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)

Quantitative assessment of high-energy phosphate levels, including degradation or utilization during ischemia, has not previously been performed in infants and children. Animal experiments suggest that high-energy phosphate metabolism varies with maturation. To help answer these questions, 24 patients aged 2 months to 8 years underwent myocardial biopsy immediately after the institution of cardiopulmonary bypass (16 to 20 degrees C). Additional samples were obtained at 16 and 45 minutes after aortic cross-clamping and administration of cardioplegia (St. Thomas's solution) (in vivo ischemia). Seven patients also underwent major myocardial resection. Resected specimens were placed in a 37 degrees C bath and divided into equal-sized samples that were removed at ten-minute intervals (in vitro ischemia). All samples were immersed in liquid nitrogen and analyzed for adenine nucleotide pool metabolites using high-performance liquid chromatography. Levels of adenosine triphosphate were high before cross-clamping but diminished during the period of protected ischemia. Adenosine triphosphate loss was much more pronounced in patients less than 18 months old (p less than 0.05) and was associated with accumulation of adenosine monophosphate and inosine, a finding not seen in patients more than 18 months old (p less than 0.05). The same trends documented during in vivo ischemia were noted during in vitro ischemia. Immaturity of 5'-nucleotidase results in accumulation of adenosine monophosphate during ischemia. It is known that 5'-nucleotidase is present in neonatal myocardial cell membranes and absent from the cytosol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial adenine nucleotide metabolism in pediatric patients during hypothermic cardioplegic arrest and normothermic ischemia. 273 Jan 89

Ischemic insult has been considered a cause of cellular injuries under certain circumstance, such as the disturbance of energy metabolism, the alternation of calcium homeostasis, the production of oxygen radical and the release of lysosomal protease. The present study was designed to clarify the pathophysiological effects of coenzyme Q10 (CoQ10), diltiazem, superoxide dismutase (SOD) and urinastatin on the development and progression of ischemic acute renal failure (IARF) of the rat. At 24 hours after reflow following 45 minutes ischemia, serum urea nitrogen, creatinine and fractional excretion of sodium were 99.3 mg/dl, 3.14 mg/dl, 5.95% respectively, in non-treated IARF rats. Renal ATP content was reduced to 0.91 micrograms/mg. prot. from 10.59 micrograms/mg. prot. at 10 minutes after ischemic insult, and remained at almost the same level throughout the entire 45 minutes ischemia. Although the subsequent blood reflow resulted in the recovery of ATP content, it was up to 50% of normal level at 24 hours after reflow following 45 minutes ischemia. During the ischemic period, the pathological changes were mild, whereas, after reflow, tissue involvement was mainly localized in the S3 segment of the proximal tubule. Major alteration were the loss of brush border, high amplitude swelling of mitochondria with matrical densities and fragmentation of the epithelial cell. At 24 hours after reflow, it was observed that renal function was superior in IARF rats treated with CoQ10, diltiazem, SOD and urinastatin. The treated rats also had higher ATP contents and showed less pathological changes than non-treated rats. Among these inhibitory agents, diltiazem exerted the most reliable effect. From these results, it was concluded that IARF was obviously caused by such pathophysiological mechanisms as mentioned above. Especially, Ca influx into the cells is one of the most important factors on pathogenesis of IARF.
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PMID:[Pathophysiological mechanism of ischemic acute renal failure: protective effect of coenzyme Q10, Ca channel blocker, superoxide dismutase and protease inhibitor against ischemic acute renal failure]. 274 96

