Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effect of nizofenone on pyramidal response (PR), electrocorticogram (ECoG) and regional cerebral blood flow (rCBF) following recirculation after complete global brain ischemia was compared with that of pentobarbital in gallamine-immobilized cats. The basilar artery and the branches of both carotid arteries (superior thyroid artery, dorsal muscular branch, internal carotid artery, occipital artery and ascending pharyngeal artery) were all ligated. The cats were subjected to complete brain ischemia by occluding both common carotid arteries for 45 min, followed by 180 min recirculation. rCBF of the cortex (suprasylvian gyrus) and the internal capsule was monitored by the hydrogen clearance method. Blood gases were regulated within a range determined previously in freely-moving cats throughout the experiment. Nizofenone (1 mg/kg, i.v.) facilitated the recovery of PR and ECoG, and it inhibited the phenomenon of secondary suppression evidenced by interruption and reversion of the recovery process. rCBF showed good recovery throughout the recirculation period. Pentobarbital (20 mg/kg, i.v.) facilitated the recovery of PR during the early period of recirculation, but secondary suppression of PR, associated with the decline of rCBF, was evident. These results suggest that the ameliorative effect of nizofenone on the recovery of neuronal functions is due to its ability to protect neurons against ischemic anoxia and to prevent interruption of postischemic circulation, and also the good recovery of rCBF is due to its ability to protect vasculature against ischemic anoxia.
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PMID:[Effect of nizofenone on pyramidal response, electrocorticogram and regional cerebral blood flow following recirculation after complete global brain ischemia in cats]. 651 84

We previously reported that whole-brain free fatty acids (FFA) rose almost linearly for up to 1 h after decapitation of unanesthetized rats and was significantly attenuated by pentobarbital anesthesia. However, our values for total FFA and arachidonic, stearic, oleic, and palmitic acids were severalfold higher than those obtained by previous investigators. Based upon the suggestion that this may be due to FFAs released from di- and triglycerides in the quantitation of FFAs, we have now analyzed and improved our procedures for TLC separation of FFA and reassessed the accumulation of FFA in whole brain during decapitation ischemia in unanesthetized and pentobarbital-anesthetized rats. FFA levels in whole brain after 0.5 min of ischemia were one-half to one-fourth the levels previously reported after 1 min of ischemia. The rise in FFA between 0.5 and 60 min of ischemia was 9-fold for total FFA, and between 7 and 12-fold for each of the FFAs quantitated. Pentobarbital significantly attenuated the rise of all FFAs with, however, greater effects on oleic and palmitic acids than previously reported.
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PMID:Reassessment of brain free fatty acid liberation during global ischemia and its attenuation by barbiturate anesthesia. 682 83

Uteroplacental ischemia is associated with uterine renin release in pregnant nephrectomized rabbits. In the present study, uterine and renal renin release after uteroplacental ischemia were investigated in 10 Australian white rabbits at 24 to 28 days' gestation. Pentobarbital was administered, and both uterine arteries were ligated close to their origins. Blood samples were taken for plasma renin activity (PRA) determinations from the femoral artery, uterine vein, and right renal vein before ligation and at 30 and 60 minutes after ligation. Mean arterial blood pressure (MAP) was monitored throughout. In five additional pregnant rabbits renal blood flow (RBF) was measured with an electromagnetic flowmeter. The preligation uterine vein-artery PRA difference was not significant (1.9 +/- 1.1 ng/ml/hr). Postligation uterine vein-artery PRA was 11.4 +/- 3.2 at 30 minutes and 6.6 +/- 1.9 ng/ml/hr at 90 minutes (p less than 0.02). Preligation renal vein-artery PRA was 32.3 +/- 10.5 ng/ml/hr (p less than 0.02) and did not change significantly after ligation. MAP remained stable and RBF was unchanged after uterine artery ligation. These observations confirm the finding that the kidney is the primary source of renin in the normal pregnant rabbit and demonstrate that following acute uteroplacental ischemia there is significant uterine renin release even when the kidneys are intact.
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PMID:Uterine and renal renin release after ligation of the uterine arteries in the pregnant rabbit. 698 78

