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

The spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN) reduced the ischemia-reperfusion induced acute renal failure in the rat. Renal ischemia was produced in unilateral nephrectomized rats by complete occlusion of the left renal artery for 60 min. Perfusion of the kidney was then reestablished, and the rats were sacrificed 48 h later. PBN (100 mg/kg i.p.) administered 30 min prior to renal artery occlusion significantly reduced the increase in serum creatinine and urea and renal failure index, as well as the decrease in urine/plasma creatinine ratio and creatinine clearance compared to saline-injected ischemic rats. PBN injected to control rats had no effect on these parameters. These data support the hypothesis of an involvement of reactive free radicals in the pathogenesis of ischemia-reperfusion induced acute renal failure in the rat and suggest that PBN may be a useful agent for the prevention of renal ischemia-reperfusion damage.
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PMID:Ischemia-reperfusion induced acute renal failure in the rat is ameliorated by the spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN). 146 97

In the acute phase of ischemic renal failure, the severe depression of the glomerular filtration rate (GFR) is due to obstruction of the tubules by cells and cell debris rejected from the proximal tubules, a blockade which can be prevented at least partly, by treatment with osmotic diuretics. The isosthenuria, the second typical sign in ischemic acute renal failure, probably derives from the medullary ischemia that results from an intracapillary trapping of red cells. This, in turn, is suggested to be caused by oxygen-derived free radicals, which via increasing the capillary macromolecular permeability result in a massive extravasation of plasma and hence in hemoconcentration. As expected from this hypothesis, scavengers may ameliorate both the trapping and the consequent medullary ischemia. Unfortunately, however, a therapy using both osmotic diuretics and scavengers fails to improve the long-term outcome. Hemodilution would seem more promising, since it will both prevent the medullary ischemia seen in the acute phase and substantially improve the long-term outcome. At a hematocrit of 0.30, rat kidneys exposed to 45-min ischemia will show a GFR 1 month after the insult of more than 50% of the normal GFR as against 15% in untreated animals.
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PMID:Osmotic diuretics and hemodilution in postischemic renal failure. 150 60

Two patients with carbon monoxide poisoning are presented, both of whom suffered rhabdomyolysis complicated by acute renal failure. One patient, an attempted suicide, developed a compartment syndrome of the right thigh that required fasciotomy and recovered after a period of hemofiltration and hemodialysis. Muscle biopsy appearances were consistent with partial muscle infarction. The other patient, rescued from a smoke filled room, exhibited raised creatine kinase but no evidence of muscle swelling. He developed anuric renal failure and adult respiratory distress syndrome and died despite maximum intensive care. Muscle biopsy showed early evidence of muscle necrosis. In both cases there was a marked reduction of enzyme activities in the muscle biopsy consistent with metabolic derangement. Although there was a clinical compartment syndrome in the first case, there was no muscle swelling at the time of biopsy or subsequently in the second case. A direct toxic effect of carbon monoxide may thus have been an important mechanism contributing to the muscle necrosis in the second case, although local ischemia may have been an exacerbating factor in the first case.
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PMID:Rhabdomyolysis and acute renal failure following carbon monoxide poisoning: two case reports with muscle histopathology and enzyme activities. 151 16

Between May 1966 and June 1991, 129 patients underwent surgical repair of thoracoabdominal aneurysms, with an overall 30-day mortality rate of 35%. In 75 operations (58%) performed electively, 11 deaths (15%) occurred, and in 54 cases (42%) of either symptomatic or ruptured aneurysms 34 deaths (63%; p less than 0.001) occurred. No one survived among six patients with preoperative hypotension (less than 90 mm Hg) or cardiac arrest. In 16 patients (12%) the etiology of aneurysms was a result of chronic aortic dissection, and the mortality rate in this subgroup was 44%. In the remaining 113 patients (88%) where the etiology was atherosclerosis, 38 deaths occurred (34%; p = 0.433). Spinal cord ischemia occurred in 25 cases (21%) among 116 patients who survived operation. Partial ischemia occurred in six cases (25%), and complete paraplegia occurred in the remainder. Complete and partial paraplegia occurred in 16 of 42 cases (38%) when all of the thoracic aorta was replaced (Crawford groups I, II) and in 9 of 74 cases (12%) when only the abdominal or lower thoracic aorta was replaced (Crawford groups III, IV; p = 0.016). Other complications included myocardial infarction (14 cases, 11%), respiratory failure (46 cases, 36%), and renal failure (33 cases, 27%). The major prospect for improved early survival of patients with thoracoabdominal aneurysms seems to be early detection and elective repair before the occurrence of symptoms.
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PMID:Thoracoabdominal aneurysm repair: a representative experience. 157 33