Previous observations and clinical manifestations suggest the presence of ischemia in the disproportionately thickened septum of patients with hypertrophic cardiomyopathy. Metabolic consequences of ischemia can be demonstrated with positron emission tomography. Therefore, 10 patients with hypertrophic cardiomyopathy and an echocardiographic septum to posterior wall thickness ratio of 1.8 +/- 0.4 cm (range 1.3 to 2.5) were studied with the use of nitrogen (N)-13 ammonia, carbon (C)-11 palmitate and fluoro (F)-18 2-deoxyglucose as tracers of myocardial blood flow, fatty acid metabolism and exogenous glucose utilization. The results of positron emission tomography in 9 patients with hypertrophic cardiomyopathy were compared with those in 10 normal volunteers. In the hypertrophic cardiomyopathy group, observed myocardial activity of N-13 ammonia and C-11 palmitate in the septum was similar to that in the lateral wall. Septum to lateral wall tissue activity ratios averaged 1.04 +/- 0.15 for N-13 ammonia and 1.04 +/- 0.18 for C-11 palmitate, and were similar to those in the normal volunteers (0.98 +/- 0.07 and 0.98 +/- 0.03, respectively; p = NS). Myocardial clearance half-time and residual fraction of C-11 palmitate did not differ significantly between the septum and lateral wall. However, F-18 2-deoxyglucose uptake was significantly lower in the septum than in the lateral wall (15,768 +/- 4,314 versus 19,818 +/- 5,234 counts/pixel; p less than 0.003). The mean septum to lateral wall activity ratio of 0.83 +/- 0.21 was less than that observed in normal volunteers (0.92 +/- 0.07; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional myocardial blood flow and metabolism at rest in mildly symptomatic patients with hypertrophic cardiomyopathy. 252 4

To assess myocardial glucose metabolism and perfusion in 142 myocardial segments with defects seen at thallium-201 single photon emission computed tomography (SPECT), 27 studies with positron emission tomography (PET) utilizing nitrogen-13 ammonia and fluorine-18 deoxyglucose were performed in 26 patients. Myocardial infarction was defined on the basis of concordant reductions in segmental perfusion and glucose utilization; myocardial ischemia, on the basis of preservation of glucose utilization (metabolic viability) in segments with hypoperfusion at rest. Of the 142 segments analyzed, 101 had fixed defects, 31 had partially reversible defects, and ten had completely reversible defects. Preserved glucose utilization was identified in 47 (46.5%) of the segments with fixed defects and 20 (64.5%) of the segments with partially reversible defects. Of the ten segments with completely reversible defects, five (50%) were normal, and five (50%) exhibited ischemia at PET. Visual improvement in a persistent thallium defect at delayed imaging was not associated with residual glucose metabolic activity. Thus, PET can be used to detect glucose metabolic activity in a significant proportion of myocardial segments with fixed or partially redistributing defects seen at thallium SPECT, which suggests that the extent of tissue viability in patients with ischemic heart disease is underestimated at thallium scintigraphy.
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PMID:PET detection of viable tissue in myocardial segments with persistent defects at T1-201 SPECT. 278 37

Two simple cerebral ischemic models of mice were used for studying brain energy metabolism and the effects of drugs. Model one is partial occlusion of the left carotid artery and total occlusion of the right one including the vagus. The behavior of the animals appeared splaying of the contralateral extremities, circling around counterclockwise and in a comatose motionless state. Following the designated ischemic time, the animals were put into liquid N2. Model two is decapitation induced ischemia of mouse brain. The whole animal (control) and the severed head were rapidly frozen in liquid nitrogen 0, 10, 30, 60 s after decapitation. Brain samples were powdered at liquid N2 temperature, extracted and determined for ATP, phosphocreatine (Pcr) and lactic acid (LA). The data from model one indicate that after an ischemic period of 10 min, brain LA level increased significantly compared with values from the sham operated group, while no significant alteration was observed in brain ATP, and Pcr level. At 180 min of ischemia, levels of ATP and Pcr were considerably reduced while LA level increased significantly. The degree of symptoms induced by brain ischemia showed good correlation with brain energy metabolism. In model 2 brain LA level was found to be increased, while ATP and Pcr levels decreased after whole brain ischemia. However, brain ATP and Pcr levels were increased and LA level was decreased significantly in the normal and ischemic animal after administration of phenobarbital (225 mg/kg ip). LA level decreased significantly in the unischemic mice treated with Rb1 (100 mg/kg ip). It is indicated that both models of cerebral ischemia were simple and sensitive methods for studying brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain energy metabolism of cerebral ischemic mice and the effects of some drugs]. 280 Nov 43

