Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

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

Changes in biochemical and electroencephalographic parameters were followed over time during the development of acute hepatic encephalopathy (HE) in two different experimental models. In the rat, (sub)acute liver failure was obtained either by ligation of the hepatic artery in previously portacaval-shunted animals or by intraperitoneal injection of a high dose of galactosamine (GALN). The EEG changes were characterized in both models by a significant increase in low-frequency activity of the EEG power density spectra: the so-called 'left shift'. This 'left shift' was significant in liver ischemia after 4-5 h and in GALN hepatitis after about 30 h. The changes in plasma biochemical indices also showed a great similarity in both models. The concentration of all measured plasma amino acids (except histidine and arginine in GALN hepatitis and arginine in liver ischemia), NH3 and ALAT were significantly increased during the development of (sub)acute HE. Correlation of the combined data of electroencephalographic and biochemical indices showed a significant (P less than 0.01) correlation between the 'left shift' and NH3, taurine, threonine, proline, alanine, methionine, cystathionine, phenylalanine, tryptophan, ornithine and histidine. It is concluded that EEG spectral analysis is a useful parameter for following the development of (sub)acute hepatic encephalopathy in relation to biochemical parameters.
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PMID:Correlation between electroencephalographic and biochemical indices in acute hepatic encephalopathy in rats. 359 63

Reversible ischemia reduced renal cortical brush border membrane (BBM) Na+-dependent D-glucose uptake (336 +/- 31 vs. 138 +/- 30 pmol/mg per 2 s, P less than 0.01) but had no effect on Na+-independent glucose or Na+-dependent L-alanine uptake. The effect on D-glucose uptake was present after only 15 min of ischemia and was due to a reduction in maximum velocity (1913 +/- 251 vs. 999 +/- 130 pmol/mg per 2 s; P less than 0.01). This reduction was not due to more rapid dissipation of the Na+ gradient, altered sidedness of the vesicles, or an alteration in membrane potential. Ischemia did, however, reduce the BBM sphingomyelin-to-phosphatidylcholine (SPH/PC) and cholesterol-to-phospholipid ratios and the number of specific high-affinity Na+-dependent phlorizin binding sites (390 +/- 43 vs. 146 +/- 24 pmol/mg; P less than 0.01) without altering the binding dissociation constant (Kd). 20 mM benzyl alcohol also reduced the number of Na+-dependent phlorizin binding sites (418 +/- 65 vs. 117 +/- 46; P less than 0.01) without altering Kd. The reduction in Na+-dependent D-glucose transport correlated with ischemic-induced changes in the BBM SPH/PC and cholesterol-to-phospholipid ratios and membrane fluidity. Taken together these data indicate the cellular site responsible for ischemic-induced reduction in renal cortical transcellular glucose transport is the BBM. We propose the mechanism involves marked alterations in BBM lipids leading to large increases in BBM fluidity which reduces the binding capacity of Na+-dependent glucose carriers. These data indicate that reversible ischemia has profound effects on the surface membrane function of epithelial cells.
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PMID:Ischemia induces surface membrane dysfunction. Mechanism of altered Na+-dependent glucose transport. 362 82

Changes in cerebral free amino acids, catecholamines and uric acid levels were explored for up to 7 days after cerebral ischemia in the rat. Fifty male Sprague-Dawley rats were subjected to occlusion of the middle cerebral artery on the olfactory tract, under halothane anesthesia. The animals were decapitated at 2, 4, 6, 12, 24 hours and 2, 3, 5, 7 days after the surgery, respectively. The brains were rapidly removed. The cerebral hemispheres were divided into right and left halves, and homogenized in sulfosalicylic acid solution. Free amino acids were analyzed by colormetric method. Cathecholamines and uric acid were analyzed by high-performance liquid chromatography. Each parameters were measured both on the ischemic and contralateral hemispheres. The time course of changes in each parameters were observed by means of the ratio, which is the value of ischemic side divided by that of contralateral side. Free amino acids Dicarboxylic group; Decreases in glutamate and increases in glutamine suggest one aspect of detoxication of ammonia within the ischemia tissue. Monocarboxylic group; GABA, glycine, alanine were increased in early ischemic state, and gradually lowered to the normal values. These suggest the impairment of tricarboxylic acid (TCA) cycle in the ischemic tissues, since these amino acids are closely related to TCA cycle. Essential amino acids, except for tryptophan, were increased until the end of study. These increases suggest the utilization of essential amino acids for protein synthesis might be disturbed in the ischemic tissues. Catecholamines and precursors; Norepinephrine and dopamine were lowered gradually. On the other hand, phenylalanine and tyrosine were increased during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Biochemical studies of the cerebral ischemia in the rat--changes in cerebral free amino acids, catecholamines and uric acid]. 370 75

