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)

The influence of transient myocardial ischemia on recovery uridine incorporation into RNA and histone acetylation was investigated in an isolated perfused rat heart. Hemodynamically, hearts recovered from 15 min of ischemic arrest and were stable for at least 60 min of perfusion. Uridine incorporation was reduced (P less than 0.05) in ischemic hearts by 24 and 26% after 30 and 60 min of recovery perfusion. The incorporation of uridine into RNA from purified myocytes was decreased by 50% in the ischemic muscle cells. The covalent acetylation of total nucleohistones was diminished by 37%. Histone fractionation by urea polyacrylamide gel electrophoresis clearly indicated that histones H3 and H4 preferentially incorporated less acetate during ischemic recovery. However, histone acetylation for proteins H2A + H2B was not effected. These data suggest that a brief period of ischemia disrupts nucleotide incorporation during the recovery phase, with marked decrease associated with the muscle cell. The similar change in histone acetylation indicates a possible link between nucleoproteins and chromatin function during ischemic insult to the heart.
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PMID:Effect of myocardial ischemia on uridine incorporation and histone acetylation. 617 4

Models of post-ischemic acute renal failure were prepared in rats. The effects of adenosine triphosphate-magnesium chloride (ATP-MgCl2) administration following renal ischemia on possible changes in renal function and renal cellular metabolism following ischemia were studied using the model. The results obtained revealed the following: 1) Over 40 minute-renal ischemia led to significant lowerings of renal cellular ATP level and energy charge (EC) by as much as 45 to 57% and 4.1 to 7.4% of the control, respectively, at 90 min following re-establishment of renal blood flow. Significant increases in Na+ in renal tissues were observed, but no changes in K+. Further, lactate level in renal tissues tended to increase with prolonged ischemic time by as much as 27 to 31% of the control, with a renal cellular anaerobic metabolism observed. On the other hand, at 24 hr following recirculation of the kidney, plasma creatinine (P-Cr), blood urea nitrogen (BUN) and fraction excretion of sodium (FENa) increased significantly, and creatinine clearance (C-Cr) and urine osmotic pressure decreased significantly, as compared with the control, indicating ischemic acute renal failure. 2) Intravenous injection of ATP-MgCl2 at a dose of 25 mumole/kg and a rate of 1.0 mumol/min after 40 min of renal ischemia led to significant lowerings of P-Cr, BUN and FENa to 36, 35 and 35% of the control (injected with physiological saline solution), respectively, and to significant elevation of C-Cr and urine osmotic pressure by as much as 41 to 31% of the control respectively, at 24 hr after reperfusion. The above results suggested that the ischemic acute renal failure was caused by the decreases in renal cellular ATP and EC with ischemia, resulting in renal cellular metabolic disturbances. It was further suggested that ATP-MgCl2 administered for such a pathological condition could make significant improvements in renal function.
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PMID:[Effect of adenosine triphosphate-magnesium chloride administration for post-ischemic acute renal failure (I)]. 660 69

Revascularization syndrome is one of the dangerous postoperative complications which results sometimes in loss of a limb, renal shutdown and death due to myoglobin-nephrosis and hyperkalemia. During the past 3 years, 2 cases of revascularization syndrome were experienced in 16 cases of thrombo-embolectomies for acute peripheral arterial occlusion. One patient died from hyperkalemia 100 minutes after revascularization. Another patient suffered from a renal shutdown, and was treated with hemodialysis and thigh amputation. It is sometimes very difficult to predict whether the revascularization syndrome will occur or not. When revascularization is performed within 12 hours after an onset of acute occlusion and when the amount of ischemic muscle is not large, the syndrome may not occur. When the time-interval between the onset of ischemia and revascularization is longer than 24 hours and when the mass of ischemic muscle is large, the syndrome will occur. Preoperative serum creatinine and urea nitrogen level are important parameters predicting the prognosis.
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PMID:[Pathogenesis and prevention of the revascularization syndrome]. 667 83

