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)

Sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (POCA) inhibits carnitine palmityltransferase I and fatty acid oxidation. The effects of POCA on cardiac function and on tissue levels of carnitine and coenzyme A esters were studied in the isolated rat heart subjected to 90 minutes of ischemia with and without 15 minutes of reperfusion. The perfusion medium contained 1.2 mM palmitate and 5.5 mM glucose plus or minus 0.5 mM POCA. This compound prevented accumulation of long-chain acylcarnitine and coenzyme A esters during ischemia and significantly improved the recovery of cardiac output after ischemia and reperfusion. Short-chain acylcarnitine levels were increased during ischemia by POCA. No effects were noted on tissue ATP and lactate levels. POCA may protect the ischemic heart by preventing accumulation of these toxic metabolites and by stimulating glucose utilization during ischemia.
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PMID:Effects of POCA on metabolism and function in the ischemic rat heart. 374 56

Sodium-independent binding of [3H]gamma-aminobutyric acid ([3H]GABA) to membranes prepared from ischemic-damaged rat striatum was studied by kinetic and time-course analysis. Three days after 40 min of ischemia, [3H]GABA binding increased fourfold over control values. Scatchard analysis of the binding showed that ischemia significantly increased the affinity (KD) and the total number of binding sites (Bmax) for the high-affinity GABA receptor. These results support the conclusion that transient forebrain ischemia damages striatal GABAergic neurons.
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PMID:Increased binding of [3H]GABA to striatal membranes following ischemia. 630 Mar 37

Sodium thiopental was administered to 10 dogs following embolization of the middle cerebral artery. Its effect on the "grace period" for revascularization was investigated by performing embolectomies 6 hours later. We observed a striking reduction in the size of infarction in the animals treated with thiopental at moderate and prolonged dosage levels. The control animals treated with pentobarbital received less protection against ischemia although blood levels were similar to those of the experimental groups during the period of vascular occlusion.
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PMID:The controlled delivery of thiopental and delayed cerebral revascularization. 725 21

It has been proposed that electrophysiological changes following coronary artery occlusion result from inhibition of the adenine nucleotide translocase and that these changes can be reduced by carnitine infusion or reproduced by infusion of K+-atractyloside. In the present study, we recorded bipolar electrograms during serial 3- to 5-min occlusions of the left anterior descending coronary artery in open-chest, anesthetized dogs. DL-Carnitine (100-200 mg/kg iv) prior to coronary artery occlusion did not significantly alter ischemia-induced electrogram changes. L-Carnitine (100 mg/min ia) distal to the site of occlusion during coronary artery occlusion partially reversed ischemia-induced electrogram changes, but these effects resembled those produced by intra-arterial infusion of NaCl. During normal perfusion, intra-arterial infusion of K+-atractyloside (750 mumol/10 min) or equimolar KCl produced similar reversible flattening of perfused zone electrograms. Sodium atractyloside (750 mumol/10 min ia) did not produce electrogram changes. We conclude that 1) carnitine does not attenuate ischemia-induced electrogram changes in this model and 2) K+-atractyloside-induced electrogram changes are primarily due to K+.
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PMID:Effects of carnitine and atractyloside on canine cardiac electrical activity. 731 75

Mongolian gerbils were observed for the effects of beta-methasone on ischemic brain edema which developed during ischemia or after blood flow restoration. The severity of brain edema was determined by measuring water content of the ischemic cerebral hemisphere, using the wet and dry methods. Sodium and potassium ions were extracted from homogenized brains with 0.75N HNO2 and ion concentration measured by flame photometry. Passage of RISA from blood into the cerebral parenchyma, as an indicator of blood-brain barrier change, was determined with a gamma-scintillation counter. In the cytotoxic edema model, animals were killed after 9 h permanent ischemia or 3 h after 1 h ischemia. In the simultaneous cytotoxic and vasogenic edema model, the animals were killed either 20 h or 3 days following 1 h ischemia, or 3 h after blood flow restoration following 6 h ischemia. Steroid treatment was ineffective in ischemic brain edema of the cytotoxic or vasogenic type.
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PMID:Effect of steroid on ischemic brain edema. Analysis of cytotoxic and vasogenic edema occurring during ischemia and after restoration of blood flow. 736 44

