Mouse paw oedema induced by Habu snake (Trimeresurus flavoviridis) venom: inhibition by morphine, naloxone and methylnaloxone alone or in combinations.

The oedema produced in the mouse by intraplantar injection of the venom of Trimeresurus flavoviridis was inhibited by morphine (Mo) and by naloxone (Nx); the action of Mo increased with the dose, whereas that of Nx first progressed and thereafter regressed with the dose; very small doses of Nx antagonized Mo. Methylnaloxone (MeNx), a quaternary ammonium derivative of Nx was much less effective than Nx by the subcutaneous route but almost as effective by the intraplantar route. Peripheral opioidergic receptors are thus likely to be involved. Very high doses of Mo acted an synergistically with an optimal dose of EDTA or zymosan; complex interactions occurred between lower doses of Mo or Nx and EDTA or zymosan.

Antagonists of mouse paw oedema induced by Habu snake (Trimeresurus flavoviridis) venom. Inhibitions by various antagonists administered alone or in combinations.

When injected into the sole of the hind paw of mice, Habu snake (Trimeresurus flavoviridis) venom produced a prolonged oedema (72 hours). When administered alone, most of the studied drugs (mepyramine, methysergide, cyproheptadine, indomethacin, aspirin, dexamethasone and aprotinin) inhibited this oedema only partially and transiently (less than 7 hours). Some drugs however (EDTA, Biogel P4, zymosan and celluloses) were able to abolish it progressively. Combinations of some of these drugs resulted in various synergisms; in particular important and prolonged inhibitions were observed with aprotinin-dexamethasone, one of these drugs and EDTA, and especially EDTA-zymosan, which abolished totally the oedema from 2 hours after the injection of the venom to its end (72 hours). Antagonisms between components of combinations were also observed. The mechanisms of these synergisms and antagonisms are discussed. In particular, it is suggested that the blockade of the two pathways "classical" and "alternative", of the complement by EDTA and zymosan respectively might account for their important and early synergism. Antagonisms also helped in indicating some mechanisms of action.

[Study of Vipera seoanei venom, Lataste, 1879 (Reptilia, Viperidae)]. / Etude du venin de Vipera seoanei Lataste, 1879 (Reptilia, Viperidae).

The venom of Vipera seoanei, species from the north-western Iberic Peninsula and adjacent territories in France, is completely neutralised by different anti-venomous immune sera against European vipers. Its toxicity, sensibly lower than V. berus berus and V. aspis zinnikeri venoms, is close to V. aspis aspis venom.