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)

Once brain ischemia was induced in the gerbil cerebral fronto-parietal cortex, serial changes occurred in energy metabolites and various lipids. The amounts of inositol-containing phospholipids began to decrease immediately after energy failure, followed by an increase in the amount of 1,2-diacylglycerol with a subsequent liberation of arachidonic acid and other free fatty acids. The fatty acid compositions of inositol-containing phospholipids, of 1,2-diacylglycerols produced by ischemia, and of free fatty acids liberated during ischemia were quite similar. The amount of stearic acid liberated was much larger than that of arachidonic acid between 30 s and 1 min of ischemia. On the other hand, there was no significant decrease in the amount of the other phospholipids except for phosphatidic acid. Furthermore, there was also no change in the fatty acid composition of phosphatidylcholine or phosphatidylethanolamine throughout 15 min of ischemia. The amount of cytidine-monophosphate reached a peak (36.7 nmol/g wet wt) at 2 min of ischemia. These results indicated that arachidonic acid was predominantly liberated from inositol-containing phospholipids by phospholipase C, and by the diglyceride lipase and monoglyceride lipase system rather than from phosphatidylcholine or phosphatidylethanolamine by phospholipase A2 or plasmalogenase or choline phosphotransferase during the early period of ischemia.
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PMID:Mechanism of arachidonic acid liberation during ischemia in gerbil cerebral cortex. 379 19

Gas liquid chromatography was used to study fatty acid (FA) composition of lysophosphatidylcholine (lyso-PC) and phosphatidylcholine in isolated rabbit heart mitochondria. In control, lyso-PC and PC were found to contain 95 and 66% of unsaturated FA, respectively. At 1 hour of ischemia (autolysis at 37 degrees C) the percentage of saturated FA in lyso-PC noticeably increased whereas FA composition remained unchanged. It is concluded that changes in FA composition of lyso-PC are caused by phospholipase A2 action.
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PMID:[Fatty acid composition of mitochondrial phospholipids of the ischemic heart]. 396 69

It is generally known that free fatty acids (FFA) are liberated from membrane phospholipids in the brain tissue during the early period of ischemia. However, the precise mechanism of FFA liberation from phospholipids is still unclear, even though it is a central topic of neurosurgery. As an initial step toward a better understanding of the molecular mechanism, we have investigated the effects of global ischemia upon brain lipid metabolism. Brain ischemia was evoked by rat decapitation without anesthesia. Removed brains were incubated for 1, 5, 15 or 30 min at 37 degrees C and then quickly frozen in liquid nitrogen. After extraction of total lipids from the brains by Bligh & Dyer's method, the compositions of neutral lipids and phospholipids were analyzed by thin-layer and gas-liquid chromatography. For assaying deacylating enzyme (phospholipase A) activity, the brain homogenate was used as a crude enzyme. The reaction mixture including radioactive substrate, buffer (pH 7.3 & 4.0) and enzyme was incubated for 1 hour at 37 degrees C. Lipids were extracted from reaction mixture and separated by TLC. The enzyme activity was estimated by measuring the radioactivity in FFA or lysophosphatidylcholine liberated from L-alpha-di [1-14C] palmitoyl phosphatidylcholine. The reaction mixture for the assay of reacylating enzyme (acyl CoA: lysophospholipid acyltransferase) activity, contained acyl CoA, lysophosphatidylcholine, DTNB and microsomes, and the enzyme activity was determined by the amount of released CoA-SH detected spectrophotometrically. The results demonstrated that FFA, either unsaturated or saturated, rapidly accumulated in the brain during the early period of ischemia. Di-acylglycerols were also produced in the ischemic brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain lipid metabolism during early period of global ischemia--with reference to the enzymes related to membrane phospholipid metabolism]. 402 85

