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At least 325 records · Page 18Linked to original sources
PubMed1978

Effect of dimercaptosuccinic acid on toxicity of Habu snake (Trimeresurus flavoviridis, Hallowell) venom.

Habu venom (HV) incubated with dimercaptosuccinic acid (DMS) or thiosuccinic acid (TMA), was given subcutaneously to mice. The LD50 of HV was 19.7 mg/kg, and after treatment with TMA and DMS, it was 38.1 and 47.1 mg/kg, respectively. The logarithm concentration--mortality curve for the DMS-treated HV shifted to the right compared with the curve for crude HV. The curve for the TMA-treated HV was intermediate between these two. Decimal two mg of HV was then incubated with DMS, and such was given intramuscularly to mice. Hemorrhage and edema which occurred after administration of crude HV were markedly decreased with injection of DMS-treated HV, but the myonecrosis was not greatly affected. At 24 hr after the intramuscular dosing of 1 mg of HV into rats, lymphopenia, acute involution of lymphatic tissue, decrease in liver glycogen and lipid granules in zona fasiculata were apparent, indicating the mark of a stressor. When the DMS-treated venom was administered, the blood picture and histological findings did not differ greatly from the controls. As DMS has marked anti-HV activity, it may be used to investigate treatments for cases of Habu snake bite.

Adrenal Cortex↗
PubMed1983

Enhancement of hepatic microsomal aniline hydroxylation by Habu snake (Trimeresurus flavoviridis) venom fractions.

Enhancement of aniline hydroxylation by Habu snake venom was studied in vitro. The fraction which was isolated from Habu venom through column chromatography caused the enhancement of aniline hydroxylation of hepatic microsomes obtained from untreated rats. This fraction was heat stable and free from phospholipase activity. Enhancement of aniline hydroxylation was not clear in crude Habu venom or the unheated fraction, but appeared after heating of the fraction. This fraction enhanced aniline hydroxylation at low concentrations, followed by inhibition at high concentrations, but inhibited aminopyrine N-demethylation dose-dependently. Aniline hydroxylation was enhanced by the heated fraction at more than 1 mM aniline, and the enhancement was rather decreased at more than 10 mM aniline. The degree of the enhancement by the heated fraction increased with increasing pH.

Aminopyrine↗
PubMed1990

Characteristics of cardiovascular effects of the venom of habu (Trimeresurus flavoviridis) in rats.

Characteristics of the cardiovascular effects of habu venom were studied in vivo and in vitro in rats. Aortic pressure (AoP), heart rate (HR) and renal cortical blood flow (RCBF) assessed by a laser-Doppler flowmeter were measured in anesthetized rats. Administration of habu venom (0.2-1.6 mg/kg, i.v.) dose-dependently produced a fall in AoP without a marked change in HR. RCBF decreased significantly along with the decline in AoP. Heated habu venom (70 degrees C for 5 min) or the residual venom by dialysis produced similar hemodynamic responses to nonheated crude habu venom. Although habu antivenin significantly reduced the effects of habu venom, indomethacin, aprotinin, atropine, captopril and chlorpheniramine did not. Methylprednisolone significantly attenuated these effects. Habu venom (10(-5) to 3 x 10(-4) g/ml) produced dose-dependent relaxations of the isolated rat aorta preparations precontracted with norepinephrine or KCl, which were not affected by indomethacin, nordihydroguaiaretic acid, p-bromophenacyl bromide, mepacrine, methylene blue or de-endothelialization. These results indicate that habu venom, particularly its heat-stable component(s) which has at least more than 10,000 molecular weight, produces hypotensive and vasorelaxant effects in rats, and suggest that eicosanoids, kinins, histamine, ACh, and endothelium are scarcely involved in these effects.

Animals↗
PubMed1980

Electron microscopic observations on the pit organ of a crotaline snake Trimeresurus flavoviridis.

The pit membrane in the pit organ of a crotaline snake is about 15 micron thick. Myelinated nerve fibers from the trigeminal nerve enter the pit membrane and swell into palmate structures on demyelination. Demyelinated fibers repeat branchings and their terminals contain many mitochondria. The terminal portion is not surrounded with Schwann cell processes. There are many small vesicles (30-60 nm in diameter) in the extra-cellular space in close association with the nerve terminal membranes. The spreading of branches from each palm seemed to have a definite territory which would correspond to the unit area detected with electrophysiological methods. But no "unit structure" was revealed by electron microscopy. intraepithelial free nerve endings exist in the outer epithelial layer. The nerve bundles from the trigeminal branches contain some unmyelinated fibers which come in close contact with vascular elements in the pit membrane.

Animals↗