A. Tarasiuk et al., EFFECTS OF SCORPION-VENOM ON CENTRAL AND PERIPHERAL CIRCULATORY RESPONSE IN AN OPEN-CHEST DOG-MODEL, Acta Physiologica Scandinavica, 161(2), 1997, pp. 141-149
Scorpion venom can induce in dogs severe haemodynamic changes leading
to rapid rise in systemic blood pressure and cardiac output, followed
by reduction of cardiac output and blood pressure within 1 h. The decr
ease in cardiac output is not related to myocardial dysfunction (Taras
iuk et al. 1994). We hypothesized that scorpion venom affects cardiac
output by reducing venous return to the heart. Venous return was studi
ed by steady-state measurements of cardiac output, the pressure gradie
nt and resistance to venous return, in 16 dogs following injection of
0.05 mg kg(-1) venom obtained from the scorpion species Leiurus quinqu
estriatus. In eight of the 16 dogs, atropine (0.1 mg kg(-1)) was given
15 min prior to venom injection (n = 4) or 85 min (n = 4) after venom
administration. In five additional dogs, the stability of the prepara
tion over time was evaluated following the same protocol without the i
njection of the venom. At 15 min, the venom induced an increase in blo
od pressure (80%) and cardiac output (250%) (P < 0.001) with little ef
fect on heart rate. At 90 min, cardiac output and heart rate declined
considerably below baseline (P < 0.001). Atropine prevented the decrea
se in heart rate, but did not affect the reduction of cardiac output.
Five minutes after venom injection, mean circulatory pressure increase
d by 300% (P < 0.001), which was accompanied by a rightward shift of t
he venous return curve with no effect on resistance to venous return.
At 120 min, mean circulatory pressure recovered and resistance to veno
us return remained at 40% (P < 0.01) above baseline. This study indica
tes that, in dogs, scorpion venom affects cardiac output by modifying
the determinants of venous return. The initial increase in cardiac out
put is related to increased mean circulatory pressure since resistance
to venous return did not change. The later fall in cardiac output. is
related to the reduction of mean circulatory pressure and increased r
esistance to venous return.