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

To clarify the changes that occur during marked hypocarbia in the neonate, we measured brain blood flow and metabolite levels after 90 minutes of hyperventilation in neonatal dogs. Brain blood flow decreased significantly in diencephalon, brainstem, and spinal cord but not in cerebral cortex or white matter. There was no substantial change in the electroencephalogram. Lactate concentrations, both in telencephalon and in superior sagittal sinus blood, increased significantly, although there was no alteration in levels of ATP or phosphocreatine. Marked hypocarbia in the neonatal dog produces an elevated brain lactate level that may be related to changes in glycolytic rate rather than to tissue ischemia or hypoxia.
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PMID:Cerebral physiological and metabolic effects of hyperventilation in the neonatal dog. 643 4

The application of selective saturation (or solvent suppression) techniques in nuclear magnetic resonance (NMR) imaging offers the opportunity to significantly expand the range of NMR studies. Data acquired at 1.44 T are presented using a two-dimensional spin-echo sequence preceded by a selective (saturating) radiofrequency pulse. Individual water or lipid proton resonances were eliminated (greater than 90% reduction in signal intensity) resulting in images of H2O or -CH2- distribution with resolution and imaging time equivalent to conventional proton images. Data are also presented demonstrating the feasibility of using selective saturation to image proton metabolites at low concentrations with a three-dimensional chemical shift imaging approach. Lactate was investigated because of its importance in the pathophysiology of ischemic insult. Phantom studies without solvent suppression failed to detect lactate at 80 mM; however, with solvent suppression, lactate at 40 mM was imaged in a reasonable time (approximately 50 min). With the favorable NMR characteristics of the methyl protons of lactate and with improvements in imaging systems, this technique may play an important role in the noninvasive evaluation of tissue ischemia using 1H NMR.
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PMID:Selective saturation NMR imaging. 647 Feb 46

It was the aim of this study to define biochemical parameters of hepatic ischemia. In seven dogs portal vein and hepatic artery were occluded subsequently. During this ischemia the lactate concentration in the hepatic veins rose from a basal value of 15 mg% to 57 mg%. Lactate levels measured in portal vein, femoral artery, and femoral vein were significantly lower. Furthermore, hepatic ischemia caused an increase in potassium and glucose levels in the hepatic vein. Primarily, production of lactate by the liver seems to be an appropriate parameter for hepatic ischemia. Measuring lactate metabolism could be used to examine patients with portal hypertension before performing a shunt procedure. By cannulating the umbilical vein it is possible to occlude the portal vein with a balloon catheter. Portal vein occlusion with hepatic vein blood sampling may identify those patients in whom hepatic arterial reserve is inadequate to support portosystemic shunting.
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PMID:[Biochemical parameters of hepatic ischemia in experimental animals]. 647 4

Pulmonary changes in acute cerebral ischemia were studied in anesthetized Mongolian gerbils, in which both carotid arteries were occluded simultaneously. Lactate, pyruvate and adenosine triphosphate (ATP) in the brain were measured as indicators of the severity of cerebral ischemia. Microscopic changes in the lung were arbitrarily scored from 0 (normal) to 3 points (severely affected) by the grade and the extent of lesions. Mean arterial pressure (MAP) was also measured through the cannulated femoral artery before and after carotid artery occlusion in a separate group of animals. Cerebral lactate was increased while ATP decreased in ischemic animals in which pulmonary changes such as intra-alveolar hemorrhages were prominent and frequent. The lung pathology score averaged 1.3 in animals with severe ischemia (lactate greater than or equal to 10 mM/Kg), 0.7 in moderate ischemia (5-10 mM/Kg) and 0.3 in mild or no ischemia (less than 5 mM/Kg), respectively, suggesting that severe brain ischemia may cause fulminant pulmonary changes. The mechanism of pulmonary lesions in acute cerebral ischemia is discussed.
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PMID:Pulmonary hemorrhage in experimental cerebral ischemia in mongolian gerbils. Brain metabolism and lung pathology. 653 Jul 49

