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

The evaluation of myocardial metabolic changes in ischemic heart disease remains centered on the coronary sinus pacing and sampling techniques established over the last 25 years. Lactate remains the marker of choice for most institutions, though centers with more sophisticated laboratories will always be trying to improve on the sensitivity and specificity for ischemia, perhaps using ATP catabolites and nucleotides and measuring coronary sinus flow. The diagnostic value of lactate changes is limited and probably not superior to a well-conducted 12-lead treadmill exercise electrocardiogram test, but it does provide an objective marker for reliable further study and evaluation of interventions. It is almost certainly in the research context that metabolic studies have their place--evaluating drugs, surgery, or angioplasty and perhaps shedding light on obscure entities, such as chest pain with normal coronary arteries and cardiomyopathies. Attention to detail and simplicity of study are more likely to lead to valuable results rather than concentrating on the complexities. Each laboratory should establish the reproducibility of its results before commencing any procedures.
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PMID:Laboratory diagnosis of myocardial ischemia. 287 36

The effect of free radical scavengers on free radical-induced myocardial injury during heart preservation and transplantation was examined. Four groups of nine hearts each were harvested from mongrel dogs (12.5 to 16.5 kg) and orthotopically transplanted to size-matched recipients. All hearts received a continuous perfusion of oxygenated modified Collins' solution (group A). In addition, groups B, C, and D received Fluosol DA and albumin. Preservation perfusion was performed for 18 hours, at 4 degrees C, pH = 7.4, and 20 mm Hg. In group C, recombinant human superoxide dismutase (4,080 U/mg, 20 mg/kg) and bovine catalase (46,200 U/mg, 20 mg/kg) were administered only during preservation perfusion. In group D, these scavengers were administered just before and during reperfusion for 1 hour. Hemodynamic studies were performed before excision of the donor hearts and 1 hour after the termination of cardiopulmonary bypass. Creatinine kinase MB isoenzyme and thiobarbituric acid reactive substance levels in the coronary effluent were determined during preservation perfusion and reperfusion. Only group A showed a significant heart weight gain (p less than 0.05) and a decline in passive compliance (p less than 0.05) during preservation. Lactate release was higher in group A than in the groups receiving Fluosol DA. In contrast, pyruvate levels in group A were lower than in other groups. The generation of free radicals stayed at a low level during preservation, but significantly increased during reperfusion and was associated with a corresponding increase in creatinine kinase MB isoenzyme. Perfusion with a perfluorochemical solution (group B) inhibited the sharp rise in levels of thiobarbituric acid reactive substances and of creatinine kinase MB isoenzyme and improved cardiac function during reperfusion (versus group A). Exogeneous free radical scavengers administered just before and during reperfusion (group D) significantly ameliorated thiobarbituric acid reactive substances and creatinine kinase MB isoenzyme levels and also induced a significant hemodynamic improvement during reperfusion. However, administration of scavengers during preservation did not. This study demonstrates that the generation of free radicals is primarily significant during reperfusion and reoxygenation after ischemia. Thus the best time for administration of scavengers is just before and just after the onset of reperfusion. Furthermore, perfusion with perfluorochemicals effectively maintains aerobic metabolism and ameliorates free radical damage during this period.
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PMID:Oxygenated perfluorocarbon, recombinant human superoxide dismutase, and catalase ameliorate free radical induced myocardial injury during heart preservation and transplantation. 305 92

Ischemia, hypoglycemia, and epilepsy have long been thought to produce similar or identical brain damage. Furthermore, these insults have been assumed to be additive in their damaging effects. These notions have been based on neuropathological observations in the hippocampus and cerebral cortex, and on the tenet that energy failure (ischemia, hypoglycemia) and increased demand for energy (epilepsy) similarly give rise to selective neuronal necrosis. Recently, other bases for considering these three insults identical have grown out of observations that loss of calcium homeostasis is common to all and that an excitotoxic mechanism of selective neuronal necrosis exists in all three conditions. Fundamental differences between ischemia, hypoglycemia, and epilepsy include the underlying neurochemical changes induced, the neuronal revival times, the time course of neuronal death, the distribution of selective neuronal necrosis, and the likely excitotoxins released. Lactic acid accumulation, implicated in damage to the neuropil as well as to neuronal cell bodies, also occurs to different degrees and in different distributions in the three conditions. The degree and distribution of pannecrosis is thus also different in ischemia, hypoglycemia, and epilepsy.
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PMID:Biological differences between ischemia, hypoglycemia, and epilepsy. 306 62