Intracellular calcium mediates a wide array of cell functions in mesenchymal as well as in epithelial and endothelial cells. These comprise regulation of vascular tone, cell proliferation and synthesis of prostanoids and cytokines. Therefore, it is not surprising that a substantial body of evidence has emerged to suggest a crucial role of calcium in the initiation and perpetuation of renal disease. Increased deposition of calcium was found in the renal cortex of rats with remnant kidney and in kidney tissue of patients with end-stage renal failure. Calcium plays an important role in altered intrarenal and glomerular hemodynamics with increased glomerular wall tension as well as in cellular proliferation and in recurrent ischemic events leading to glomerulosclerosis and interstitial fibrosis. Besides hemodynamic mechanisms, additional calcium-dependent mechanisms must be considered for glomerular hypertrophy and/or mesangial proliferation to develop, namely the role of growth factors, prostanoids and cytokines. Their signals include receptor-regulated production of inositol-trisphosphate and diacylglycerol and the consecutive stimulation of protein kinase C and the Na/H-antiport. Full activation of this antiport, which raises intracellular pH and thereby stimulates protooncogenes, again requires the presence of calcium. Recurrent focal glomerular ischemia may result in cellular and mitochondrial calcium overload that may interfere with cellular energy metabolism. Calcium also activates proteinases and the production of oxidants to enhance neutrophil-mediated cell injury. These deleterious effects of calcium may initiate and perpetuate the progression of renal disease and eventually lead to end-stage renal failure.
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PMID:Role of calcium in the progression of renal disease: experimental evidence. 161 63

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.
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PMID:Ischemic hepatitis: widening horizons. 848 Jul 56

We identified 47 patients with nonocclusive ischemia of the large intestine over a seven-year period. The mean age at presentation was 56.2 years, with a 2:2:1 male predominance. Associated medical illnesses were diabetes (17 percent), renal failure (5 percent), and hematologic disorders (5 percent). Six patients developed ischemic colitis after aortic surgery. The mean delay in diagnosis was 1.8 days (range, three hours to 23 days). The right colon was involved in 21 patients (46 percent). Overall, 15 of 16 patients were successfully treated nonoperatively with bowel rest and antibiotics; one patient who was managed nonoperatively died. Among the 31 requiring intestinal resection, enteric continuity was reestablished in 14. Second-look laparotomy in eight patients revealed further ischemia in two (20 percent). Mortality in the operative group was 29 percent (9 of 31). No patient has developed recurrent ischemia (mean follow-up, 5.3 years). Ischemic colitis often occurs without an obvious predisposing event, may involve all segments of the large intestine, and frequently requires surgery. While its course may be self-limited, elderly and diabetic patients, as well as those developing ischemia following aortic surgery or hypotension, continue to have a poor prognosis.
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PMID:Ischemic colitis: patterns and prognosis. 164 95

Twelve patients underwent transabdominal, supraceliac aortomesenteric bypass for celiac and superior mesenteric artery occlusive disease. Nine patients had bypass for intestinal ischemia (five acute, four chronic), and one patient each had bypass for arcuate ligament syndrome, thoracoabdominal aneurysm, and an infected aortic stump "blowout." Three aortoceliac, 9 aortohepatic, and 10 aortosuperior mesenteric artery bypasses were performed. Prosthetic grafts were used for the bypasses in 11 of the 12 patients. One death occurred in a patient with preexisting hepatic necrosis and renal failure secondary to acute mesenteric ischemia. During a mean follow-up of 26 months, one graft thrombosis occurred and required revision for recurrent symptoms. Supraceliac aortomesenteric bypass appears to be a safe and effective procedure for visceral revascularization.
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PMID:Role of supraceliac aortic bypass in visceral artery reconstruction. 167 Feb 36

In a 73-year-old woman with trimalleolar fracture, secondary acute ischemia of the limb and renal failure developed in association with heparin-dihydroergotamine thromboprophylaxis. Earlier cases of thromboprophylaxis-related angiospasm are briefly reviewed. The condition is infrequent, but trauma of extremities and shock are risk factors. Renal failure is rare.
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PMID:Lower-limb vasospasm and renal failure during postoperative thromboprophylaxis. Case report. 167 86

Recent studies in animal models suggest that glomerular capillary hyperperfusion and hypertension, rather than ischemia, cause renal injury. Interventions that control glomerular capillary hypertension may protect against progressive injury, even in the presence of continued systemic hypertension. In the absence of systemic hypertension, diabetes mellitus is a prominent clinical example of glomerular hypertension. Animal studies have shown that glomerular hemodynamic abnormalities, especially elevations in glomerular pressure, play an important role in the pathogenesis of diabetic glomerulopathy. A number of clinical observations suggest that angiotensin converting enzyme (ACE) inhibitors may delay the progression of diabetic nephropathy by their effects on renal hemodynamics. In experimental animals, comparisons between calcium channel blockers and ACE inhibitors have shown the latter to be more effective in protecting the kidneys. Preliminary clinical studies indicate that ACE inhibitors may have advantages in preserving renal function in hypertensive and diabetic patients with renal failure.
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PMID:Renal effects of converting enzyme inhibitors in hypertension and diabetes. 169 12


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