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

The synthesis and release of PGs by the isolated perfused rabbit heart upon bradykinin stimulation results from lipase stimulation which liberates arachidonic acid for PG biosynthesis. The [14C]-labelled fatty acids, arachidonate, linoleate, and oleate, when infused into the heart preparation, were efficiently incorporated into the phospholipid pool in the heart mostly in the 2-position of phosphatidylcholine. On the other hand, [14C]-palmitate was esterified into both the 1- and the 2-position. Bradykinin released bioassayable PG when injected into the rabbit hearts, regardless of which fatty acid label was incorporated into the phospholipid pool. However, only [14C]-arachidonic acid (but not [14C]-linoleate, oleate or palmitate) was liberated from the variously labelled hearts upon hormone stimulation. This selective bradykinin effect on fatty acid release suggests that hormone stimulation either activates a specific lipase that distinguishes different fatty acids in the 2-position or activates lipase which is selectively compartmented with arachidonate-containing phospholipids. Ischemia, on the other hand, appeared to non-specifically stimulate tissue lipases, resulting in a non-selective release of oleic as well as arachidonic acid. A disproportionally large release of arachidonic acid was observed accompanying a relatively small PG (10:1 arachidonate: PG ratio) production during ischemia, as compared to bradykinin (3:1 ratio), suggesting distinct mechanisms for PG biosynthesis induced by bradykinin and ischemia.
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PMID:Hormone selective lipase activation in the isolated rabbit heart. 88 98

In this study, the release of lysophospholipids (to depict phospholipase A2 activity) and diacylglycerols (DG) (to depict stimulated hydrolysis of polyphosphoinositides) was related to the decapitation-induced release of free fatty acid (FFA) in the mouse brain. To assay for lysophospholipids, Balb/c mice were injected intracerebrally with either [3H]choline or [3H]inositol for 16 h in order to label their respective phospholipids. These lipids were examined at various times (30 s to 30.5 min) after decapitation. Between 30 s and 1.5 min after decapitation, the rate of FFA release (3 micrograms FA/mg FA in phospholipids/min) was three times more rapid than that between 10 and 15 min (0.8 microgram FA/mg FA in phospholipids/min). FFA released during the initial phase were enriched in 20:4 and 18:0 whereas those released during the latter phase were nonspecific. The DG fatty acids are enriched in 18:0 and 20:4. Ischemia induced a rapid release of DG as measured by its fatty acid content (3.2 micrograms FA/mg FA in phospholipids/min). Unlike FFA, the level of DG reached a plateau after 1.5 min and remained elevated for the entire 30.5 min. In agreement with previous notions indicating the involvement of phospholipase A2 in ischemic insult, steady increases in radioactivity of both lysophosphatidylcholines and lysophosphatidylinositols were observed with time after decapitation. Based on the preferential increase in both 18:0 and 20:4 during the initial time period, the results suggest that poly-PI hydrolysis coupled to DG-lipase may contribute to the initial release of FFA, whereas the FFA released subsequent to the initial phase may be mainly a result of activation of phospholipase A2 acting on phosphatidylcholines and phosphatidylinositols.
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PMID:Decapitation ischemia-induced release of free fatty acids in mouse brain. Relationship with diacylglycerols and lysophospholipids. 138 50

In order to examine the toxic effects on the pancreas of oxygen free radicals which are generated at reperfusion after ischemia, a short term-ischemia/reperfusion model was prepared in rats. Both the anterior mesenteric artery and the celiac artery were ligated and then released to restore blood flow. In a group where the anterior mesenteric and the celiac arteries were ligated for 60 minutes, the serum levels of amylase and lipase rose 7 and 6 times, respectively, 7 hours after reperfusion. In a group ligated for 30 minutes, both levels remained unchanged. Histologically, vacuolization of the pancreatic acinar cells was observed, only in a group rats ischemic for 7 hours. In rats ligated for 60 minutes with a continuous venous infusion of superoxide dismutase (SOD) (3600 U/Kg/hour), the secretion of amylase and lipase decreased to 25 percent of that in the non-injected group. These results confirm that the oxygen free radicals, which are generated by the short term-ischemia/reperfusion method, injure the pancreas. This may lead to pancreatitis with hyperamylasemia and hyperlipasemia. Pretreatment with an active oxygen scavenger, SOD, markedly reduces the rise in serum amylase and lipase levels. This suggests that active oxygen free radicals are involved in the pathogenesis of acute pancreatitis.
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PMID:[Effect of short-term-ischemia and reperfusion on the rat pancreas]. 182 5