Dichloroacetate (DCA) is known to prevent the phosphorylation of the pyruvate dehydrogenase complex (PDHC) by blocking the action of PDH kinase. This action allows the active PDHC to exert its effect on the metabolism of glucose, lactate and alanine to acetyl CoA. DCA has been shown to reduce serum lactate levels in humans and animals in such conditions as diabetes, phenformin-induced hepatic failure, exercise, and endotoxin-induced shock. Lactic acidosis in the brain has often been postulated as a cause of neuronal damage following ischemia and hypoxia. Therefore, we examined the effect of intravenously administered DCA (100 mg/kg) in rats that were rendered hyperglycemic by intravenous glucose (2 g/kg), and then made to undergo 15 minutes of incomplete cerebral ischemia by bilateral carotid ligation and systemic hypotension (mean arterial pressure of 50 mm Hg). DCA significantly reduced serum lactate levels pre-ischemia, but had no effect on serum lactate levels after ischemia induction. Brain levels of lactate, ATP and PCr after 15 minutes of incomplete ischemia were unaffected by DCA. We conclude that in this in-vivo model the control of PDHC activity in the brain may be different than that in the periphery, and that DCA was not effective in reducing brain tissue lactate levels.
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PMID:The effect of dichloroacetate on brain lactate levels following incomplete ischemia in the hyperglycemic rat. 371 55

During repeat exercise testing in 10 patients with stable angina, individual optimal doses of nicardipine were determined. Hemodynamic values and cardiac metabolism were studied during 2 pacing periods carried out before and after this dose (mean 5.3 mg). Postpacing ST-segment depression diminished (1 mm) after nicardipine administration (p less than 0.05), whereas pacing time to onset of angina did not change. Nicardipine administration increased heart rate 16% (p less than 0.005) and reduced systolic (10%) and diastolic (8%) blood pressures (both p less than 0.005). Coronary blood flow increased 16% (p less than 0.05) and coronary vascular resistance decreased 24% (p less than 0.01). Myocardial oxygen consumption was unchanged despite an 11% decrease in rate-pressure product during pacing (p less than 0.02). In the control state before nicardipine administration, metabolic signs of ischemia included release of lactate across the heart in 7 patients, decreased mean free fatty acid and glutamate uptake and alanine release during pacing, together with increased glucose uptake and citrate release during recovery. After nicardipine lactate release decreased in 5 of the 7 patients, pacing no longer changed free fatty acid, glutamate and alanine uptake/release from the level at rest. During recovery glucose uptake was reduced and citrate release was unaffected. The hemodynamic data indicate that nicardipine is a systemic and coronary vasodilator, increasing oxygen supply to the ischemic myocardium. The metabolic results indicate a change in substrate utilization toward that of normal heart, suggesting improved aerobic energy supply.
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PMID:Metabolic and hemodynamic effects of nicardipine during pacing-induced angina pectoris. 381 68

The relation between the amount of exercise-induced ischemia and alterations in left ventricular (LV) function and metabolism at rest was studied in 18 coronary patients with stable angina pectoris. An ischemic defect area score was computed from quantitative exercise thallium-201 (Tl-201) scintigraphy; this estimation of the amount of ischemic myocardium was used to classify the patients in group I (n = 8; score less than 15%, mean 6.7 +/- 2.5%) and II (n = 10; score greater than 15%; mean 27.2 +/- 8.9%). Hemodynamics and metabolism were studied in basal state. No patient had anginal pain during the study, and the extent of angiographic coronary artery disease (CAD) was comparable in the two groups. Heart rate, aortic pressure, coronary blood flow, and myocardial oxygen uptake were also similar in both groups. However, ejection fraction was reduced in group II (51 +/- 13 vs 63 +/- 5%; p less than 0.01) and LV relaxation was impaired as shown by the increase in time-constant of isovolumic pressure fall (55 +/- 16 vs 44 +/- 6 ms in group I; p less than 0.05); the LV end-diastolic pressure was also increased in group II (19 +/- 8 vs 10 +/- 4 mmHg in group l; p less than 0.05). Furthermore, in group II, myocardial lactate uptake was reduced (4 +/- 19 vs 30 +/- 29 mumole/min in group I; p less than 0.01) and the productions of alanine and glutamine were augmented (-7.5 +/- 4.4 vs -4.6 +/- 1.6 mumole/min in group I; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in myocardial metabolism and function at rest in stable angina pectoris: relations with the amount of exercise-induced thallium-201 perfusion defect. 381 6