The cardioprotective effects of L-659,989, a specific platelet-activating factor (PAF) receptor antagonist, were investigated in an ischemia/reperfusion model in rats. Pentobarbital-anesthetized rats were subjected to left main coronary artery occlusion (1 h) followed by reperfusion (1 h) (MI/R); Sham-operated rats were used as controls (Sham MI/R). Rats receiving vehicle showed reduced survival rate (60%), marked myocardial injury (necrotic area/total area = 54.5 +/- 6%; necrotic area/area at risk 76.6 +/- 6.7%), high serum creatine phosphokinase (CPK) activity (150 +/- 10 U/ml), and increased myocardial myeloperoxidase (MPO) activity in the area at risk (AR, 6.2 +/- 0.5 U x 10(-3)/g protein) and in the necrotic area (6.6 +/- 0.7 U x 10(-3)/g protein). PAF plasma levels increased significantly during reperfusion and peaked at 15 min of reperfusion. Administration of L-659,989 enhanced survival rate (80%), reduced myocardial damage (necrotic area/total area 25.6 +/- 3.5%; necrotic area/AR 34.6 +/- 5.4%), attenuated the increase in serum CPK (50 +/- 6 U/ml) and decreased MPO activity both in the AR (2.8 +/- 0.3 U x 10(-3)/g tissue) and in the necrotic area (2.3 +/- 0.5 U x 10(-3)/g tissue). Our results suggest that PAF-inducing adhesion and activation of polymorphonuclear leukocytes (PMN) plays a significant role in the injury associated with ischemia/reperfusion.
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PMID:Protective effects of L-659,989, a platelet-activating factor receptor antagonist, in myocardial ischemia and reperfusion in rats. 751 38

We tested the hypothesis that inhibition of nitric oxide synthase (NOS) activity in brain before ischemia decreases postischemic hyperemia. Pentobarbital-anesthetized piglets underwent 15 min of complete global cerebral ischemia induced by elevation of intracranial pressure followed by 20 min of reperfusion. Before ischemia the animals were randomly assigned to receive either intravenous N omega-nitro-L-arginine methyl ester (L-NAME 10 mg/kg, n = 6, or 50 mg/kg, n = 6) or an equal volume of saline (10 ml, n = 8). Serial cerebral blood flow (radiolabeled microspheres) was measured at baseline and during ischemia and reperfusion. Forebrain postischemic hyperemia was documented after administration of saline (42 +/- 4 to 88 +/- 10 ml.min-1.100 g-1) and 10 mg/kg L-NAME (36 +/- 4 to 59 +/- 9 ml.min-1.100 g-1) but not after 50 mg/kg L-NAME (29 +/- 3 to 34 +/- 7 ml.min-1.100 g-1). However, the percent reduction in cerebral vascular resistance (CVR) fell during reperfusion to a similar extent in all three groups because of differences between groups in cerebral perfusion pressure changes during the protocol. CVR fell to the lowest level at 8 min of reperfusion in the saline-treated animals (2.0 +/- 0.16 to 0.68 +/- 0.05 mmHg.ml-1.min.100 g) compared with the L-NAME-treated animals (50 mg/kg: 4.0 +/- 0.3 to 1.8 +/- 0.2 mmHg.ml-1.min.100 g).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of nitric oxide synthase inhibition on postischemic cerebral hyperemia. 754 58

We investigated the effects of vinconate and pentobarbital against the alterations in spirodecanone binding in the gerbil striatum and hippocampus 5 h and 7 days after 10 min of cerebral ischemia, using receptor autoradiography. Vinconate and pentobarbital were given intraperitoneally 10 and 30 min prior to ischemic insult, respectively. The spirodecanone binding in vehicle-treated gerbils subjected to ischemia was unchanged in the brain 5 h after recirculation, compared with that in sham-operated animals. Seven days after ischemia, a significant elevation in the spirodecanone binding was observed in the striatum and the stratum radiatum of the hippocampal CA1 sector and the hippocampal CA3 sector of the vehicle-treated animals. Other regions showed no significant change in the binding. Vinconate and pentobarbital showed no significant change in the striatum and hippocampus 5 h after ischemia. However, the administration of vinconate inhibited a significant elevation in the spirodecanone binding in the lateral striatum and the stratum radiatum of hippocampal CA1 sector 7 days after ischemia. Pentobarbital also prevented a significant elevation only in the lateral striatum. A histological study revealed that cerebral ischemia caused severe neuronal damage in the lateral striatum and hippocampal CA1 and CA3 sectors. However, ischemic neuronal damage was not observed in the dentate gyrus. An immunohistochemical study also showed that numerous reactive astrocytes were evident in the hippocampus, particularly in the hippocampal CA1 sector, 7 days after ischemia. The present study demonstrates that cerebral ischemia can cause a conspicuous elevation in spirodecanone binding in the striatum and hippocampus. They also suggest that the postischemic elevation in the spirodecanone binding is partly prevented by treatment with vinconate and pentobarbital. These results suggest that the postischemic elevation in spirodecanone binding sites may reflect expression of reactive astrocytes.
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PMID:Effects of vinconate and pentobarbital against postischemic alterations in spirodecanone binding sites in the gerbil brain. 786 40