DT, a 63-year-old white male with insulin-dependent diabetes mellitus and severe peripheral vascular disease, was admitted with a five-day history of vague abdominal pain and diarrhea. On the day of admission he vomited three times, was noted to have a bloody stool, and came to the emergency room. DT denied hematemesis, fever, or chills. He had bilateral leg amputations and had sustained three myocardial infarctions, the last one 15 months before this admission. He had never experienced symptoms of abdominal angina. Of significance was his history of congestive heart failure, mitral regurgitation, and atrial fibrillation. His medications on admission included digoxin 0.25mg per day, furosemide 40mg per day, and NPH insulin 15 units per day. On admission to the hospital his oral temperature was 38 degrees C, pulse was 90/min, respiratory rate was 24/min, and blood pressure was 134/80mmHg. Abdominal examination revealed a distended abdomen with hypoactive bowel sounds and mild tenderness. Chest x ray revealed cardiomegaly. The electrocardiogram demonstrated atrial fibrillation. A plain film of the abdomen was positive for gallstones and edema of the bowel wall (thumb-printing). Laboratory results included blood urea nitrogen 48mg%, creatinine 1.2mg%, hemoglobin 18g/dl, and hematocrit 52.9%. White blood cell count was 11,900 cells/cc with 33% polymorphonuclear leukocytes, 47% bands, 8% lymphocytes, 11% monocytes, and 1% atypical lymphocytes. The prime considerations for differential diagnosis were mesenteric ischemia and infectious gastroenteritis. While it was appreciated that mesenteric ischemia, if present, might warrant surgical intervention, the risk of anesthesia itself in this patient was felt by his attending physicians to exceed 30%. Furthermore, the clinical findings were only "suggestive" of mesenteric eschemia. They were certainly not "diagnostic." In view of this dilemma, a consultation with the Division of Clinical Decision Making was requested.
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PMID:Abdominal pain, atherosclerosis, and atrial fibrillation. The case for mesenteric ischemia. 716 38

Ischaemia of the dog intestine lasting 1 h causes desquamation of the epithelium at the villus tips and congestion in the villus capillaries. The crypt cells are relatively undamaged. These changes are associated with a loss of active transport of organic solutes, determined in vitro, a reduction in mucosal sucrase activity and an abolition of glucose absorption in vivo. A profuse net loss of water and electrolytes into the lumen in vivo develops. The net sodium loss is due primarily to an inhibition of the lumen-blood flux of this ion, the blood-lumen flux being relatively unchanged. In uraemic dogs, the loss of urea into the lumen is the same in control and ischaemic loops, testifying to the lack of change in the unidirectional water flow from blood to lumen. Perfusion of the dog intestine with 1% Triton X-100 leads to morphological changes that have certain similarities with those provoked by ischaemia. Damage was restricted to the villus tips, protection from further alterations apparently being provided by a mucus layer that forms on the mucosal surface; the crypt region remained unchanged. After 10 min exposure, organic solute transport in vitro and glucose absorption in vivo were both reduced by not abolished; sodium and water absorption in vivo were suppressed, but no net secretion occurred. To account for these observations, we have suggested that the normal crypt cell is a secretory element with respect to sodium and water. During maturation, its absorptive properties develop such that the mature enterocyte, possessing both absorptive and secretory mechanisms, is capable of net absorption of sodium. After destruction of the villus tips, net secretion continues in the crypts; if there are insufficient villus cells remaining to ensure reabsorption, a net secretory capacity is observed.
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PMID:Source of net water and electrolyte loss following intestinal ischaemia. 736 61

A study of renal disease in familial dysautonomia identified excess glomerulosclerosis in 10 or 13 autopsied and biopsied patients. Sympathetic nerve terminals could not be found on renal vessels in biopsied tissue; they were invariably demonstrable in controls. Altered renovascular responsivity to systemic hypotension in familial dysautonomia may lead to ischemia and subsequent sclerosis of glomeruli. Review of 79 living outpatients showed that clinically overt renal disease was rare in familial dysautonomia. Nevertheless, frequent observations of elevations of serum creatinine concentrations (32% of patients) and blood urea concentrations (76% of patients) indicated a high prevalence of abnormality. An association was found between hypotension and renal dysfunction.
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PMID:Renal disease in familial dysautonomia. 737 14

Coronary occlusion was carried out in 58 dogs in an acute experiment and the content of ammonia and urea was studied in venous blood draining directly from the zone of ischemia. Early increase in the concentration of free ammonia in the zone of ischemia was revealed. The administration of l-aspartic acid, potassium asparaginate, magnesium asparaginate, and glutamic acid led to intensification of urea-producing processes in the myocardium and reduction in hyperammoniemia and the degree of ischemic damage to the myocardium.
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PMID:[Correction of nitrogen metabolic disorders in the myocardium in experimental ischemia]. 741 82