To clarify the mechanism of stress-induced ST segment elevation in patients with previous anterior myocardial infarction, we examined myocardial lactate metabolism during atrial pacing in 32 patients with previous anterior myocardial infarction (MI group) and 11 control subjects (control group). In the MI group, atrial pacing resulted in new or additional ST segment elevation in leads with Q waves in 15 patients (ST elevation group), ST segment depression in 7 (ST depression group), but induced no appreciable ST segment changes in the remaining 10 patients (ST unchanged group). In all patients, the ST segment changes were identical to the results of exercise stress testing which was carried out prior to the atrial pacing. Lactate extraction ratio increased moderately during the atrial pacing in the control group (p less than 0.01). Although marked reduction of the myocardial lactate extraction ratio was noted in the ST depression group (p less than 0.05), no significant change in the ratio was evoked in the ST elevation group or the ST unchanged group during atrial pacing. Left ventricular end-diastolic pressure (LVEDP) increased markedly in the ST depression group during atrial pacing, but the elevation was less evident in the other groups. The ST elevation group demonstrated the lowest left ventricular ejection fraction and the severest degree of left ventricular asynergy. Thus, the present study indicates that aggravated left ventricular asynergy in the infarcted area and associated left ventricular dysfunction, rather than peri-infarction zone ischemia is a possible mechanism of stress-induced ST segment elevation in leads with Q waves following previous anterior myocardial infarction.
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PMID:Clinical significance of stress-induced ST segment elevation in patients with previous anterior myocardial infarction. Analysis of lactate metabolism with atrial pacing. 317 72

Lactate, pyruvate and adenosine triphosphate (ATP) concentrations in the brain were measured at the end of various periods of cerebral ischemia induced by bilateral carotid occlusion at 1-hour recirculation after the ischemia in spontaneously hypertensive rates (SHR). In both male and female SHR, a progressive and consistent increase in lactate and lactate/pyruvate ratio and a concomitant decrease in ATP were observed in the ischemic periods of 1, 3 or 5 h. Changes of these cerebral metabolites in females were two thirds to one half of those in males at corresponding periods of ischemia. At 1 h after recanalization of the occluded carotid arteries, metabolic derangements of the ischemic brain were little recovered in male SHR exposed to only 1-hour ischemia, whereas in female SHR the decreased ATP levels were recovered close to the nonischemic control level even after 7-hour ischemia. Furthermore, the increased lactate in female was attenuated to only one sixth of that in male at 1-hour recirculation after 5-hour ischemia. It is concluded that the recovery of the cerebral ischemic metabolism by reperfusion is better in female than male SHR, probably because of the smaller metabolic changes during the ischemic insult, and the fact that the degree as well as the duration of ischemia seem to be important factors for sufficient recovery from ischemic impairment of the brain.
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PMID:Effect of recirculation on the recovery of cerebral metabolism after experimental cerebral ischemia in male and female spontaneously hypertensive rats. 318 66

The present study was designed to clarify whether or not a difference between arterial and venous lactate (delta lactate) levels is useful for evaluation of mitochondrial function in ischemia-reperfused myocardium. In the first experiment, 12 dogs were divided into 2 groups: 10-min occlusion of the left anterior descending coronary artery (LAD) followed by 10-min reperfusion, or 30-min occlusion followed by 40-min reperfusion, were performed. The lactate levels in the femoral artery and the great cardiac vein were measured enzymatically. delta Lactate was reversed immediately after occlusion. Ten min and 20 min were required for the recovery of delta lactate in the 10-min-occlusion with 10-min-reperfusion, and 30-min-occlusion with 40-min-reperfusion groups, respectively. In the second experiment, 36 dogs were divided into 6 groups: 10-min occlusion of LAD; 10-min occlusion with 10-min reperfusion; 30-min occlusion; and 30-min occlusion with 10-, 20-, or 40-min reperfusion were performed. Mitochondria from normal and occluded or reperfused areas were prepared, and the respiratory function of the mitochondria was measured polarographically. No significant decreases in the mitochondrial function were observed in the 10-min-occlusion, and 10-min-occlusion with 10-min-reperfusion groups. On the other hand, respiratory function of mitochondria was impaired by 30-min occlusion and was not improved by 10- or 20-min reperfusion. Significant recovery in the mitochondrial function was observed after 40-min reperfusion. That is, differing recovery time courses between delta lactate and the mitochondrial function were observed.
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PMID:Differing time courses between delta lactate and mitochondrial respiration during coronary occlusion and after reperfusion in canine hearts. 324 82