It has been well recognized that acyl groups of phospholipids play an important role for structure and function of biomembrane. The turnover of these acyl groups in normal brain biomembrane is also well known. Some types of enzymic system related to this turnover has been investigated. Phospholipase A, PI-specific phospholipase C, lipase, lysophospholipase and acylCoA: lysophospholipid acyltransferase belong to these enzymic systems. In this report, the sequential changes of phospholipase A, PI-specific phospholipase C, lipase, lysophospholipase and acylCoA: lysophospholipid acyltransferase activities in ischemic rat brain were examined. The purpose of this study was to examine the enzymic changes of deacylation-reacylation cycle of biomembrane phospholipid in ischemic brain. Ischemic brain were produced by decapitation and activities of 5 enzymes were assayed in microsomal fraction. The activities of phospholipase A, PI-specific phospholipase C, lipase showed high value during early stage of ischemia for 15 or 30 min and then decreased gradually. Lysophospholipase activity was not changed for 120 min. On the other hand, acylCoA: lysophospholipid acyltransferase activity showed gradual decrease from the beginning of ischemia. There are some reports that in early ischemic stage, the concent of free fatty acids increase, while that of phospholipid decrease. The present results may suggest that the changes of free fatty acid and phospholipid in ischemic brain are related to these enzymic system.
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PMID:[The activities of phospholipase A, PI-specific phospholipase C, lipase, lysophospholipase and acylCoA: lysophospholipid acyltransferase in ischemic brain microsomal fraction]. 402 86

After periods of 5 and 30 min following decapitation, rat cerebral cortices were removed and subcellular fractions were prepared. Fractions P1A (large myelin), P1B (nuclei), P1C (cells and debris), P2A (small myelin), P2B (synaptosomes), P2C (mitochondria), and P3 (microsomes) were isolated. Free fatty acid levels of 1.0 and 1.4 mumol/g tissue were found in the homogenates at the early and late times of ischemia. In the 30-min samples, P1A, P1C, and P2A had relatively high specific contents of total free fatty acids in comparison with other subfractions. At this time P2C was relatively enriched in arachidonate, P1A and P2A were enriched in palmitate, and P2B and P3 were enriched in stearate in comparison with the homogenate. P2C had the highest ratio of polyunsaturates/saturates in its free fatty acid pool. Comparing the 5- and 30-min samples, a large increase in the quantity of free fatty acids was found in fractions P1A and P2A, so that at the later time P1A + P2A contained 60 mol% of the free fatty acid in the total subfractions derived from cerebral cortex. In comparison with the homogenate, the lack of accumulation of free fatty acids in certain membranes known to possess phospholipase activities (e.g., phospholipase A2 in P2C) and the buildup of free fatty acids in P1A and P2A led to the hypothesis that free fatty acids may be migrating outwards from intracellular sites of production and accumulating in the multilamellar structure of myelin.
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PMID:The subcellular distribution of free fatty acids released during post-decapitative ischemia in rat cerebral cortex. 408 56

Lysolecithin (lysoglycerophosphocholine, LPC) was isolated from rat cerebral cortex and quantitatively analyzed at various times after postdecapitative ischemic treatment. In addition, different procedures for extraction and analysis of the LPC in brain were evaluated. Results indicated that LPC can be quantitatively extracted into the organic phase using the conventional extraction procedure with chloroform-methanol (2:1, vol/vol). However, care should be taken to avoid using strong acids, which can hydrolyze the alkenylether side chain of the plasmalogens, resulting in the release of 2-acylphospholipids. Quantitative GLC analysis using myristoyl-LPC as internal standard revealed a level of 1.8 nmol LPC/mg protein in brain with acyl groups comprised mainly of 16:0, 18:0, and 18:1. The acyl group profile reflects that the LPC are derived mainly from phospholipase A2 action. An increase of 46% in the LPC level was observed at 1 min after ischemic treatment, but this was followed by a steady decline. Ischemia induced an increase in the LPC species that are enriched in 18:0 and 18:1 fatty acids. The transient appearance of LPC during ischemia further suggests that this phospholipid is undergoing active turnover, possibly hydrolysis by the lysophospholipase. This mechanism of action may account, at least in part, for the increase in both saturated and unsaturated fatty acids during the early phase of the ischemic treatment.
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PMID:On the status of lysolecithin in rat cerebral cortex during ischemia. 647 Jul 8

