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)

Medical records of 53 burn and trauma patients were reviewed to assess the possibility of myocardial damage. Except for electrophoretically detectable creatine kinase MB isoenzyme, none showed evidence of myocardial injury. Lactate dehydrogenase isoenzyme tests, electrocardiograms, myocardial pyrophosphate scans, clinical course, and results of (two) autopsies were all negative for myocardial necrosis or ischemia. Types of patient, number, mean peak value (U/L) for serum creatine kinase, and ranges of percentage MB isoenzyme were as follows. Burns from direct electrical contact: 28, 16 600, 0-29; electrical flash or other thermal burns: 10, 4340, 0-22; blunt trauma (mostly from automobile accidents): 15, 3430, 0-18; myocardial infarction: 57, 1520, 4-46. Evidently creatine kinase MB isoenzyme is nonspecific in burn and trauma patients and should not be the only test result used to assess myocardial involvement.
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PMID:Creatine kinase and lactate dehydrogenase isoenzymes in serum of patients suffering burns, blunt trauma, or myocardial infarction. 674 81

Coronary artery disease is considered a contraindication to inducing hypotension during surgery because the combined effects of stenosis and hypotension in reducing distal coronary artery perfusion pressure might produce myocardial ischemia. To study the effect of deliberate hypotension (mean systemic pressure, 50 mmHg) on regional myocardial perfusion, oxygenation, and lactate extraction, we constricted the left-anterior descending coronary artery (LADCA) in dogs. Two degrees of stenosis were studied: "critical" stenosis, which reduced resting coronary blood flow from 34.4 to 31.2 ml/min and abolished reactive hyperemia of the LADCA in response to 10 s of total coronary artery occlusion; and a more "severe" stenosis, which reduced resting coronary blood flow by 40%. LADCA pressure was measured distal to the stenosis, and LADCA perfusion pressure was obtained by subtracting the left ventricular end-diastolic pressure from the coronary artery diastolic pressure measured past the stenosis. Hypotension was induced by administering sodium nitroprusside, halothane at a high concentration, or trimethaphan. Lactate extraction and oxygen consumption were measured across the myocardium distal to the stenosis (from the coronary artery to the great cardiac vein) and across the whole heart (from the coronary artery to the coronary sinus). Regional myocardial blood flow was measured using radioactive microspheres. A transmural electrocardiogram was obtained from electrodes implanted in the subendocardium and the subepicardium in the distribution of the LADCA distal to the stenosis. Although the combination of critical stenosis and hypotension reduced regional myocardial blood flow and lowered LADCA perfusion pressure to 27 +/- 3 (SE) mmHg, myocardial ischemia did not occur, as evidenced by continued lactate extraction and no redistribution of transmural blood flow or change in ST segment. On the other hand, the combination of severe stenosis and hypotension reduced LADCA perfusion pressure to 17 +/- 2 (SE) mmHG and produced evidence of ischemia by regional lactate production, reduction of the subendocardial/subepicardial flow ratio, and depression of the ST segment.
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PMID:A canine model of acute coronary artery stenosis: effects of deliberate hypotension. 688 88

1. Cerebral energy metabolism and electroencephalogram (EEG) power spectra were evaluated before, during and after 1 minute of global compression ischemia induced in N2O anesthetized rats. 2. Before ischemia, the EEG of rats was characterized by theta and delta frequencies. During ischemia, the EEG flattened after 14 +/- 1 sec and the electrical activity reappeared 55 +/- 4 s after recirculation and was characterized by high amplitude slow waves. After ischemia, the total power showed a rapid rebound mainly due to a 10 fold increase of delta band. 10 minutes after recirculation, the EEG was normal. 3. The ischemia induced a decrease of phosphocreatine, ATP and glucose, and an increase of ADP, AMP and lactate, while pyruvate remained normal. During recirculation phosphocreatine, ATP, glucose and energy charge potential showed a rapid recovery. AMP normalized after 10 minutes, while ADP was slightly higher for up to 30 minutes. Lactate returned to normal levels after 30 minutes and pyruvate showed a high peak at 3 minutes and returned to normal values after 30 minutes. 4. The results suggest that there is not a correlation between EEG and the metabolic pattern of recovery after a short complete ischemia.
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PMID:Cerebral energy metabolism and computerized EEG. Analysis following transient ischemia in the rat. 715 67