Ischaemia has profound effects on myocardial metabolism and cell function in general. High energy phosphate and glycogen stores are depleted. Lactate, inorganic phosphate and hydrogen ions accumulate, exerting negative effects on the initially accelerated glycolytic flux. Fatty acid oxidation is inhibited. The cellular content of lipid intermediates, such as hydroxy-fatty acids, acyl CoA and acylcarnitine, increases in low-flow ischaemia hearts. Non-esterified fatty acid (NEFA) accumulation occurs after 30-60 min ischaemia. Endogenous triacylglycerol and phosphoglyceride turnover is most likely impaired, ultimately resulting in accumulation of lipid droplets in the oxygen deprived cells and in degradation of myocardial membranes. Accumulated lipid substances such as NEFA, acyl CoA, acylcarnitine and lysophosphoglycerides, are likely to be involved in the mechanism underlying ischaemia-induced damage to myocardial cells.
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PMID:Lipid and carbohydrate metabolism in the ischaemic heart. 331 Oct 2

The effect of insulin-induced reduction in blood glucose to 65 +/- 20 mg/dl (mean +/- standard deviation) on recovery of electrophysiological function and extracellular lactate concentration was studied in a rabbit model of spinal cord ischemia. These results were compared to findings in animals with spinal cord ischemia that either were fasted overnight (fasted group: blood glucose 97 +/- 26 mg/dl) or had no pretreatment (control group: blood glucose 172 +/- 65 mg/dl). The aorta was occluded until the postsynaptic waves of the spinal somatosensory evoked potentials (SSEP's) had been absent for 20 minutes, a period of ischemia that produces paraplegia in 100% of untreated rabbits. The total aortic occlusion time was not significantly different in the three groups. Recovery of the SSEP's was significantly better in the insulin-treated animals than in the fasted or control animals. The N3 wave of the SSEP's, which has been found to correlate best with neurological recovery, returned to 65% +/- 48% of the preischemia amplitude in the insulin-treated animals, compared to 40% +/- 34% in the fasted group and 26% +/- 24% in the control animals. Extracellular lactate concentration in the spinal cord increased immediately after occlusion of the aorta, reached a plateau as the postsynaptic waves disappeared from the SSEP's, and then increased a second time during the first 15 minutes of reperfusion. The peak lactate concentration during ischemia and during reperfusion correlated with the preischemia glucose concentration (r = 0.60336 and r = 0.76930, respectively). Lactate concentration in the spinal cord was higher during ischemia and throughout the first 2 hours of reperfusion in the control and fasted animals than in the insulin-treated animals. During the 2nd hour of reperfusion, lactate concentration was significantly higher in the control animals than in the fasted animals. Reduction in blood glucose with insulin improves recovery of electrophysiological function after spinal cord ischemia, probably because of reduced lactic acid production, especially during the early reperfusion period.
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PMID:Protection against spinal cord ischemia with insulin-induced hypoglycemia. 331 14

Lactate dehydrogenase has been measured in the small-intestinal mucosa in order to assess its value as a marker for the effects of ischemia and of reperfusion. The decrease in specific activity of the enzyme illustrates the deleterious effect of reperfusion on the quality of the remaining epithelial cells. However, this parameter fails to detect the loss of epithelial cells, which is the major event during ischemia as well as during reperfusion. In contrast, the expression of enzyme activity per g protein of the underlying intestinal muscle allowed us, in addition, to assess quantitatively the loss of epithelial cells, in good agreement with the histological data.
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PMID:The use of biochemical parameters for a qualitative and quantitative assessment of ischemic damage to the small-intestinal mucosa. 345 49

Animal studies suggest that hyperglycemia (glucose concentrations greater than 225 mg/dl) occurring prior to periods of brain ischemia exacerbates neurologic damage. Neurosurgical patients, a group at risk for intraoperative brain ischemia, often receive glucose. Therefore, the effects of intraoperative glucose administration (IGA) on these patients were studied. Sixteen patients undergoing supratentorial craniotomy were randomly assigned to receive either 5% glucose in 0.9% sodium chloride solution (G) or 0.9% sodium chloride solution (S) infusion (both at a rate of 3-4 ml X kg-1 X h-1) during the first 4 h of surgery. All patients received glucose infusions postoperatively. Plasma glucose, insulin, free fatty acids, alanine, ketones, base excess, pH, triglycerides, and lactate were measured during the infusion period and 24 h postoperatively. Urinary nitrogen was measured, commencing with the infusion and continuing for 24 h. Neurologic testing included preoperative and postoperative neurologic and psychomotor exams, time to extubation (min), and degree of alertness at the completion of anesthesia. The G group had significantly greater intraoperative plasma glucose concentrations at all time periods studied during the infusion (P less than 0.05). Glucose levels ranged from 200-242 mg/dl compared with 120-160 mg/dl in G and S groups, respectively. G group hyperglycemia was within the range associated with exacerbation of ischemic brain damage in animal studies. Free fatty acids and ketones were significantly greater (P less than 0.05) intraoperatively in the S group. Lactate and insulin were significantly greater in the G group at 4 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intraoperative glucose on protein catabolism and plasma glucose levels in patients with supratentorial tumors. 351 17


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