Renal oxygen and lactate metabolism as well as central and renal hemodynamics were investigated in hemorrhagic shock in dogs. The animals were bled progressively until a 40-50% blood loss was achieved. Following a 20-, 40-, 60-, or 80-minute shock phase the shed blood was gradually returned. The effect of acute total ischemia on renal oxygen metabolism was studied during arterial occlusion. The renal cortical and medullary PO2 and PCO2 were recorded by means of implanted Silastic tonometers. The mean baseline cortical PO2 was 35 mmHg and the corresponding medullary PO2 25 mmHg. The renal cortical PO2 responded promptly to hemorrhage and declined in parallel with the cardiac output and renal blood flow. Hypoxia became more severe in the cortex than in the medulla during hemorrhagic shock. The response of both the cortical and the medullary PO2 to blood return increased with prolongation of the preceding shock phase. After one hour of shock, or more, the tissue oxygen tensions exceeded the prehemorrhage levels. Concomitantly, the renal blood flow and oxygen consumption were depressed below the initial values. The results of the studies of tissue PO2 decay curves after renal arterial occlusion suggested that the mean critical PO2 level for oxygen consumption is 15 mmHg for the cortex and 13 mmHg for the medulla. Aerobic oxidative metabolism ceased at a PO2 value of 6 mmHg in both tissue layers. In hemorrhagic shock, the critical PO2 level for oxygen consumption was reached earlier in the cortex than in the medulla. The minimum PO2 for aerobic oxidative metabolism was recorded in the cortex during severe shock, but not in the medulla. Renal lactate uptake remained rather unaffected during graded hemorrhage. The extreme impairment of renal perfusion associated with hemorrhagic shock produced a parallel decrease in the cortical PO2 and lactate utilization. Renal lactate utilization became limited at the cortical PO2 level, which coincided with the critical PO2 measured during the arterial occlusion. Lactate utilization ceased at a cortical PO2 level that was analogous with the minimum PO2 for aerobic oxidative metabolism determined after arterial occlusion. After reinfusion of shed blood renal lactate uptake failed to return to the prehemorrhage level. The renal lactate uptake was inversely related to the arterial pH under baseline conditions whereas after blood return the correlation between these parameters was less significant. The present findings suggest that in hemorrhagic shock renal metabolism may become limited by hypoxia and the susceptibility to the development of hypoxia is greater in the cortex than in the medulla.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal oxygen and lactate metabolism in hemorrhagic shock. An experimental study. 659 13

Excessive tissue lactic acidosis has earlier been shown to aggravate structural damage of both neurons and glial cells in the rat cerebral cortex. To study the reactions of cortical capillaries, light- and electronmicroscopic morphometry was used. Rats were subjected to severe incomplete ischemia (cerebral blood flow below 5% of normal) for 30 min by clamping their carotid arteries and by lowering the blood pressure. Lactate production during ischemia was modified by preischemic administration of either saline (low lactic acidosis group) or glucose (high lactic acidosis group). In the animals with low lactic acidosis, only minimal vascular changes were seen after both 5 min and 90 min recirculation. In the high lactic acidosis group, the endothelial cells were swollen after 5 min of recirculation, and the changes grew markedly worse during 90 min of recirculation. Nuclear chromatin coarsened and mitochondria swelled up. Morphometry showed that the lumen narrowed as a result of endothelial swelling. In spite of variable degree of perivascular astrocytic edema, the outer capillary diameter was little changed in the experimental groups. It seems likely that endothelial swelling hampers postischemic circulation in incomplete ischemia accompanied by high lactic acidosis.
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PMID:Brain lactic acidosis and ischemic cell damage: quantitative ultrastructural changes in capillaries of rat cerebral cortex. 661 33

The reproducibility of myocardial ischaemia provoked by atrial pacing was studied in two groups of patients. The heart rate was slowly increased (10 beats per fourth min) until angina in group A, and quickly increased (10 beats per 20 s) in group B. Cardiac venous flow was measured by thermodilution and blood was sampled for metabolic studies at rest and during the maximum obtained heart rate and repeated after 20 min of rest. Ischaemia was defined as a reduction in myocardial lactate extraction ratio by 50% and to a ratio lower than 0.15. Lactate metabolism changed from production (-0.06 +/- 0.05) during the first pacing to extraction (0.05 +/- 0.05) during the second in group A (p less than 0.02). Lactate metabolism was quite reproducible in group B. All the other metabolic and haemodynamic parameters were unchanged in both groups. We conclude that the duration of atrial pacing is important for the reproducibility of pacing-induced myocardial ischaemia.
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PMID:Reproducibility of ischaemic lactate metabolism during atrial pacing in man. 664 May 58