Brain ischemia was induced for 10 or 30 min by clamping the common carotid arteries in rabbits whose vertebral arteries had previously been electrocauterized. EEG and tissue content of high energy phosphates were used to verify the ischemic state and to evaluate the degree of postischemic recovery. Extracellular levels and total contents of amino acids were followed in the hippocampus during ischemia and 4 h of recirculation. At the end of a 30-min ischemic period, GABA had increased 250 times, glutamate 160 times, and aspartate and taurine 30 times in the extracellular phase. The levels returned to normal within 30 min of reflow. A delayed increase of extracellular phosphoethanolamine and ethanolamine peaked after 1-2 h of reflow. Ten minutes of ischemia elicited considerably smaller but similar effects. With respect to total amino acids in the hippocampus, glutamate and aspartate decreased to 30-50% of control while GABA appeared unaffected after 4 h of reflow. Alanine, valine, phenylalanine, leucine, and isoleucine increased severalfold. The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, are considered in relation to the pathophysiology of neuronal cell loss during cerebral ischemia.
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PMID:Ischemia-induced shift of inhibitory and excitatory amino acids from intra- to extracellular compartments. 403 Sep 18

Tissue sections of kidneys from 172 patients with various pathologic conditions, such as hydronephrosis, interstitial nephropathies, ischemia, chronic graft rejection and renal cancer, were evaluated by an image analysis technique. Structurally defined kidney alterations were monitored for enzymatic, immunologic and other histochemical changes. Indicator enzymes of the proximal tubule, alanine-aminopeptidase (AAP), alkaline phosphatase (AP), beta-glucoronidase (beta-Gl) and gamma-glutamyltranspeptidase (GGTP), were used as parameters for screening. Enzyme concentrations were found to be significantly decreased in kidney sections of patients with various renal diseases (AP less than 15%, AAP less than 55% and beta-Gl less than 60%) as compared to normal kidney tissues (100%). AAP concentration was measured quantitatively by specific immunofluorescence using an antienzyme antibody. Immunofluorescence of AAP was comparable to that of AAP calculated by the colorimetric technique (substrate: DL-alanine-beta-naphthylamide-HCl) and decreased to less than 50% in altered kidney tissues. Furthermore, kidney cancer (less than 20%) and kidney tissue adjacent to tumours (less than 65%) displayed significantly decreased levels of kidney marker enzyme activity. This study suggests that (1) the diseased kidney is characterized by a defined change in key enzymes of the cell surface and (2) renal cancer exhibits partial depletion of these constituents. Image analysis of the pattern of enzyme activity appears to be a useful tool in the analysis of renal pathology.
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PMID:Quantitative enzymatic, immunologic and histochemical studies of clinically relevant human kidney alterations using image analysis. 611 96

The tissue concentration of tubular marker enzymes were evaluated in sections of kidneys from 86 patients with various underlying diseases such as hydronephrosis, interstitial nephropathies, ischemia due to renal arterial stenosis and chronic allograft rejection. In addition, as an experimental model, kidney tissue sections of 166 Wistar rats were analyzed due to hydronephrosis caused by ureteral obstruction, ischemia and obstruction of the renal vein. The tissue concentration of indicator enzymes, such as alkaline phosphatase (AP) and alanine-aminopeptidase (AAP), was considered as a parameter describing the extent of kidney tubule damage. Quantitative evaluation of enzymatic activity was performed by histophotometry using a computed image analysis device technique. As compared to normal human kidney (enzyme activity 100%), the concentrations of brush border enzymes were significantly (p less than 0.001) lower under pathological conditions (AP less than 15%, AAP less than 55%). In similar manner investigations of kidneys in animal experiments with rats exhibited lower enzyme concentrations following kidney injury caused by ureteral obstruction for 10 and 21 days (AP less than 12%, AAP less than 65%; 2p less than 0.01). Kidneys after an ischemic period of 2 h and a subsequent 14-day recirculation period displayed a significant (2p less than 0.01) decrease of normally present indicator enzyme concentrations (AP less than 22%, AAP less than 77%) as compared to normal renal organs (100%). Computed image analysis of kidney tissue sections might be a useful aid in evaluating morphologic and enzymatic patterns of human and animal kidney alterations.
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PMID:Quantitative enzymatic histophotometry of morphologic alterations caused by urologically relevant tubular kidney damages using computed image analysis device technique. 611 5


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