A. Tarasiuk et al., EFFECTS OF ANTIVENOM SEROTHERAPY ON HEMODYNAMIC PATHOPHYSIOLOGY IN DOGS INJECTED WITH L-QUINQUESTRIATUS SCORPION-VENOM, Toxicon (Oxford), 36(7), 1998, pp. 963-971
In dogs, scorpion venom causes an immediate increase in cardiac output
that declines below baseline Values within one hour. We tested the hy
potheses that antivenom given before venom injection may prevent chang
es in cardiac output, while antivenom given after the inotropic stage
of envenomation cannot reverse cardiac output decline. Twenty-five ane
sthetized, mechanically Ventilated dogs were given 0.1 mg/kg IV venom
of the scorpion Leiurus quinquestriatus. The dogs were randomized into
4 groups: 5 dogs were given venom alone (control group) and 6 dogs we
re given 6 mi of antivenom one minute before venom injection while 8 a
nd 6 dogs were given 6 mi of antivenom 20 and 60 min after venom injec
tion, respectively. Parameters reflecting respiratory and circulatory
functions were measured for 180 min after venom injection. Scorpion ve
nom caused a gradual decrease in heart rate, an initial elevation of s
ystemic and pulmonary blood pressure and cardiac output followed by a
decline in these parameters. PO2, pH and HCO3- gradually decreased, wh
ile PCO2 gradually increased from baseline. Antivenom given before ven
om 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 a
nd pH and a decrease in PCO2. We assume that antivenom clears free tox
ins from the circulation and since cardiac output and HCO3- did not im
prove after this clearance, we conclude that following intravenous ven
om 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 g
iven after venom injection may be secondary to reversion of cholinergi
c effects of the venom. Improvement in respiration may be also explain
ed by reversion of the toxic effects on Ca2+ activated K+ channels of
branchial smooth muscle. All these effects may be secondary to clearan
ce of toxins by the antivenom. (C) 1998 Elsevier Science Ltd. All righ
ts reserved.