A method of perfusing the isolated human colon in vitro was developed to study the effect of the short-chain fatty acid n-butyrate on sodium absorption under controlled conditions. The isolated colon was viable in vitro provided that ischemia to the colon prior to perfusion was less than 40 min. Viability was judged on glucose utilization, mucosal potential difference, an sodium absorption. Sodium absorption from the lumen was observed either with or without 20 mM n-butyrate. In a control group sodium absorption (nmol/min/cm2 /+- SEM) was 320 /+- 10 (four perfusions, nine observation intervals) and potassium secretion 26 /+- 3 (four perfusions, nine observation intervals). With 20 mM n-butyrate sodium absorption was 1960 /+- 480 (four perfusions, ten observation intervals) (P less than 0.0025). Potassium secretion was 72 /+- 2 (four perfusions, ten observation intervals) and (P less than 0.025). Butyrate absorption was 254 /+- 60 (four perfusions, ten observation intervals) and correlated linearly with the unidirectional flux (Jm leads to S) of sodium (linear coefficient of 0.714, P = less than 0.001). These results suggest that the presence of bacterial short-chain fatty acids may determine the efficiency of sodium absorption in the colon and also indicate that an absence of short-chain fatty acids in the colon could be one factor leading to diminished sodium absorption in the colon of man.
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PMID:Effect of short-chaim fatty acid on sodium absorption in isolated human colon perfused through the vascular bed. 746 Jul 12

Sodium-activated K+ channels (IK(Na)) are a class of large-conductance ion channels expressed in several populations of vertebrate neurons, mammalian cardiac myocytes and Xenopus oocytes. These channels are activated by the binding of Na+ to sites located on the cytoplasmic face of the channel. The physiological functions of IK(Na) channels have been difficult to ascertain, in part because their activation typically requires Na+ concentrations considerably higher than those that are normally present in the cytosol. However, there is now evidence suggesting that IK(Na) can play a role in the regulation of neuronal excitability, the modulation of the action-potential waveform, and the responses of excitable cells to hypoxia and ischemia.
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PMID:Na(+)-activated K+ channels: a new family of large-conductance ion channels. 751 95

Intracellular sodium accumulation, cellular swelling, and energy deficiency are ischemia-associated processes that participate in the transition to irreversible ischemic injury. This study aims to determine the relationship among these parameters in intact rat hearts during global ischemia at 4 degrees C. High-energy phosphates were determined by 31P nuclear magnetic resonance, intracellular sodium accumulation was measured by 23Na spectroscopy with the shift reagent dysprosium triethyl tetraaminohexaacetic acid [Dy(TTHA)3(-)], and cell volumes were measured by 59Co and 1H spectroscopy with use of the extracellular marker Co(CN)3-(6). Intracellular sodium flux rates were 1.53 +/- 0.17, 0.17 +/- 0.05, and 0.30 +/- 0.06 mumol.g dry wt-1.min-1 at 0-1.5, 2-7, and 9-12 h, respectively. Sodium influx resulted in accumulation of the ion: 10% after 4 h, 16% after 10 h, and 29% after 12 h. Water followed sodium into the cells at two constant molar ratios (Na+/H2O): 3.80 +/- 0.15 x 10(-3) during the first 8 h of ischemia and 7.8 x 10(-3) at 8-12 h. Relative to initial intracellular volume, cells swelled by 38% after 8 h and 46% after 12 h; reperfusion reduced cellular swelling to 25 and 36%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac energetics, cell volumes, sodium fluxes, and membrane permeability: NMR studies of cold ischemia. 757 2

High-speed MR diffusion/perfusion imaging was performed to assess variable degree stenosis of the MCA and the formation of cytotoxic edema in a cat model of acute ischemia. Sodium transport was estimated in synaptosomes isolated from moderately perfused or non-perfused brain tissue. Complete MCA occlusion for 50-75 min produced a major disruption of brain sodium transport, whereas continued preservation of ion homeostasis and the activation of adaptive cell volume regulatory systems was associated with longer duration of moderate severity of ischemia. Preservation of neuronal ion homeostasis might be one of the main mechanisms contributing to the relative tolerance of the brain to moderate reductions in cerebral blood flow.
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PMID:Mechanisms of brain injury associated with partial and complete occlusion of the MCA in cat. 797 49

Hyponatremia in cats produced brain edema, detectable by both magnetic resonance imaging (MRI) and increased brain water, with a compensatory decrease of brain sodium. Sodium transport was measured in synaptosomes from hyponatremic cat cerebral cortex. The sodium efflux via Na(+)-K(+)-ATPase was significantly higher (144%) than control, while sodium influx via the Na+/H+ antiporter was significantly decreased (74%). Both responses tend to decrease brain intracellular sodium and thus, brain cell osmolality. Ischemia following unilateral middle cerebral artery occlusion also resulted in brain edema. However, the efflux of sodium via both Na(+)-K(+)-ATPase and sodium channels actually decreased, both maladaptive responses. Furthermore, when ischemia was superimposed upon hyponatremia, all of the cerebral adaptive changes which had been induced by hyponatremia alone were rendered ineffective. This resulted in further elevations of brain water and sodium. Hyponatremia superimposed upon ischemia thus worsens the brain edema associated with ischemia alone. Thus, ischemia impairs the ability of the brain to adapt to hyponatremia, probably by eliminating the compensatory mechanisms of brain sodium transport initiated by hyponatremia.
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PMID:Severe brain edema associated with cumulative effects of hyponatremic encephalopathy and ischemic hypoxia. 797 57


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