The New Guinean small-eyed snake (Micropechis ikaheka) is a cause of life-threatening envenoming. Previous studies on M. ikaheka
venom have indicated the presence of
neurotoxins as well as
myotoxins. This study examined the in vitro myotoxic effects of M. ikaheka
venom and the efficacy of a polyvalent
antivenom in neutralizing these effects.
Venom (50 microg/ml) produced a slowly developing
contracture and inhibition of direct twitches of the chick biventer cervicis nerve-muscle preparation in the presence of
tubocurarine (10 microM).
Myotoxicity was confirmed by subsequent histological examination of tissues. This
myotoxicity was prevented by the prior addition of polyvalent snake
antivenom (30 U/ml). However, the addition of
antivenom (30 U/ml) 1 h after
venom administration failed to reverse or prevent the further inhibition of direct twitches. In addition,
venom (1-10 microg/ml) produced concentration-dependent contractions of the guinea-pig isolated ileum. These effects were dependent on
phospholipase A2 (PLA2) activity of the
venom as evidenced by the ability of the PLA2 inhibitor
4-bromophenacyl bromide (4-BPB; 1.8 mM) to prevent this activity. This study indicates that M. ikaheka
venom causes significant
myotoxicity and that polyvalent snake
antivenom may be a potential treatment for the myotoxic effects in patients envenomed by this species.