Effects of adrenergic-receptor blockade and ligation of spleen vessels on the hemodynamics of dogs injected with scorpion venom. Academic Article uri icon


  • Objective In dogs, scorpion venom evokes a rapid increase in cardiac output (CO) that decreases below baseline level in 1 hr. The changes in CO have recently been shown to be related to the effect of the venom on venous return. In the present study, we tested the hypothesis that changes in determinants of venous return are secondary to sympathoadrenal stimulation evoked by the venom, which causes splenic contracture in the first stage of envenomation leading to increased mean circulatory pressure (MCP) and CO. Persistence of adrenergic response is the main factor leading to the second stage of envenomation, characterized by an increase in resistance to venous return (Rv) and a decrease in CO. Design Repeated measures, prospective study in dogs. Setting University-affiliated research laboratory. Subjects Mixed-breed dogs injected with scorpion venom. Interventions The effects of alpha-and beta-adrenergic-receptor blockade (blockade group, n = 9 dogs) and effects of ligation of spleen vessels (spleen ligation group, n = 11 dogs) following intravenous injection of scorpion venom from Leiurus quinquestriatus (0.05 mg/kg) were tested on the determinants of venous return and compared with the effects of scorpion venom alone (control group, n = 6 dogs). Measurements and Main Results Scorpion venom in the control group caused a marked increase in CO from 2.9 +/- 0.2 SD L/min to 6.5 +/- 2.2 L/min (p < .001) and MCP from 8.7 +/- 2.7 torr (1.2 +/- 0.35 kPa) to 21.6 +/- 1.4 torr (2.9 +/- 0.19 kPa) (p < .001) within 5 mins after venom injection. Cardiac output and MCP markedly decreased at 60 mins to 1.8 +/- 0.3 L/min (p < .001) and 7.3 +/- 3.8 torr (1.0 +/- 0.5 kPa) (p < .05), respectively. Rv did not change at 5 mins but increased from 196 +/- 50 dyne[center dot]sec/cm5 to 335 +/- 102 dyne[center dot]sec/cm5 (p < .01) at 60 mins. Adrenergic-receptor blockade attenuated the increase of CO and MCP at 5 mins, from 2.1 +/- 0.5 L/min to 2.7 +/- 1 L/min (p < .001) and from 5.6 +/- 2.0 torr (0.8 +/- 0.27 kPa) to 7.5 +/- 2.3 torr (1.0 +/- 0.31 kPa) (p < .05), respectively. By 60 mins, both CO and MCP returned to baseline, while Rv was not affected and was maintained at 204 +/- 158 dyne[center dot]sec/cm5. Ligation of spleen vessels prevented a CO increase at 5 mins and it was maintained at baseline value (2.5 +/- 0.6 L/min). However, MCP increased from 7.9 +/- 0.5 torr to 12 +/- 1.3 torr (p < .05). At 60 mins, CO decreased to 1.6 +/- 0.7 L/min (p < .01) while MCP returned to baseline. The changes in MCP were accompanied by significant increases of Rv from 152 +/- 24 dyne[center dot]sec/cm5 to 383 +/- 93 dyne[center dot]sec/cm5 (p < .001) at 5 mins, and 510 +/- 175 dyne[center dot]sec/cm5 (p < .01) at 60 mins. Conclusions The changes in CO and MCP following scorpion venom injection in dogs are in part related to sympathetic stimulation. Adrenergic-receptor blockade attenuated the initial inotropic effect of the venom and completely prevented a late decrease in CO and MCP. The increase in Rv is the most important factor for late decrease in CO, and results from persistent adrenergic-receptor stimulation. In addition, an Rv increase apparently expresses vasoconstriction and redistribution of blood flow. The initial increase in CO and MCP is explained mainly by adrenergic-receptor effects on the spleen leading to augmented circulatory blood volume. (Crit Care Med 1999; 27:365-372)

publication date

  • January 1, 1999