Reference

Failure to detect chromosome damage in bone-marrow cells of mice and Chinese hamsters exposed in vivo to some ergot derivatives

Failure to detect chromosome damage in bone-marrow cells of mice and Chinese hamsters exposed in vivo to some ergot derivatives. Matter, B. E. (Biol. Med. Res. Div., Sandoz Ltd., Basel, Switz.). J. Int. Med. Res., 4(6), 382-92 (English) 1976. CODEN: JIMRBV. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) A known chem. mutagen, Trenimon (I) [68-76-8], and 3 ergot derivs. (ergotamine tartrate [379-79-3], dihydroergotoxine mesylate [8067-24-1], and methysergide hydrogen maleate [129-49-7]) were tested in mice and Chinese hamsters for mutagenic effects. In contrast to I, which proved to be a powerful mutagen, none of the ergot derivs. showed an effect. Thus, these compds., at subtoxic or therapeutic dose-levels, have no potential for damaging the chromosome complement of in vivo treated mammals.Except for chemicals metioned above, 68-76-8 and 8067-24-1 are also used. .

Failure of ergotamine to alter the lipolytic effect of somatotropin in dogs

Failure of ergotamine to alter the lipolytic effect of somatotropin in dogs. Sirek, A. M. T.; Sirek, A.; Sirek, O. V. (Fac. Med., Univ. Toronto, Toronto, Ont., Can.). Pharmacology, 15(6), 481-4 (English) 1977. CODEN: PHMGBN. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Hypophysectomized dogs were injected intravenously with bovine somatotropin (GH) [9002-72-6], and plasma free fatty acid (FFA) concns. were measured over a period of 2 h. The response consisted of an initial redn. in the concn. of plasma FFA followed by a rebound and a delayed rise above baseline values. When the animals were given a single intravenous injection of ergotamine tartrate (I tartrate) [379-79-3] 30 min prior to the administration of GH, the biphasic pattern with the sluggish rise in plasma FFA was retained. This finding is contrary to the results of identical expts. with dihydroergotamine, which proved to be a potent amplifier of the lipolytic effect of GH. Since the only difference between these two compds. is the presence of the double bond at C9 and C10 of the lysergic acid moiety, it appears that unless this bond is satd. the alkaloid is not capable of functioning as a biol. amplifier.