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)

Extracts of acetone-dried powders from ischemic gerbil brain were examined for phospholipase A1 and A2 activities with phosphatidylethanolamine at pH 7.2. Ischemia was induced by bilateral ligation, and the animals were killed by immersion into liquid nitrogen. Bilateral ligation with ketamine as general anesthetic resulted in a rapid, transient increase in phospholipase A2 activity. The activity increased from 0.46 nmol/h/mg protein at 0 time to 0.82 nmol/h/mg protein at 1 min of ligation. Phospholipase A1 activity also increased from 0.7 go 1.3 nmol/h/mg protein within the 1st min. When Nembutal was used as anesthetic, the phospholipase activation was earlier, within the first 30 s. Similar results were found for ischemia induced by decapitation of Wistar rats without anesthesia. Bilateral ligation of the carotid arteries of the gerbil is known to increase the concentration of free fatty acids, particularly arachidonate. This increase is, at least in part, due to phospholipase A activation. As ethanolamine phospholipase A2 in brain does not require Ca2+ for activity, these results suggest that phospholipase A2 activation in ischemic brain results from a covalent modification of the enzyme.
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PMID:Activation of ethanolamine phospholipase A2 in Brain during ischemia. 711 83

Changes of gastric movements and ulcerogenic mechanisms in reserpine (6 mg/kg s.c.)-induced ulcer were studied in Wistar male rats weighing 180 to 220 g after fasting for about 20 hr. Under anesthesia with Nembutal (30 mg/kg i.p.), rats were fixed on their backs. The abdomen was incised and the stomach was exposed. Gastric movements of the fundic glandular area of greater curvature (A), the fundic-antral area of lesser curvature (B), and the neighboring area of pylorus (C) were recorded electromyographically after placing a small bipolar electrode of 1 mm distance on each area. Spontaneously, many higher amplitudes were found in area B and less found in area A. In area C, there were the least number of spikes and the lowest amplitudes. These gastric movements were inhibited until 1 hr after reserpine followed by a gradual increase in spikes and higher amplitudes. This increase was long-lasting and most marked in area B. Increased gastric movements due to reserpine were completely inhibited by atropine and vagotomy, moderately inhibited by hexamethonium and diphenhydramine, and only weakly inhibited by l-phenylephrine, l-isoproterenol, phentolamine, propranolol, metiamide, and methysergide. In reserpine-induced ulcer, ischemia occurred most markedly in area A, but erosions initiated from area B as reported previously. In area B, the gastric movements were most active, and the erosions were inhibited by the drugs which suppress gastric movements. These results suggest that reserpine-induced ulcer is due not only to the ischemia in the earlier stage, but also to the long-lasting hypermotility in the later stage.
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PMID:[Gastric movements and reserpine-induced ulcer in rats]. 715 93

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

Ischemia/reperfusion (IR) damage is a major cause of dysfunction in transplanted organs. The objective of the present study was to correlate in vivo measurements of respiratory chain (RC) function with histological and physiological parameters. Non-invasive in situ (surface fluorescence) measurements of mitochondrial NADH and near infrared spectroscopic measurements of cyt aa3 were made in unstored (Group 1) and 72 hour stored (1 to 2 degrees C) (Group 2) autografted rabbit kidneys. The effect of sodium pentobarbitone on NADH levels was investigated. In Group 1, there was a significant change in the redox state of cyt aa3 in all (N = 6) kidneys on reperfusion which correlated with organ viability and increased NADH oxidation and minimal edema on histological examination. In Group 2 there was no significant change in cyt aa3 compared to baseline, and this correlated with poor long term organ viability, slower NADH oxidation, and severe cortical edema. Pentobarbitone inhibition of the RC resulted in rapid and complete reduction of NAD+ in Group 1, but none or only a slight reduction in Group 2. The results demonstrate that it might be possible in future to predict organ viability and histological changes by non-invasive measurements of RC dysfunction in the clinical transplant situation.
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PMID:Non-invasive measurement of respiratory chain dysfunction following hypothermic renal storage and transplantation. 807 62

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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