Bothrops jararacussu venom and its major toxin, bothropstoxin-I (BthTX-I), possess myotoxic and neurotoxic activities. The ability of commercial equine antivenom to neutralize these activities was studied in mouse isolated phrenic nerve-diaphragm (PND) and extensor digitorum longus (EDL) preparations by indirect stimulation (0.1 HZ, 0.2 ms). The time required to produce 50% neuromuscular blockade in the PND and EDL preparations was, respectively, 70 +/- 11.5 min and 58 +/- 8 min for B. jararacussu venom (50 microg/mL), and 31 +/- 6 min and 30 +/- 3 min for BthTX-I (20 microg/mL). After a 120-min incubation, the creatine kinase (CK) concentrations in the EDL preparations were 3464 +/- 346 U/L and 3422 +/- 135 U/L following exposure to venom (50 microg/mL) and BthTX-I (20 microg/mL), respectively. Antivenom neutralized the neuromuscular blockade induced by the venom and toxin in PND preparations in a dose-dependent fashion, but only partially neutralized this effect in EDL. Antivenom also effectively prevented the venom- and toxin-induced release of CK from EDL. In contrast, histological analysis showed that the morphological damage caused by B. jararacussu venom and BthTX-I in the EDL was only partially prevented by the anti- venom. These results indicate that commercial equine antiserum fully protects against the neurotoxic action of B. jararacussu and BthTX-I in PND preparations, but only partially protects against the neurotoxic and myotoxic actions of the venom and its toxin in EDL preparations. Care must therefore be exercized in extrapolating results from different preparations even when similar pharmacological or physiological responses are involved.
Copyright 2000 John Wiley & Sons, Inc.