Lactate accumulation was measured soon after decapitation in three adjacent lower spinal cord regions of rats with EAE. Results indicate that during EAE, and in correlation with the onset of clinical signs of both initial attack and short-term relapse, a differential focal increase in lactate accumulation occurs in rat spinal cord compared to Freund's Complete Adjuvant controls, with greater increase occurring in more caudal segments. A [14C]antipyrine method of estimating relative spinal cord blood flow failed to find evidence that the lactate accumulations were due to focal ischemia. Subsequent measurement of isotopic water and total protein increases in the same cord regions indicated that a slight but significant increase in vasogenic edema occurs in correlation with the increase in lactate accumulation and the onset of EAE clinical signs. The data are interpreted as lending support to a speculative theory of paralysis induced by edema during EAE, in which nerve root endoneurium is postulated as the functionally vulnerable site. More specifically, it is hypothesized that the ascending progression of clinical signs of EAE in rodents can be explained on an anatomical basis by progressive disturbance of the nodes of Ranvier in nerve root myelinated fibers.
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PMID:Experimental autoimmune encephalomyelitis. An anatomically-based explanation of clinical progression in rodents. 717 84

Neurological symptoms and cerebral metabolism following bilateral carotid artery occlusion (BCAO) were observed in stroke-prone spontaneously hypertensive rats (SHRSP), stroke-resistant SHR (SHRSR), normal Wistar-Kyoto rats (WKY) and the F1 and F2 hybrids between SHRSP and SHRSR or WKY. Systolic blood pressure recorded before BCAO was found to rank in the following order: SHRSP greater than F1 (SHRSP X SHRSR) greater than SHRSR greater than F1 (SHRSP X WKY) greater than WKY. The effect of BCAO in these rats tended to be proportional to the blood pressure. F1 (SHRSP X WKY) was more sensitive to brain ischemia than SHRSR. In addition, though none of the SHRSR (average blood pressure 155 mm Hg) developed acute stroke symptoms, many animals of the F2 generation, in which the blood pressure was equal to or lower than that of SHRSR, developed stroke symptoms. Lactate and ATP changes in the F2 generations did not correlate with the blood pressure. The results suggest that genetic factors may play an important role in susceptibility to brain ischemia in the stroke-prone rats.
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PMID:Mechanism of increased sensitivity to cerebral ischemia following carotid artery occlusion in stroke-prone spontaneously hypertensive rats: importance of genetic factors. 723 74

Fructose 1,6-diphosphate (FdP) reportedly protects ischemic myocardium. To determine whether this is a direct action on the heart, we used a canine model in which two coronary arteries were perfused at identical but reduced rates. Into one artery we infused FdP (total doses of 400 mg or 1.8 g) while the other received 0.9% NaCl. After 1 h, biopsies were taken from a normal region and the two ischemic regions and were analyzed for ATP, phosphocreatine (PC), and lactate content. In the 0.9% NaCl-treated ischemic tissue, ATP and PC fell to half the nonischemic levels. The FdP-treated tissue exhibited high-energy phosphate levels similar to the 0.9% NaCl-treated tissue with no significant differences between the two ischemic areas. Lactate levels in both ischemic areas were elevated threefold above nonischemic levels. Contractility studies showed that infusion of FdP directly into the coronary artery depressed contractility in both nonischemic and ischemic conditions. Our data show that, if FdP does have a protective action in ischemia, it is not through a direct action on the heart.
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PMID:Lack of a direct metabolic effect of fructose, 1,6-diphosphate in ischemic myocardium. 731 82

The effects of L-arginine on recovery of myocardial contractile function and oxidative metabolism were investigated in a model of reversible global normothermic, ischemic injury using an isolated, buffer-perfused rabbit heart preparation. One mM L-arginine was infused into hearts for 2 min at the onset (group 1) of a 35 min period of ischemia or at the onset of reperfusion (group 2). In non-ischemic hearts, L-arginine caused a slight increase in developed pressure but had no effects on diastolic pressure, oxygen consumption (MVO2), coronary flow, or lactate production. When administered either before or after ischemia-reperfusion. L-arginine caused a significant increase in the diastolic pressure-volume relationship (PVR) and decline in systolic function when compared to untreated control hearts receiving the same ischemic injury. Recovery of MVO2 and high energy phosphates (phosphocreatine and ATP), measured by 31P-NMR spectroscopy, were significantly impaired in L-arginine-treated hearts compared to reperfused control hearts. Lactate release on reperfusion was also higher in both arginine-treated groups. Nitric oxide release into the coronary circulation (measured in separate experiments by the conversion of [15N]L-arginine to [15N]nitrate/nitrite using gas chromatography/mass spectroscopy) was not increased by L-arginine administration. Thus, we conclude that L-arginine acts synergistically with ischemia reperfusion to augment myocardial injury, which includes inhibition of oxidative metabolism and mitochondrial function.
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PMID:Direct detrimental effects of L-arginine upon ischemia--reperfusion injury to myocardium. 747 86

