Tarasiuk A, Khvatskin S, Sofer S
Soroka Medical Center and Department of Physiology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Toxicon. 1998 Jul;36(7):963-71. doi: 10.1016/s0041-0101(98)00011-7.
In dogs, scorpion venom causes an immediate increase in cardiac output that declines below baseline values within one hour. We tested the hypotheses that antivenom given before venom injection may prevent changes in cardiac output, while antivenom given after the inotropic stage of envenomation cannot reverse cardiac output decline. Twenty-five anesthetized, mechanically ventilated dogs were given 0.1 mg/kg i.v. venom of the scorpion Leiurus quinquestriatus. The dogs were randomized into 4 groups: 5 dogs were given venom alone (control group) and 6 dogs were given 6 ml of antivenom one minute before venom injection while 8 and 6 dogs were given 6 ml of antivenom 20 and 60 min after venom injection, respectively. Parameters reflecting respiratory and circulatory functions were measured for 180 min after venom injection. Scorpion venom caused a gradual decrease in heart rate, an initial elevation of systemic and pulmonary blood pressure and cardiac output followed by a decline in these parameters. PO2, pH and HCO3- gradually decreased, while PCO2 gradually increased from baseline. Antivenom given before venom injection prevented all the effects induced by the venom. Antivenom given at 20 and 60 min after venom injection had no effect on cardiac output and HCO3- decline, but caused an increase in heart rate, PO2 and pH and a decrease in PCO2. We assume that antivenom clears free toxins from the circulation, and since cardiac output and HCO3- did not improve after this clearance, we conclude that following intravenous venom injection, heart and circulation are rapidly affected by the toxins or by other substances released by the venom which do not respond to antivenom. Improvements in respiration and heart rate with antivenom given after venom injection may be secondary to reversion of cholinergic effects of the venom. Improvement in respiration may be also explained by reversion of the toxic effects on Ca2+ activated K+ channels of bronchial smooth muscle. All these effects may be secondary to clearance of toxins by the antivenom.
