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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We attempted to determine if the cholinomimetic activity of the psychotropic drug minaprine was related to the amelioration of the delayed neuronal death induced by cerebral ischemia in Mongolian gerbils. Minaprine improved the passive avoidance deficit induced by cerebral ischemia, and the histopathological ischemic neuronal changes in the hippocampal CA1 neurons were diminished. These effects were completely inhibited by treatment with the cholinergic blocker scopolamine. Rectal temperature fell about 1.5 degrees C immediately after cerebral ischemia and hyperthermia occurred 30 and 60 min after recirculation. Minaprine had no effect on body temperature before or after ischemia. Physostigmine and tetrahydroaminoacridine (THA), drugs which stimulate the cholinergic system, improved passive avoidance deficits and prevented the delayed neuronal death. These effects of physostigmine and THA were completely inhibited by scopolamine. Pentobarbital and diazepam also improved the passive avoidance deficit and prevented the destruction of CA1 neurons. In contrast with minaprine, these effects of pentobarbital and diazepam were not inhibited by scopolamine. As the protective effect of minaprine against ischemia-induced delayed neuronal death is related to cholinomimetic activities, these events differ from those seen with pentobarbital and diazepam.
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PMID:Cholinomimetic activity of minaprine is related to the amelioration of delayed neuronal death in gerbils. 152 97

Using a repeated acquisition procedure in a three-panel runway apparatus, the effects of minaprine on the impairment of working memory produced by scopolamine, ethylcholine aziridinium ion (AF64A) or cerebral ischemia were investigated in rats. Minaprine (3.2-32 mg/kg IP) as well as idebenone (10-100 mg/kg IP) and physostigmine (0.1-0.32 mg/kg IP) dose-dependently reduced the increase of errors (pushes made on the two incorrect panels located at each choice point) induced by 0.56 mg/kg IP scopolamine. Cerebral ischemia for 5 min caused a significant increase of errors in the runway task. Minaprine at 3.2 and 10 mg/kg administered IP immediately after blood recirculation and again 30 min before the runway test conducted 24 h after ischemia, significantly reduced increases in errors expected to occur after 5 min of ischemia. Physostigmine 0.1 mg/kg similarly attenuated the increase in errors in ischemic rats. However, minaprine at doses up to 32 mg/kg IP failed to reduce the increase of errors induced by AF64A 2.5 nmol injected into the dorsal hippocampus. These findings suggest that minaprine exerts an ameliorating effect on amnesia produced by scopolamine and cerebral ischemia, probably through mediation of its stimulant action on central cholinergic systems.
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PMID:Minaprine improves impairment of working memory induced by scopolamine and cerebral ischemia in rats. 231 27

The cerebral protective effects of minaprine were examined using the following methods, i.e., complete ischemia by decapitation in mice, histotoxic anoxia by potassium cyanide (KCN) in mice, hypobaric hypoxia in mice, asphyxic anoxia in normal rats and cerebral ischemia induced by bilateral carotid artery occlusion (BCAO) in strokeprone spontaneously hypertensive rats (SHR-SP). Minaprine showed positive effects on all the mouse models. Minaprine led to an improvement in the hypoxia-induced impaired electroencephalogram activity, in normal rats. All vehicle-treated SHR-SP died within 20 hr after BCAO, whereas pretreatment with minaprine (50 mg/kg x 5 days) decreased the mortality within 20 hr after BCAO. Beneficial effects of minaprine for treating cerebral hypoxia, anoxia and ischemia are discussed.
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PMID:Protective effects of minaprine on the cerebrum of rodents. 317 36