The morphological factors contributing to the reduction GFR in an early phase of NE-induced ARF (0.75 microgram/kg/min) were evaluated by comparing renal morphology at the end of NE infusion with that 2 hr later in unilaterally nephrectomized dogs. GFR 2 hr after NE infusion was reduced to 50% of the preinfusion level in a 30 min infusion group (N = 6), to 13% in a 60 min infusion group (N = 7), and to 2% in a 120 min infusin group (N = 5). On the other hand, simultaneous RBF was not significantly reduced in any group. Dilated PT lumina filled with eosinophilic granular materials in paraffin sections fixed in Zenker-Formol or with impacted swollen blebs in Epon sections fixed in diluted Karnovsky's solution and osmium were found diffusely immediately following 60 and 120 min NE infusion, but patchily after 30 min infusion. Similar changes were found 2 hr after the infusion, except that some PTs came to have dilated but transparent lumina in the 60 and 120 min NE infusion groups. Electron microscopic studies revealed that a part of the membrane-bounded cytoplasm of PT cells extruded into the tubular lumen and became impacted swollen blebs during NE-induced ischemia. There was no prominent foot process fusion in any group. It is concluded that the tubular obstruction by impacted swollen blebs generated in PT during ischemia is a major factor responsible for the reduction in GFR in the early phase of NE-induced ARF.
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PMID:Morphological changes in an early phase of norepinephrine-induced acute renal failure in unilaterally nephrectomized dogs. 741 55

This work studies the role that nitric oxide (NO) plays in ischemia/reperfusion (I/R) of the rat kidney. Sprague-Dawley rats, weighing 250-300 g, were subjected to 75 min of warm ischemia and contralateral nephrectomy. The animals were divided into six groups (n = 12 per group): ischemic control (IC) with normal saline, L-NG-mono-methyl-arginine (L-NMMA) 50 mg/kg, L-arginine (L-Arg) 300 mg/kg, Na-nitroprusside (Na-NP) 2.5 mg/kg, the combination of L-NMMA+Na-NP at the doses used before, and the sham group. All animals received the drug intravenously 60 min prior to ischemia. Survival was evaluated at seven days. Renal damage was assessed by kidney function tests (serum creatinine and blood urea nitrogen) and light histology. Lipid peroxidation was measured in renal tissue using the thiobarbituric acid assay. Significantly better survival was seen in the Na-NP group, as compared to the rest of the study. Serum creatinine at 24 and 48 hr showed a significant difference between the Na-NP group and the other groups. Histological damage was minimal in the Na-NP group. Clearly, the Na-NP had the most beneficial effect in survival and histological structure. Lipid peroxidation was significantly different, with the lower levels seen in the L-NMMA group and the higher levels in the Na-NP group. In base to these results, we conclude that exogenous NO has a beneficial and protective effect of the ischemically damaged rat kidney. This protection is independent of lipid peroxidation. Endogenous NO production does not play a role in I/R injury in our model.
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PMID:Role of nitric oxide in ischemia/reperfusion of the rat kidney. 753 53

Rhabdomyolysis caused 28 out of 903 (3.1%) of cases of severe acute renal failure (ARF) treated at Leeds General Infirmary over a 14-year period (1980-1993). The commonest cause of rhabdomyolysis was muscle compression, usually due to drug- or alcohol-induced coma. Other causes included fits, infection, acute limb ischemia, trauma, and heat stroke. Prognosis was relatively good, with a 78.6% survival rate and recovery of renal function to normal in all survivors who were followed up. The creatinine/urea ratio was higher in ARF due to rhabdomyolysis than in an unselected group of patients with other causes of ARF but not when the comparison was with sex- and age-matched controls with ARF. This suggests that this previously described feature of rhabdomyolysis simply reflects the increased muscle mass of a younger group of patients, rather than a specific effect of muscle damage. Clinical features of muscle damage were often absent and so the possibility of rhabdomyolysis should be considered in appropriate settings if the diagnosis is to be made early enough to administer treatment that may prevent ARF and the consequences of the compartment syndrome.
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PMID:The clinical and biochemical features of acute renal failure due to rhabdomyolysis. 756 17


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