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)

Cadaveric kidney graft recipients, treated according to a strict, high dose CyA protocol, were followed prospectively for one year. The aim was to study the impact of donor age on transplantation outcome in a homogenously immunosuppressed patient material. The patients were divided into 2 groups; G1: donor age less than or equal to 50 years (mean 34.5 y; range 10-50; n = 49) and G2; donor age greater than 50 years (mean 58.1 y; range 51-68; n = 37). The groups were comparable in terms of recipient age, warm and cold ischemia time, number of HLA A, B, DR mismatches and number of rejection episodes. The result showed no difference in mortality between the 2 groups (12% vs. 13%). One year graft survival was 70% vs. 51% (NS), immediate onset of function was 76% vs. 46% (p less than 0.01), creatinine concentration at one year was 146 +/- 39 vs. 206 +/- 73 mumol/l (p less than 0.05) for G1 and G2, respectively. The most striking finding was a highly significant difference in the rate of graft-related surgical complications, 12% vs. 35% (p less than 0.01) for G1 and G2, respectively. We conclude, that a patient receiving a graft from an elderly donor, runs a higher risk of graft-related complications and that long term graft survival and function also might be influenced by the age of the donor. A possible reason for the inferior results in group 2 might be an increased sensitivity for the toxic effects of CyA of aging kidneys.
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PMID:Influence of the age of cadaveric kidney donors on transplantation outcome and rate of surgical complications. 207 67

The effects of chronic dietary protein restriction on ischemic renal failure were evaluated in rats subjected to 90 min of bilateral renal clamping. The rats were kept on either 20% casein (regular) diet or casein-free (protein-free) diet 10 days before and 21 days after renal injury. Rats on regular protein diet showed higher levels of BUN and serum creatinine and had a lower inulin clearance (microliter/min/100 g BW) than animals on protein-free diet (289 +/- 34 vs 582 +/- 103, p less than 0.05) 2 days after ischemia. However, the inulin clearance measured 21 days following ischemia was significantly higher in rats on regular diet (1468 +/- 181) than those maintained on protein-free diet after ischemia (560 +/- 167). When unilateral 90 min ischemia was performed in rats on regular diet, the postischemic kidneys showed an incomplete recovery of the inulin clearance (226 +/- 35) compared to the contralateral kidney (900 +/- 116), 21 days after ischemia; whereas in rats on a protein-free diet the inulin clearance averaged 106 +/- 17 in the postischemic kidney and 345 +/- 41 in the right kidney. When left renal ischemia and contralateral nephrectomy were performed, the inulin clearance was 1149 +/- 74 in rats on regular diet and 534 +/- 60 in rats on protein-free diet, 21 days following renal insult. These results suggest that protein restriction can play a protective role against renal ischemia in an initial phase, but it limits the late recovery from ischemia. The presence of a normal contralateral kidney inhibits the functional recovery of the postischemic kidney and a contralateral nephrectomy produces a compensatory functional hypertrophy of the postischemic kidney, even in rats on a protein-free diet.
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PMID:The effect of protein restriction on the severity and recovery from ischemic renal failure. 210 Aug 29

Because the intestinal mucosa is most sensitive to ischemia, serum levels of mucosal enzymes, such as diamine oxidase, may be most likely to indicate intestinal ischemia. Our aim was to compare serum levels of mucosal (diamine oxidase, alkaline phosphatase) and seromuscular (creatinine phosphokinase, lactic dehydrogenase, serum glutamic oxaloacetic transminase) enzymes during intestinal ischemia of varying extent and duration in dogs. Group 1 (n = 6) underwent sham laparotomy. Group 2 (n = 8) had 50% of the small intestine devascularized. Group 3 (n = 8) had the superior mesenteric artery occluded for 2 hours and released. Group 4 (n = 8) had the superior mesenteric artery ligated. Serum samples were obtained before and 2, 4, 8, and 24 hours after operation, and histologic specimens were examined at 4 hours. Creatinine phosphokinase levels became elevated within 4 hours of ischemic injury in group 2 (223 +/- 197 vs. 68 +/- 26, p less than 0.05) and group 4 (212 +/- 136 vs. 76 +/- 29, p less than 0.05). Significant elevation of serum enzymes levels, except diamine oxidase, occurred in groups 2, 3, and 4 at 24 hours, including those with normal histology after temporary superior mesenteric artery occlusion. Thus seromuscular enzymes, particularly creatinine phosphokinase, were more likely to be elevated during intestinal ischemia. Enzyme levels were not influenced by the extent and reversibility of the ischemic injury.
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PMID:Serum enzyme levels during intestinal ischemia. 210 44