Nineteen combined renal and segmental pancreatic transplantations with enteric exocrine diversion were performed between May 1984 and September 1985. The one year actuarial patient survival rate and pancreatic graft survival rate were 86 and 66 per cent, respectively. Thirteen pancreatic grafts are presently functioning (two to seven months) and all of the recipients are insulin-free. Although graft cold ischemia time was kept low (a mean of 4.6 hours), a moderate graft pancreatitis developed with a peak serum amylase level of 16.8 +/- 2.2 microkatal per liter. Analysis of the fluid drained through an abdominal drain tube placed at the graft site revealed an amylase activity of 280 +/- 110 microkatal per liter on the first postoperative day and rapidly decreasing to a mean of 15 +/- 5 microkatal per liter on day 6. A pancreatic duct catheter was used to divert the exocrine juice to the exterior during the first few postoperative weeks thereby promoting healing of the pancreaticoenteric anastomosis. The volume of pancreatic juice from the ductal catheter was quite low in the first postoperative days but then rose to reach a plateau level of 500 to 600 milliliters. The amylase activity and the lipase concentration in the pancreatic juice was very high (9,100 +/- 2,450 microkatal per liter and 11.1 +/- 4.4 grams per liter, respectively) during the first postoperative day but then gradually decreased to reach a steady level after four to seven days. Intravenous administration of secretin induced a sixfold increase in the flow of pancreatic juice. An intravenous infusion of somatostatin significantly reduced the flow of pancreatic juice and the amylase activity and lipase concentration in the juice but did not abolish the secretin induced increase in pancreatic secretion.
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PMID:Studies on the exocrine secretion of segmental pancreatic grafts in humans. 243 63

The present study was designed to establish an in vitro perfused porcine pancreas preparation as a model for testing the effect of organ protective solutions on stimulated pancreatic endocrine and exocrine secretion. The pancreas was prepared and perfused for 10 min with Euro Collins solution, thereafter it was stored in the cold (4 degrees C) for various times. After 3-h and 6-h ischemia pancreatic insulin release in response to glucose was not significantly affected. After 12-h ischemia reduced pancreatic insulin secretin, increased perfusion pressure, and increased amylase and lipase release indicated pancreatic damage. Complete pancreatic dysfunction was seen after 24-h and 48-h ischemia with massive increase in perfusion pressure and low insulin secretion which did not follow a glucose-dependent release pattern, while amylase and lipase concentrations in the perfusion medium increased. Stimulated exocrine pancreatic secretion was significantly decreased already after 3-h ischemia and completely lost after 12 h.
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PMID:The perfused porcine pancreas as a model for testing organ protective solutions. 247 64

Fatty acids, the preferred substrate in normoxic myocardium, are derived from either exogenous or endogenous triacylglycerols. The supply of exogenous fatty acids is dependent of the rate of lipolysis in adipose tissue and of the lipoprotein lipase activity at the coronary vascular endothelium. A large part of the liberated fatty acids is reesterified with glycerol-3-phosphate and converted to triacylglycerols. Endogenous lipolysis and lipogenesis are intracellular compartmentalized multienzyme processes of which individual hormone-sensitive steps have been demonstrated in adipose tissue. The triacylglycerol lipase is the rate-limiting enzyme of lipolysis and glycerol-3-phosphate acyltransferase and possibly phosphatidate phosphohydrolase are the rate-limiting enzymes of lipogenesis. The hormonal regulation of both processes in heart is still a matter of dispute. Triacylglycerol lipase activity in myocardial tissue has two intracellular sources: 1. the endoplasmic reticular and soluble neutral lipase, and 2. the lysosomal acid lipase. Studies in our laboratory have indicated that whereas lipolysis is enhanced during global ischemia and anoxia, overall lipolytic enzyme activities in heart homogenates were not altered. In addition we were unable to demonstrate alterations in tissue triacylglycerol content and glycerol-3-phosphate acyltransferase activity under these conditions. Lipolysis, is subject to feedback inhibition by product fatty acids. Therefore all processes leading to an increased removal of fatty acids from the catalytic site of the lipase will stimulate lipolysis. These studies will be reviewed. In addition, studies from our department have demonstrated the capacity of myocardial lysosomes to take up and degrade added triacylglycerol-particles in vitro. Such a process, stimulated by Ca2+ and stimulated by acidosis, offers another physiological target for hormone actions.
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PMID:Hormones and triacylglycerol metabolism under normoxic and ischemic conditions. 267 63

