Cardiovascular effects of scorpionfish (Scorpaena plumieri) venom

Abstract

The aim of the present study was to investigate the cardiovascular activity of Scorpaena plumieri venom in both in vivo and in vitro models. In anesthetized rats, doses of the venom (14-216 microg protein/kg) induced a transient increase in the mean arterial pressure. However at higher dose (338 microg protein/kg) this effect was followed by a sudden hypotension and the animal evolved to death. The heart rate was temporarily increased and followed by bradycardia using doses > or =108 microg/kg. In isolated rat hearts the crude venom (5-80 microg protein) produced dose-dependent positive ventricular chronotropic, inotropic, lusitropic and coronary vasoconstriction responses. Partial purification of an active fraction (CF, cardiovascular fraction) which reproduced the cardiovascular effects induced by crude venom on isolated hearts was achieved by conventional gel filtration chromatography. Adrenergic blockades, prazosin and propranolol, significantly attenuated these responses. The coronary vasoconstriction response to CF was also attenuated by chemical endothelium denudation. In conclusion, the data showed that S. plumieri fish venom induces disorders in the cardiovascular system. It also suggests that alpha(1) and beta-adrenergic receptors, and the vascular endothelium, are involved at least partially, in these cardiac effects.

Bioactive Components in Fish Venoms

“…A previous study on G. marmoratus venom also found that the relaxation response was most likely due to NO but via a muscarinic receptor independent mechanism [ 68 ]. In isolated rat hearts positive lusitropic effects were seen after exposure to both crude venom from the scorpionfish Scorpaena plumieri and from an isolated fraction with cardiovascular activity [ 71 ].…”

A review on the Scorpaena plumieri fish venom and its bioactive compounds

“…SpV was found to perform lethal, hemolytic, cardiovascular, inflammatory, integrin-binding-inhibitory and proteolytic activities [20, 22–24, 27, 29]. This spectrum of activities — observed in experimental animals — resembles those of other fish venoms previously described [1, 2].…”

“…Similarly, it was observed in animal models that SpV increases mean arterial pressure (MAP) in a dose-dependent manner. However, biphasic responses — characterized by an initial increase followed by a pronounced fall of the MAP — are achieved using higher doses (338 μg/kg), leading to the death of the animal after a few minutes [22]. This phenomenon was also observed in other fish venoms, such as P. volitans , S. horrida and S. guttata .…”

“…These responses are attenuated by a non-selective β-adrenergic antagonist, evidencing that the venom compounds could act — at least in part — directly through the presence of some adrenergic agonist in the venom and/or indirectly via the release of endogenous stores of norepinephrine from the sympathetic varicosities in the heart [22]. …”

“…SpV induces a dose-dependent increase in perfusion pressure (CPP) on the coronary bed, and a biphasic effect on intact and pre-contracted rat aortic rings — characterized by an initial and transient relaxing phase followed by a sustained contractile phase [22, 24]. It is noteworthy that variations in vascular responses induced by the same fish venom have been observed in studies applying different experimental models [1].…”