Despite evidence from animal experiments to the contrary, nitrous oxide (N2O) reportedly does not induce myocardial ischemia when used as an adjunct to fentanyl anesthesia in patients with coronary artery disease who have well-preserved left ventricular (LV) function. However, the incidence of ischemia with N2O administration in similar patients with poor LV function may be different. The effects of N2O on segmental LV function, as determined by two-dimensional transesophageal echocardiography, changes in the ST-segment of the electrocardiogram were compared with the effects of an equal concentration of nitrogen (N2) (crossover design) in 70 patients who required elective coronary artery bypass grafting. Of these patients, 24% had left ventricular ejection fraction (LVEF) less than or equal to 40%. Myocardial ischemia was diagnosed in 14 patients during the study: four while awake, seven during induction of anesthesia and tracheal intubation, and four during the remainder of the study (one during N2O and three during 100% oxygen; one patient had two distinct periods of ischemia). No value for LVEF could be found that would distinguish between patients who did or did not have ischemia during the study. Patients treated with beta-adrenergic blocking drugs preoperatively were less likely to develop ischemia (P less than 0.05). Preoperative calcium channel blockers made no such differences. Onset of ischemia was not closely associated with hemodynamic changes. Thus, N2O does not induce clinically detectable myocardial ischemia in patients who have coronary artery disease, and poor LV function in situations in which the effects of deepening anesthetic depth and mild depression of global myocardial function are deemed desirable or harmless.
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PMID:Nitrous oxide does not induce myocardial ischemia in patients with ischemic heart disease and poor ventricular function. 280 10

The purpose of this study was to assess the degree, time sequence, and biochemical correlates of hypothermic protection against ischemic acute renal failure. Rats subjected to 40 minutes of bilateral renal artery occlusion (RAO) were made mildly hypothermic (32 degrees-33 degrees C, by cold saline peritoneal lavage) during the following time periods: 1) RAO only, 2) reperfusion only (beginning at 0, 15, 30, or 60 minutes after RAO and maintained for 45 minutes), or 3) during and after (0-45 minutes) RAO. Continuously normothermic (37 degrees C) RAO rats served as controls. The control rats developed severe acute renal failure (blood urea nitrogen [BUN], 95 +/- 4 mg/dl; creatinine, 2.2 +/- 0.1 mg/dl; and extensive tubular necrosis at 24 hours). Hypothermia confined to RAO was highly protective (BUN, 33 +/- 5 mg/dl; creatinine, 0.62 +/- 0.07 mg/dl; and minimal necrosis). Hypothermia partially preserved ischemic renal adenylate high-energy phosphate (ATP and ADP), increased AMP and inosine monophosphate concentrations, and lessened hypoxanthine/xanthine buildup (assessed at end of RAO). Hypothermia confined to the reflow period (beginning at 0, 15, and 30 minutes) was only mildly protective (e.g., BUN, 58-63 mg/dl); the degree of protection did not differ according to the time of hypothermic onset. Lowering reflow temperature to 26 degrees C had no added benefit. Hypothermia that started at 60 minutes after RAO conferred no protection. Combining ischemic and postischemic hypothermia abolished all renal failure (assessed at 24 hours). This study offers the following conclusions: Mild hypothermia can totally prevent experimental ischemic acute renal failure. Hypothermia is highly effective during ischemia, and it is mildly protective during early reflow; these benefits are additive. During early reflow, hypothermic protection is not critically time dependent. By 60 minutes of reflow, no effect is elicited; this absence of effect possibly signals completion of the reperfusion injury process. Hypothermia's protective effects may be mediated, in part, by improvements in renal adenine nucleotide content and, possibly, by decreasing postischemic oxidant stress.
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PMID:Degree and time sequence of hypothermic protection against experimental ischemic acute renal failure. 280 43