Calcium is believed to be responsible for initiating a deleterious cascade of events that leads to irreversible cell injury during prolonged ischemia. Theoretically, the calcium-dependent cascade of events can be interrupted at three distinct points: a) by reducing calcium inflow into the cytosol using a calcium channel blocker such as verapamil, b) by increasing the mitochondrial capacity to sequester calcium using ethane-1-hydroxy-1:1-diphosphonic acid (EHDP), and c) by inhibiting the activation of the calcium-calmodulin complex using trifluoperazine (TFP). To evaluate the protective role of these agents in prolonged ischemia, 190 unilaterally nephrectomized rats underwent total occlusion of the renal artery for 90 min. One hour before surgery, all the rats received an i.p. injection of either saline or one of the drugs. Of the 190 rats, 130 were used to determine survival and optimal drug doses; the remaining 60 rats were used to determine blood urea nitrogen and serum creatinine at 40 h and 5 days after surgery. Only 33% of the rats in the control group survived for 10 days. However, 87.5% (P less than 0.005), 90% (P less than 0.005), and 60% (P less than 0.01) of the rats pretreated with verapamil, TFP and EHDP respectively survived for 10 days. No differences, however, were seen in renal function tests among the control, TFP or EHDP groups. This suggests that calcium antagonists are successful in protecting the kidney from prolonged ischemic injury despite impaired renal function tests. It may also indicate that these agents delay or prevent the ischemic cells from undergoing irreversible damage.
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PMID:Blocking the calcium cascade in experimental acute renal failure. 211 82

So far two methods for prolonging the tolerance of renal ischemia are available: 1) surface cooling with crushed ice and 2) perfusion cooling with an extracellular-like solution. Both methods use only the principle of reducing metabolism through cooling. While rewarming during surgery the ischemic protection is lost, or the kidney must be cooled once again. Therefore, a new preservation solution should reduce energy consumption due to its composition in addition to cooling. For open heart surgery, the HTK solution by Bretschneider is already used clinically. In 71 dog kidney experiments, the ischemic time kidneys could tolerate was prolonged by this solution from 15 to 120 min at 35 degrees C and from 45 to 360 min at 25 degrees C. After 2 h of ischemia at 30 degrees C glomerular filtration rate was about 20 ml/min.100gww within 3 h of reperfusion. After six postoperative days the filtration rate was 40 ml/min.100 gww. No ischemic damage could be recognized by histological investigations. The clinical effectiveness of this method was shown in 7 clinical applications. Ischemic duration lasted up to 113 min, and blood creatinine was between 0.8 and 2.4 mg% at the 6th postoperative day. Use of this preservation technique thus leads to improved kidney function immediately following operation. Longer ischemia can be tolerated by a kidney thus protected, and using this technique excellent visibility can be achieved during intrarenal surgery, simplifying, for example, tumor extirpation.
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PMID:A new method for conservative renal surgery--experimental and first clinical results. 212 22