The protective effects of fructose-1,6-biphosphate (FBP) during hypoxia/ischemia are thought to result from uptake and utilization of FBP as a substrate for glycolysis or from stimulation of glucose metabolism. To test these hypotheses, we measured CO2 and lactate production from [6-14C]glucose, [1-14C]glucose, and [U-14C]FBP in normoxic and hypoxic cultured astrocytes with and without FBP present. FBP had little effect on CO2 production by glycolysis, but increased CO2 production by the pentose phosphate pathway. Labeled FBP produced very small amounts of CO2. Lactate production from [1-, and 6-14C]glucose increased similarly during hypoxic hypoxia; the increase was independent of added FBP. Labeled lactate from [U-14C]FBP was minimal. We conclude that exogenous FBP is not used by astrocytes as a substrate for glycolysis and that FBP alters glucose metabolism.
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PMID:Energy metabolism in hypoxic astrocytes: protective mechanism of fructose-1,6-bisphosphate. 747 71

Single or multiple brief periods of regional or global ischemia and reperfusion prior to a prolonged ischemic insult showed cardioprotective effects. Although this phenomenon (ischemic preconditioning [IPC]) has been described in ischemic reperfusion models, the effect of IPC on heart preservation has not been previously reported. We, thus, investigated the effect of IPC on heart preservation. Hearts isolated from male Wistar rats (250-350 g) were mounted on a Langendorff apparatus to estimate baseline function (aortic flow, coronary flow, cardiac output, heart rate, systolic pressure, and rate pressure product). All hearts were divided into 5 groups. In groups 1 and 4, the hearts were subjected to 8 and 12 hr of preservation, respectively. The hearts in group 2 were subjected to a single 2.5-minute cycle of normothermic global ischemic episode (IPC) before 8 hr of preservation. In groups 3 and 5, the hearts were subjected to two 2.5-min IPC cycles and stored for 8 or 12 hr. The hearts were arrested with University of Wisconsin solution and stored at 4 degrees C. Following storage, the hearts were reperfused and measured postpreservative function to assess cardiac functional recovery. Lactate and troponin-T leakage in the coronary perfusate was also measured. In group 3, the treatment of two 2.5-min IPC cycles significantly increased cardiac output, but the treatment of single 2.5-min IPC cycle did not affect the result. In the extended preservation group (group 5), the recovery (%) of both coronary flow and cardiac output were significantly increased compared with group 4. Furthermore, lactate leakage was significantly reduced in groups 2 and 3. These results suggest that IPC improves cardiac functional recovery following simple cold storage and has cardioprotective effects in rat heart preservation.
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PMID:Ischemic preconditioning improves cardiac functional recovery following preservation with University of Wisconsin solution. 748 11

We designed the present study to examine whether or not the inhibition of acetylcholinesterase modulates cerebral microcirculation in hypotension and improves brain metabolism in ischemia induced by bilateral carotid artery occlusion in hypertensive rats. Blood flow to the parietal cortex was determined by the H2 clearance method. Lactate, pyruvate, and ATP were estimated by enzymatic methods. Acetylcholinesterase inhibitor (AChEI, ENA-713), at 0.05, 0.1, or 0.5 mg/kg, was intravenously injected 10 min before either hemorrhagic hypotension or cerebral ischemia. The levels of acetylcholine in the control were 29.3 +/- 8.1 (mean +/- SD) and 39.5 +/- 8.1 pmol/mg in the cortex and hippocampus, respectively, and they were significantly decreased by 15-19% after 60 min of ischemia in the vehicle-treated rats. AChEI preserved the levels to 93-98% of the control (p < 0.05 versus vehicle). The lower limit of autoregulation was 74 +/- 9% of the resting values. The administration of AChEI helped preserve blood flow and lowered the limit to 64 +/- 6% (p < 0.05 versus control). After 60 min of ischemia, lactate increased 6.5-fold and ATP decreased to 64% of the control value. The administration of AChEI dose-dependently reduced the lactate level 1.9- to 3.9-fold and well preserved the ATP level to 94-97% of the control. The inhibition of acetylcholinesterase activity may preserve cerebral autoregulation during hypotension and protect cerebral metabolism against ischemic insult.
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PMID:Inhibition of acetylcholinesterase modulates the autoregulation of cerebral blood flow and attenuates ischemic brain metabolism in hypertensive rats. 767 77


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