Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have observed that pial arteriolar dilation in response to hypercapnia and hypotension is abolished after cerebral ischemia in newborn pigs. We determined whether direct generation of activated oxygen on the brain surface (OX: xanthine oxidase, hypoxanthine, FeCl3, and FeSO4) or topical arachidonate altered pial arteriolar responsiveness in a manner similarly to cerebral ischemia. OX, which generated more brain surface superoxide than reperfusion after ischemia, dilated pial arterioles. This dilation was reversed within 10 min of the end of exposure. OX produced ultrastructural changes in pial vessel endothelium and appeared to cause intravascular aggregation of granulocytes. After OX, prostanoid-dependent pial arteriolar dilations in response to hypercapnia and hypotension were attenuated, whereas constrictor responses to norepinephrine and acetylcholine and dilator responses to prostaglandin E2 and isoproterenol were not affected. After OX, hypercapnia increased cortical periarachnoid cerebrospinal fluid prostanoids modestly, whereas acetylcholine produced the normal strong stimulation of prostanoid synthesis. Arachidonate (10(-4) M and 7 x 10(-4) M) also caused reversible pial arteriolar dilation but did not alter subsequent pial arteriolar responses. Therefore, although arachidonate did not mimic the effects of ischemia-reperfusion on pial arteriolar reactivity, OX produced alterations that are qualitatively similar, although quantitatively less, than those produced by ischemia.
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PMID:Activated oxygen and arachidonate effects on newborn cerebral arterioles. 212 Oct 51

TJ-960 is a Japanese Kampo (traditional herbal) medicine used for the treatment of epilepsy. It's a crude drug, an extract of nine herbs, and consists of many known and unknown components. Among the known components of TJ-960, we found that 5,6,7-trihydroxy-2-phenyl-4H-1-benzopyran-4-one (baicalein) might be the most potent scavenger for radicals. In the present study, we examined in vitro the radical scavenging effect of baicalein in detail using electron spin resonance spectrometry. Furthermore, we examined in vivo its effect on the thiobarbituric acid-reactive substances (TBARS) levels and superoxide dismutase in the brain of rats with FeCl3-induced epilepsy and on hippocampal delayed neuronal death in gerbils with transient ischemia. In in vitro experiments, baicalein quenched in a dose-dependent manner 1,1-diphenyl-2-picrylhydrazyl, superoxide, and hydroxyl radicals. In the FeCl3-induced epileptic model, baicalein suppressed the increase in the TBARS level at the FeCl3-injected site. Baicalein also inhibited hippocampal neuronal death induced by 5 min of cerebral ischemia in gerbils. Hence the present study suggested that baicalein is one of the active components in TJ-960, which partially contributes to the antiepileptic and neuronal protective effects of TJ-960, and that the mechanism of its pharmacological action is based upon radical quenching and antioxidative effects.
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PMID:Free radical scavenging action of baicalein. 821 13

The purpose of this study was to develope a rat model of cerebral artery thrombosis by adding FeCl3 to the surface of right middle cerebral artery (MCA) for 30 min. After 4 h, 8 h, 24 h, 48 h, 72 h, 1 week and 2 week, the extent of neurologic deficits of rats was evaluated and after 24 h and 48 h the size of cerebral infarction was measured. The results indicate that the features of neurologic deficits and infarction were similar to those of the rat focal cerebral ischemia model established by Tamura et al (1981). The nature of thrombus formed in our experiment is combined-thrombus. The antithrombotic effect of aspirin and the thrombolytic effect of urokinase were also examined. Aspirin (50 mg.kg-1) was given by duodenum 30 min before adding FeCl3 to the surface of the right MCA and urokinase (4000 U.kg-1, iv) was given 30 min after thrombosis. After operation, the behavior of rats were observed. The cerebral infarction was evaluated 24 h after thrombosis. The infarcted areas in the aspirin and the urokinase groups were reduced to 20% and 11% those of the control group, respectively. The neurologic deficits were also attenuated. These studies suggest that this rat model may be used for testing not only antithrombotic but also thrombolytic agents.
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PMID:[A rat middle cerebral artery thrombosis model for evaluation of thrombolytic and antithrombotic agents]. 870 41

In the present paper, the role played by Na+/Ca2+ exchanger (NCX) in focal cerebral ischemia was investigated. To this aim, permanent middle cerebral artery occlusion (pMCAO) was performed in male rats. The effects on the infarct volume of some inhibitors, such as tyrosine-6 glycosylated form of the exchanger inhibitory peptide (GLU-XIP), benzamil derivative (CB-DMB) and diarylaminopropylamine derivative (bepridil), and of the NCX activator, FeCl3, were examined. FeCl3, CB-DMB, bepridil and GLU-XIP, a modified peptide synthesized in our laboratory in order to facilitate its entrance into the cells through the glucose transporter, were intracerebroventricularly (i.c.v.) infused. FeCl3 (10 microg/kg) was able to reduce the extension of brain infarct volume. This effect was counteracted by the concomitant icv administration of CB-DMB (120 microg/kg). All NCX inhibitors, GLU-XIP, CB-DMB and bepridil, caused a worsening of the brain infarct lesion. These results suggest that a stimulation of NCX activity may help neurons and glial cells that are not irreversibly damaged in the penumbral zone to survive, whereas its pharmacological blockade can compromise their survival.
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PMID:Evidence for a protective role played by the Na+/Ca2+ exchanger in cerebral ischemia induced by middle cerebral artery occlusion in male rats. 1497 99