We describe two brothers, 25 and 19 years-old, with muscle pain and decreased strength after prolonged exercise; these symptoms are worsened by cold whether of fasting. One of the patients developed recurrent myoglobinuria and had one episode of renal failure. Laboratory investigations were normal between the crises, but during myoglobinuria, serum creatine kinase activity increased 100 times. Electromyography was suggestive of denervation. Muscle biopsy showed increased lipid droplets by the "oil red O" stain and increased activity of succinic dehydrogenase histochemical reaction. Lactate production during ischemia was normal. Biochemical analysis showed decreased carnitine-palmityl-transferase activity in muscle (7.23 and 10.58 nmoles/min/gr; normal range 66.7 +/- 17.3), with normal values for carnitine-octanoyl-transferase and carnitine-acetyl-transferase. The metabolic pathway of fatty acid utilization as an energy source for muscle during exercise in normal and in pathological conditions is discussed.
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PMID:[Myopathy due to carnitine palmitoyltransferase deficiency. Report of 2 cases with enzymatic analyses on muscle tissue]. 666 Nov 2

Twenty-five patients undergoing aortic valve replacement were administered two different electrolyte solutions pre- and intraoperatively: patients in group A (n = 9) received a balanced solution of electrolytes and trace metals with aspartate as anion (Inzolen), patients in group B (n = 16) received Ringer's solution with potassium chloride referenced to frequently-measured serum potassium levels. From the left ventricular apex region, needle biopsies were obtained at three points in time: 1. beginning of CPB, 2. end of ischemia, 3. after ten minutes of reperfusion. The tissue samples were enzymatically analyzed for the content of ATP, CP, ADP and lactate. In group A (patients with aspartate) ATP (moderately) and CP (markedly) decreased after ischemia with a marked increase after reperfusion. ADP and lactate in this group (A) increased at the end of ischemia and decreased after reperfusion. ATP and CP in group B (KCl) showed a similar course during the investigation. Lactate (markedly) and ADP (moderately) increased after ischemia without changing after reperfusion. Mean values of ATP and CP in group A were significantly higher than those of group B at all times. Mean values of ADP and lactate, however, in group A were below those of group B. The data indicate an improvement in energetic metabolism of myocardium in man. The results point out the possible importance of aspartates in compound with electrolytes and trace metals in preservation of biochemical energy.
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PMID:[Effect of aspartate compounds on the biochemical characteristics of myocardial energy metabolism in man]. 666 81

The objective of this study was to determine the effects of single or intermittent infusions of cardioplegic solution with glucose (5 gm/L) or without glucose on myocardial tissue lactic acid and recovery of myocardial contractility following 80 minutes of total ischemia at 28 degrees C in the isolated, blood-perfused, beating rabbit heart. Ischemia without cardioplegia increased tissue lactic acid (6.79 mg/gm tissue) above the control value (0.9 mg/gm tissue), p less than 0.0025). Lactic acid following single infusions with (4.19 mg/gm tissue) or without glucose (3.67 mg/gm tissue) was significantly greater (p less than 0.0025) than tissue lactic acid following intermittent infusions with (1.06 mg/gm tissue) or without glucose (1.05 mg/gm tissue). Cardioplegic arrest in all cases significantly decreased tissue lactate accumulation when compared to arrest without cardioplegia (p less than 0.01). The decrease in myocardial contractility demonstrated when no cardioplegic protection was employed (86% recovery) was completely eliminated (100% recovery) with a single-bolus infusion of cardioplegic solution containing glucose (p less 0.025). Intermittent infusions of cardioplegic solution containing glucose (92% recovery) and single infusions without glucose (93% recovery) also improved recovery of contractility following ischemia, but the results were not statistically significant.
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PMID:Effect of intermittent infusions of glucose-containing crystalloid cardioplegic solution on myocardial tissue lactic acid and recovery of contractility. 672 13


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