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)

Both Mg2+ and Ca2+ have been implicated as having roles in the pathomechanisms of cerebral ischemia. To further study the effects of these ions on postischemic histologic outcome, fasted rats were given one of three intravenous infusions: 5.0 mmol/kg MgCl2, 5.0 mmol/kg MgCl2 + 0.035 units/kg regular insulin, or 1.0 mmol/kg CaCl2. This resulted in elevated plasma Mg2+ or Ca2+ concentrations in the corresponding groups. A fourth group received 0.9% NaCl (saline). Preinfusion plasma glucose concentration was similar for all groups and was unchanged after infusion in rats receiving either saline or MgCl2 + insulin. In contrast, postinfusion glucose concentration was increased in the MgCl2 group (p less than 0.001) and decreased in the CaCl2 group (p less than 0.001) relative to saline-treated rats. Following respective infusions, all rats underwent 10 minutes of reversible forebrain ischemia (bilateral carotid artery occlusion and systemic hypotension) followed by 7 days' recovery. Six of 12 CaCl2-treated rats died 2-3 days after ischemia; all other rats remained neurologically indistinguishable, without gross neurologic deficits. Histologic injury in the neocortex and caudate was moderate in all groups. In the hippocampus, MgCl2 + insulin resulted in 66 +/- 6% (mean +/- SD) dead CA1 pyramidal cells, which was similar to the amount in saline-treated rats (68 +/- 10%). Injury was increased in the MgCl2 group (79 +/- 4% dead cells), while in surviving CaCl2-treated rats, injury was decreased (54 +/- 13%). We conclude that the increased injury in MgCl2-treated rats and the decreased injury noted in surviving rats receiving CaCl2 are due to the plasma glucose concentrations present prior to ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of elevated plasma magnesium versus calcium on cerebral ischemic injury in rats. 264 53

Verapamil and pentobarbital were compared for their actions on isolated canine cerebral (basilar and middle cerebral) and peripheral (mesenteric) arteries of similar diameter. The two agents shared several nonselective actions on canine arteries, but differed widely in potency. Both agents produced direct relaxation of cerebral, but not peripheral, arteries, and both agents inhibited constriction of cerebral and peripheral arteries by KCl and CaCl2 (in K+-depolarizing, Ca2+-deficient media). However, 1 mM pentobarbital was required to produce the same maximal effects as 4 uM verapamil. In addition, verapamil selectively blocked constriction of cerebral arteries by a receptor-mediated agent, prostaglandin F2a, while pentobarbital was nonselective in its blockade. On the basis of their comparative actions on isolated cerebral and peripheral arteries, calcium channel blockers such as verapamil may be a more rational choice in the treatment of cerebral ischemia than the barbiturates.
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PMID:Comparative actions of pentobarbital and verapamil on canine cerebral and peripheral arteries in vitro. 386 6

The effects of AMG-1 [6(5-hydroxy-2-methylpyridylamino)-9 ribofranosylpurine], an adenosine analogue, and adenosine on Ca2+-dependent and independent release of glutamate from rat synaptosomes induced by KCl 30 mmol.L-1 were studied with an enzyme-linked fluorometric assay. The synaptosomes were prepared and preincubated for 30 min at 37 degrees C. Two ml of incubation mixture containing synaptosomes (1.27 mg protein), NADP+ 1 mmol.L-1, L-glutamic dehydrogenase 50 U, CaCl2 1.3 mmol.L-1 (or EGTA 1.3 mmol.L-1) was transferred to the stirred cuvette in the fluorometer at 37 degrees C for 5 min. Then, AMG-1 (or adenosine) was added. Released glutamate (eg. fluorescent intensity) was monitored following the addition of 30 mmol.L-1 KCl. The results indicate that Ca2+-dependent glutamate release from depolarized synaptosomes is inhibited by AMG-1 (0.1 mmol.L-1) or adenosine (0.3 mmol.L-1). The action of AMG-1 seems to be similar to that of adenosine. However, no change was found on Ca2+-independent release of glutamate. This implies that the protective effect of AMG-1 against cerebral ischemia may be partially due to inhibiting glutamate release from nerve terminal via the activation of adenosine A1 receptor.
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PMID:[Effect of AMG-1 and adenosine on glutamate release from synaptosomes in rats]. 803 Apr 10

A characteristic event during reperfusion after cerebral ischemia in vivo, and reoxygenation after anoxia in vitro, is hyperoxidation of the electron carriers of the mitochondrial respiratory chain. Current studies have tested the hypothesis that there is a relation among calcium molecules derived from extracellular sources, mitochondrial hyperoxidation, and electrical recovery after anoxia in hippocampal slices. Rat hippocampal slices were superfused with artificial cerebrospinal fluids (ACSF) containing calcium chloride (CaCl2) in concentrations of: 0.5, 1, 2, and 4 mmol/L. Slices were made anoxic and then allowed to recover for 60 minutes. Reduction-oxidation shifts of NADH were measured by rapid-scanning spectrofluorometry. Synaptic activity was indicated by population spike amplitudes in the CA1 pyramidal cell subfield of the hippocampus in response to stimulation of the Schaffer collaterals. Low calcium ACSF concentrations ameliorated NADH hyperoxidation and improved synaptic transmission recovery after anoxia. High calcium ACSF concentrations had opposite effects. These data suggest a link between mitochondrial hyperoxidation and electrical recovery after postanoxia reoxygenation and support the hypothesis that cytosolic calcium overload promotes mitochondrial hyperoxidation and limits electrical recovery.
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PMID:Calcium influx from the extracellular space promotes NADH hyperoxidation and electrical dysfunction after anoxia in hippocampal slices. 946 65

Intracellular free calcium concentration ([Ca2+]i) was measured with Ca(2+)-sensitive fluorescent indicator, Fura-2/AM, in cultured brain cells using AR-CM-MIC cation measurement system, and the effects of berberine (Ber) on the changes in [Ca2+]i induced by CaCl2, norepinephrine, KCl and H2O2 were studied. The results indicate that the resting [Ca2+]i was 35 +/- 8 nmol.L-1 in Ca(2+)-free Hank's solution. Ber showed no effect on the resting [Ca2+]i when the extracellular Ca2+ were 0.01-10 mmol.L-1. Ber 1-100 mumol.L-1 dose-dependently inhibited norepinephrine and H2O2 induced [Ca2+]i elevation. Ber at high concentration (10-100 mumol.L-1) inhibited K(+)-induced [Ca2+]i elevation. This suggests that the inhibitory effects of Ber on norepinephrine, K(+)-, and H2O2-induced [Ca2+]i elevation may be one of the mechanisms against cerebral ischemia.
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PMID:[Effect of berberine on intracellular free CA2+ concentration in cultured brain cells]. 1124 11