
DA
Endrenyi
L
L
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004195:Disease Models, Animal; D004333:Drug Administration Routes; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007022:Hypotension / Q000139:chemically induced / Q000209:etiology*; D007262:Infusions, Intravenous; D007545:Isoproterenol; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D016627:Oxidopamine / Q000494:pharmacology; D010496:Pericardium; D051381:Rats; D017208:Rats, Wistar; D013233:Stellate Ganglion / Q000502:physiology; D013575:Syncope / Q000209:etiology* / Q000503:physiopathology; D013924:Thrombophlebitis / Q000150:complications*; D013997:Time Factors; D014628:Vagotomy; D014682:Vena Cava, Inferior / Q000502:physiology*
D001285:Atropine; D016627:Oxidopamine; D008012:Lidocaine; D007545:Isoproterenol