The purpose of the present study was to elucidate the effect of duodenal juice on development of gastric ulcer, in relation to changes of lipid composition and energy metabolism of the gastric mucosa in dogs. For regurgitation of duodenal juice and stagnation of gastric contents in the stomach, the duodenum was constricted below the papilla of Vater, accompanying with pyloroplasty and upper gastro-jejunostomy. Furthermore, to induce ischemia in the gastric mucosa, 0.5 ml of 1% formalin solution was injected into a descending branch of the left gastric artery. Three weeks later, U1 II-III gastric ulcer developed at the formalin injected area with severe gastritis but not with hyperacidity, and the histologic findings were similar to the one of a human gastric ulcer with hypoacidity. On assay of lipid composition in the gastric mucosa, lecithin decreased and both lysolecithin and NEFA increased, showing that lecithin of the gastric mucosa was decomposed by phospholipase A2 of the duodenal juice. In the gastric mucosa, ATP and energy charge decreased, and AMP and lactate increased, indicating that the energy metabolism was led to anaerobic glycolysis. These results revealed that the gastric mucosa becomes very fragile when duodenal juice regurgitates into the stomach and that gastric ulcer may develop even without hyperacidity when the microcirculation is disturbed in this condition.
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PMID:Effect of duodenal juice on pathogenesis of gastric ulcer. 683 47

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

Brain ischemia was produced in gerbils by contemporary occlusion of both carotid arteries. Definite changes of the energy state in brain demonstrated that carotid occlusion was effective. At short time intervals from occlusion the free fatty acid content, their distribution, and their concentration and specific activity in arachidonate were determined in brain. A noticeable increase of the arachidonate pool and that of other free fatty acids was detected at very early times from occlusion. Specific activity by arachidonate increased after 30-60 seconds from ligation. By examining arachidonate distribution and specific activity in neutral and polar lipids of brain, it is concluded that phosphatidylcholine and phosphatidylinositol represent the more important source for the release of arachidonate during ischemia. Enzymic-mediated phenomena produced free arachidonate from lipids by a mechanism yielding diglycerides further transformed into fatty acids and by lipid degradation through phospholipase A activity.
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PMID:The effect of transient ischemia on fatty acid and lipid metabolism in the gerbil brain. 722 34

A myocardial membrane fraction enriched in sarcolemma was used to determine the susceptibility of the lipids to hydrolysis by a phospholipase A2 from granulocytes. After incubation (37 C, pH 7.0, 5 mM Ca2+) with the phospholipase A2 for 30 min, a more than 3-fold increase in unesterified fatty acids was found (up to 47 nmol/mg protein; P < 0.001) relative to a control incubated without phospholipase A2 or Ca2+. This included a 10-fold increase in the arachidonic acid content (up to 42 mol%) and at least a 7-fold increase in lysophosphatidylethanolamine (up to 7.4 mol% total phospholipid-P). However, the exogenous phospholipase did not augment the quantity of lysophosphatidylcholine produced by endogenous phospholipases in the presence of Ca2+ (5 mM). These results demonstrate the in vitro susceptibility of phospholipids of myocardial membranes, particularly phosphatidylethanolamine, to the neutral-active, Ca2+-dependent phospholipase A2 from granulocytes. This work may be relevant to myocardial inflammation and tissue damage during ischemia, where heterolytic injury of the myocardium may occur subsequent to the accumulation of granulocytes.
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PMID:Lipids of myocardial membranes: susceptibility of a fraction enriched in sarcolemma to hydrolysis by an exogenous mammalian phospholipase A2. 741 9


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