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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thiopental, a well-known barbiturate, is often used in patients who are at high risk of developing cerebral ischemia, especially during brain surgery. Although barbiturates are known to affect a variety of processes in the cerebral cortex, including oxygen consumption by the mitochondria, the interrelation between mitochondrial function and anesthetics has not been investigated in detail under in vivo conditions. The aim of this study was to examine the effects of thiopental on brain functions in normoxia and under partial or complete ischemia. The use of the multiparametric monitoring system permitted simultaneous measurements of microcirculatory blood flow, NADH fluorescence, tissue reflectance, and ionic and electrical activities of the cerebral cortex. Thiopental caused a significant, dose-dependent decrease in blood flow and a significant decrease in extracellular levels of potassium, with no significant changes in NADH levels in normoxic and ischemic rats. Following complete ischemia (death), the increase in the reflectance was significantly smaller in the anesthetized normoxic group versus the awake normoxic group. The time until the secondary increase in reflectance, seen in death, was significantly shorter in the anesthetized ischemic group. In conclusion, it seems that the protective effect of thiopental occurs only under partial ischemia and not under complete ischemia.
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PMID:Effects of anesthesia on brain mitochondrial function, blood flow, ionic and electrical activity monitored in vivo. 1922 49

Thiopental is an anesthetic used for controlling high intracranial pressure (ICP) caused by brain surgery, brain trauma, and severe stroke. However, it remains controversial whether Thiopental is detrimental or beneficial in ischemic stroke. In this study, we used an animal model of ischemic stroke in spontaneously hypertensive rats to determine whether or not Thiopental is neuroprotective in the setting of brain ischemia. We observed that Thiopental caused a prolonged duration of unconsciousness with a high rate of mortality, that Thiopental created exaggerated neurological deficits that were revealed through limb placement tests at 4 days and 4 weeks after brain ischemia, and that infarct volume was increased in Thiopental-anesthetized rats. These data suggest that Thiopental is detrimental in ischemic stroke. Thus, our findings raise a caution about the use of Thiopental in the setting of ischemic stroke.
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PMID:Thiopental exaggerates ischemic brain damage and neurological deficits after experimental stroke in spontaneously hypertensive rats. 1964 67

The effects of membrane lipid disturbances induced by ischemia and exogenously added lipids on the uptake of GABA and Ca(2+) were investigated in gerbil brain synaptosomes. Ischemia was produced by bilateral ligation of common carotid arteries in Mongolian gerbil for 10 min. The level of the free fatty acids (FFA) increased significantly in ischemic synaptosomes. Incorporation of [1-(14)C]arachidonate into membrane phosphatidylinositol and phosphatidylcholine was decreased by about 20-35%. Furthermore ischemia exerted an inhibitory effect on GABA uptake but remained without effect on calcium accumulation. Thiopental application in dose of 100 mg per kg body weight 30 min before ischemia caused a protective effect on membrane lipid disturbances induced by ischemia and enhanced GABA uptake. Unsaturated fatty acids (arachidonate and docosahexanoate) in concentration of 10(?5)?10(?4) mol/l and lysocompounds (lysophosphatidylcholine and lysophosphatidylethanolamine) in concentrations higher than 10(?4) mol/l decreased GABA and Ca(2+) uptake in synaptosomes from normoxic brains. No effect was seen with saturated stearic acid. These results suggest that the inhibition of GABA uptake into ischemic synaptosomes resulted from an action of unsaturated fatty acids, arachidonic and docosahexanoic acids which were liberated during ischemia. Moreover the transient higher local concentration of lysophospholipids close to GABA carrier system may also have contributed to the inhibition observed during ischemia.
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PMID:Modification of GABA and calcium uptake by lipids in synaptosomes from normoxic and ischemic brain. 2049 30


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