A recent study has indicated that the generation of an oxygen radical in freeze-clamped myocardium on reperfusion can be directly demonstrated using electron-spin resonance spectroscopy (ESR). However, the results need to be analyzed with caution, since artifactual radicals are misleading problems common to this method. To test whether that reported superoxide is truly the biologically existing radical or an artifactual radical, we performed experiments using isolated, perfused rat and rabbit hearts and open-chest canine hearts subjected to ischemia/reperfusion. Radicals were freeze trapped at 77 degrees K, and ESR measurements were made. The ESR spectra exhibited four free radicals. Among these, two radicals which had been previously claimed as superoxide and a nitrogen-centered radical were shown as mechanically yielded artifactual radicals. These were produced by pulverization of the frozen sample. In artifact-free samples, superoxide could not be detected. The radicals native to the myocardium were identified as coenzyme Q10-. and another radical the species of which remains unclear.
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PMID:Is superoxide demonstration by electron-spin resonance spectroscopy really superoxide? 283 95

Ischaemic rat brains were examined for temporal changes in phospholipase C activity with phosphatidylinositol; the effects of pentobarbital on the activity also were investigated. Ischaemia was produced by decapitation. Pentobarbital (60 mg/kg) was administered i.p. for 15 min before decapitation. The removed heads were incubated at 37 degrees C for 1, 5, 15 or 30 min and then quickly frozen in liquid nitrogen. After isolation of subcellular fractions from the brains, phospholipase C activity was measured for cytosol and microsomes, using radioactive phosphatidylinositol as a substrate. The results demonstrated that brain phospholipase C predominantly localized in the cytosol was dependent on Ca2+ for full activity and had neutral pH optima. Although the enzyme activity did not increase during ischaemia, pentobarbital inhibited phospholipase C activity in the cytosol but not in the microsomes. These observations suggest that pentobarbital may exert a cerebral protective action due to, at least in part, the repression of phospholipase C followed by a reduction of phosphatidylinositol breakdown, preventing perturbation to the integrity of membranes, during ischaemia.
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PMID:Inhibitory effect of pentobarbital on phospholipase C activity in ischaemic rat brain. 289 Oct 63

The results of several recent studies have demonstrated that reactive oxygen metabolites are responsible for a major portion of ischemia/reperfusion (I/R) injury in skeletal muscle. Presumably, the cytotoxic oxidants are produced during reperfusion when molecular oxygen (the source of the reactive oxygen metabolites) is reintroduced to the tissues. The purpose of this study was to test the hypothesis that molecular oxygen must be provided at reperfusion to produce I/R injury in skeletal muscle. Isolated, maximally vasodilated (papaverine) canine gracilis muscles were reperfused, after 4 h of inflow occlusion, from reservoirs containing autologous blood equilibrated with either 95% O2-5% CO2 or 95% N2-5% CO2 gas mixtures. Arterial PO2 fell from approximately 120 mmHg to less than 3-5 mmHg, during the use of nitrogen. The solvent drag reflection coefficient for total plasma proteins (sigma f) and total vascular resistance was determined for the following conditions: control (no ischemia), reperfusion with oxygenated blood after 4 h ischemia; and reperfusion (after 4 h ischemia), first with anoxic blood and then oxygenated blood. Reperfusion with oxygenated blood, after 4 h of ischemia, significantly reduced solvent drag reflexion coefficient (sigma f) from 0.93 +/- 0.02 to 0.63 +/- 0.02, indicating a dramatic increase in vascular permeability. Total vascular resistance increased from 6.1 +/- 1.1 mmHg.ml-1.min.100 g during the preischemic period to 12.9 +/- 3.0 mmHg.ml-1.min.100 g during normoxic reperfusion. In muscles reperfused with anoxic blood, sigma f averaged 0.82 +/- 0.06, whereas vascular resistance increased by 56 +/- 13%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoxic reperfusion attenuates postischemic microvascular injury. 291 94


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