Increased morbidity and mortality in patients with spinal cord injuries present the anesthesiologist with many problems. The extent of neuronal damage is determined not only by the initial trauma, but also by subsequent activation of lipid peroxidation and lipase reactions due to local ischemia of the spinal cord. Complete transection of the spinal cord is characterized by impairment of diaphragmatic function and cardiovascular depression due to functional sympathectomy. Since hypoxemia is a common finding in high tetraplegics, immediate, careful intubation is mandatory at the trauma site. Because of rotational instability of the cervical spine, any brisk movement of the neck must be avoided. Therefore, orotracheal intubation may be performed only after sufficient stabilization of the spine in a neutral position has been guaranteed. Functional sympathectomy of the cardiovascular system is responsible for the hypotension frequently seen in high tetraplegics. Adequate volume replacement is provided based on central venous and pulmonary capillary wedge pressures. Reduced sympathetic tone causes increased sensitivity to volatile and intravenous anesthetics, so that myocardial depressants (e.g. halothane) should preferably be avoided. Opioid-induced anesthesia and nondepolarizing muscle relaxants should, therefore, be the anesthetic technique of choice.
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PMID:[Traumatic spinal cord lesion. An interdisciplinary challenge--a synopsis of the early trauma phase]. 268 84

We studied lipolysis in the isolated rat heart, measured as glycerol release during anoxia, low-flow ischemia and subsequent reperfusion. It was found that the rate of lipolysis was enhanced during ischemia/anoxia while the lipase activities in tissue extracts involved in the myocardial lipolysis and the amount of triglycerides were not affected. This indicates the dominant occurrence of a lipolysis-reesterification principle in ischemic and anoxic tissue. A common observation of ischemia/anoxia is an increase in the tissue NADH/NAD+ ratio. Therefore we investigated the effect of lactate and malate, both of which enhance the tissue redox state on myocardial lipolysis. Perfusion in the presence of lactate (10 mM) and malate (10 mM) both stimulated myocardial lipolysis by about five times. This suggests that the rate of reesterification of product fatty acids to triglycerides, which is determined by the NADH/NAD+ ratio, because of the increased formation of glycerol 3-phosphate from dihydroxy acetone phosphate, plays an important role in the regulation of lipolysis. The existence of triglyceride-fatty acid-triglyceride cycle is discussed.
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PMID:Enhanced lipolysis of myocardial triglycerides during low-flow ischemia and anoxia in the isolated rat heart. 273 May 23

To study the dynamics of pathomorphologic alterations in the development of acute pancreatitis (AP) and the corresponding changes of the patterns of pancreatic enzymes in rats AP was induced by: 1) combination of a pancreatic juice edema and temporary pancreatic ischemia, ii) by intraductal instillation of trypsin, and iii) by trypsin instillation in combination with ischemia. At 4, 8 and 24 h postoperatively the histologic findings and the activities of lipase and alpha-amylase in the pancreas and the serum were analyzed. The histologic sum score of the individual rats did not correlate with their enzymic patterns in pancreas and in serum. In all three models there was a development of parenchymal necrosis independent of the existence of pancreatic fat necrosis. Therefore, it is not probable that fat necrosis represents an obligatory precondition for the initiation of autodigestion.
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PMID:Experimental acute pancreatitis--a quantification of dynamics at enzymic and histomorphologic levels. 281 89

The reversibility of phosphoethanolamine transferase (EC 2.7.8.1) in rat brain is demonstrated in this paper. Microsomal ethanolamine glycerophospholipids were prelabeled with an intracerebral injection of [3H]ethanolamine 4 h before killing young rats. Labeled CDPethanolamine was produced by incubation of the microsomes with CMP, although to a lesser extent than for the previously observed release of CDPcholine. Ethanolamine and choline glycerophospholipids were labeled with [2-3H]glycerol by incubation with primary cultures of rat brain. Microsomes from rat brains, with diisopropyl phosphofluoridate for inhibition of lipases, were incubated with the labeled glycerophospholipids separately, and labeled diacylglycerols were produced. The kinetic parameters of phosphoethanolamine transferase and phosphocholine transferase (EC 2.7.8.2) were compared by incubating rat brain microsomes with [3H]CMP. Inclusion of AMP in the reaction mixture was necessary in order to inhibit the hydrolysis of CMP by an enzyme with the properties of 5'-nucleotidase (EC 3.1.3.5). For phosphoethanolamine transferase and phosphocholine transferase respectively, the Km values for CMP were 40 and 125 microM and the V values were 2.3 and 21.6 nmol/h per mg protein. The reversibility of both enzymes permits the interconversion of the diacylglycerol moieties of choline and ethanolamine glycerophospholipids. During brain ischemia, a principal pathway for degradation of ethanolamine glycerophospholipids may be by reversal of phosphoethanolamine transferase followed by hydrolysis of diacylglycerols by the lipase.
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PMID:A comparison of the reversibility of phosphoethanolamine transferase and phosphocholine transferase in rat brain microsomes. 301 Nov 1


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