We examined clinical recovery from repeated brain ischemic insults that have been reported to affect cytologic outcome. Brain ischemia was induced in the rat by four-vessel occlusion. A 30-min ischemia was given as a single insult or induced in animals made ischemic 24 h earlier by a 10-min insult but exempt both of brain hypoperfusion and neurologic deficit in spite of a partial necrosis of the CA1 sector of hippocampus. Repeated ischemia was associated with a significantly poorer clinical outcome as indicated by an increase in percentage of rats that exhibited postischemic seizure activity combined with the percentage of unconvulsive rats exhibiting neurologic deficits after 72 h of reperfusion (81% vs. 50% after a single 30-min ischemia). Examination of hippocampal damage showed that neurons surviving the first ischemia did not acquire resistance to the second ischemia. Pentobarbital given from start of overt seizures (30 to 60 mg/kg, IP, thrice daily) was able to stop convulsions and to antagonize processes involved in ischemia-induced neuronal death of CA1 hippocampus.
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PMID:Neurologic and cytologic outcome following repeated ischemia. Effect of pentobarbital. 795 72

We investigated the postischemic alterations in dopamine D1 receptor and Ca2+/calmodulin independent cyclic adenosine monophosphate (cyclic AMP) selective phosphodiesterase in gerbils and examined the effect of pentobarbital on these alterations. [3H]SCH 23390 and [3H]rolipram, respectively, were used to label dopamine D1 receptor and Ca2+/calmodulin independent cyclic-AMP selective phosphodiesterase. Transient cerebral ischemia was induced for 10 min, and pentobarbital (40 mg/kg) was administered intraperitoneally 30 min prior to ischemia. 5 h after ischemia, [3H]rolipram binding decreased significantly in the striatum and hippocampus, whereas no significant change was found in [3H]SCH 23390 binding. 7 days after ischemia, however, there was a marked reduction in both [3H]SCH 23390 and [3H]rolipram binding in the striatum and hippocampus, where histological neuronal damage was found. Pentobarbital significantly ameliorated postischemic decreases in [3H]rolipram binding both 5 h and 7 days after recirculation in most areas studied. Furthermore, this drug significantly prevented postischemic reduction in [3H]SCH 23390 binding (only) 7 days after ischemia. These results suggest that alteration of cyclic AMP selective phosphodiesterase is more sensitive at an earlier stage after ischemic insult than that of dopamine D1 receptors. Our results also demonstrate that pentobarbital reduces the alteration in [3H]SCH 23390 and [3H]rolipram binding after cerebral ischemia.
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PMID:Effect of pentobarbital on postischemic SCH 23390 and rolipram binding in gerbil brain. 822 65

Insoluble ubiquitin conjugates (UC) in the mitochondrial fraction of the gerbil cortex were analyzed following transient forebrain ischemia. At 1 h of reperfusion after 2-10 min of ischemia, UC increased as the duration of ischemia was prolonged. Pre-treatment with pentobarbital, rather than post-treatment immediately after recirculation, reduced the increase of UC at 1 h of reperfusion following 5 min of ischemia. Pentobarbital had no effect on in vitro ubiquitination of heat-denatured lysozyme by the extract of gerbil cortex. These results suggest that increase in UC is dependent on ischemic damage and pentobarbital attenuates the increase of UC by relieving injury during ischemia.
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PMID:Increase in ubiquitin conjugates dependent on ischemic damage. 840 94

The purpose of this study was to examine the protective effects of an N-methyl-D-aspartate receptor antagonist, MK-801, and pentobarbital against neuronal damage in a global ischemia model under controlled body temperature. Gerbils were subjected to 3 and 5 min of bilateral common carotid artery occlusion. MK-801 (1 and 5 mg/kg, i.p.), administered 30 min before ischemia, significantly attenuated the degeneration of hippocampal CA1 pyramidal cells after 3 min of ischemia in a dose dependent manner, but had no such effects after 5 min of ischemia. Pentobarbital (40 mg/kg, i.p.) also protected against CA1 damage after 3 min of ischemia but not after 5 min of ischemia. Thus, we confirmed the protective effects of these agents under normothermic conditions, although these effects were limited to shorter periods of ischemia.
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PMID:Limited but evident protective effects of MK-801 and pentobarbital on neuronal damage following forebrain ischemia in the gerbil under normothermic conditions. 847 99


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