Many renal structural and functional abnormalities have been associated with sickle cell disease. The patients have an impaired urinary concentrating ability but an intact diluting capacity. There are defects in both urinary acidification and potassium excretion, although overt metabolic acidosis and hyperkalemia occur infrequently. Proximal tubular function is supranormal, as manifested by increased reabsorption of phosphate and increased secretion of creatinine. The former results in mild hyperphosphatemia, while the latter causes substantial overestimation of the glomerular filtration rate (GFR) by creatinine clearance. Both GFR and renal plasma flow are increased in young patients with sickle cell disease, but prostaglandin inhibitors decrease the GFR. The GFR progressively decreases with increasing age. Proteinuria, and even nephrotic syndrome, are relatively frequent; the most common renal lesion in children is focal glomerular sclerosis, which may be associated with progressive deterioration in renal function. Glomerular hyperfiltration has been implicated in the pathogenesis of the glomerular lesions, as well as in the development of renal failure. In patients with end-stage renal disease, both hemodialysis and kidney transplantation have been successful. Recurrent hematuria is a relatively common problem in patients with sickle cell disease. The bleeding usually remits spontaneously, but occasionally requires therapy with aminocaproic acid. Papillary necrosis may occur, and is thought to result from medullary ischemia.
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PMID:Renal abnormalities in sickle cell disease. 217 77

We evaluated 50 consecutive patients who received thrombolytic therapy for acute myocardial infarction using thallium-201 single photon emission computed tomography in combination with oral dipyridamole (300 mg) to assess the frequency of residual myocardial ischemia. Thallium studies were performed early after myocardial infarction at a mean of 4.6 days (range 3 to 11) in 50 patients. The time from the onset of chest pain to the administration of thrombolytic therapy was 2.6 hours (range 0.5 to 5.5). Q wave myocardial infarction was evident in 46 patients; four patients had a non-Q wave infarction (anterior infarction in 31 patients and inferior infarction in 19 patients). The serum mean peak creatinine kinase was 1503 IU/L (range 127 to 6500). Coronary angiography was performed in all patients at a mean of 3.1 days (range 2 to 10) and revealed the infarct-related vessel to be patent in 36 patients (72%). The ejection fraction was 48% (range 26% to 67%). After dipyridamole administration, 13 patients (26%) developed angina that was easily reversed with the administration of intravenous aminophylline. Systolic blood pressure decreased from 122 to 115 mm Hg (p less than 0.05) and the heart rate increased from 76 to 85 beats/min (p less than 0.05). None of the patients had significant hypotension, arrhythmias, or evidence of infarct extension. Perfusion abnormalities were present on the initial thallium images in 48 patients. Redistribution suggestive of ischemia was present in 36 patients (72%). Ischemia confined to the vascular distribution of the infarct vessel was evident in 22 patients. Seven patients had ischemia in the infarct zone as well as in a remote myocardial segment. Thus 29 patients (58%) had ischemia in the distribution of the infarct vessel. Ischemia in the infarct zone was evident in 19 of 36 patients (53%) with open infarct vessels and in 10 of 14 patients (71%) with occluded infarct vessels. In conclusion, thallium-201 single photon emission computed tomography using oral dipyridamole was safely performed in patients with recent myocardial infarctions who receive thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of coronary angiography and early oral dipyridamole thallium-201 scintigraphy in patients receiving thrombolytic therapy for acute myocardial infarction. 222 May 36

The purpose of these studies was to determine if a functionally insignificant ischemic insult, occurring prior to gentamicin administration, enhanced gentamicin nephrotoxicity. Bilateral renal pedicle clamp studies demonstrated that 15 minutes of ischemia did not increase the plasma creatinine yet markedly enhanced gentamicin nephrotoxicity. Further studies, in uninephrectomized rats, demonstrated that following fifteen minutes of renal ischemia and four hours of reperfusion inulin clearance, FENa+ and cellular morphology were normal. This model, therefore, was used in all subsequent studies. While the plasma creatinine concentrations were normal 24 hours following 15 minutes of ischemia and only slightly increased following gentamicin administration (100 mg/kg, i.p.) gentamicin administered four hours following 15 minutes of renal ischemia resulted in significantly increased 24-hour plasma creatinine values. Light microscopic quantitation of tissue injury, performed 24 hours following experimental manipulation, was notable for S3 segment damage in the ischemia plus gentamicin group. This was not observed in either the ischemia group or the sham operated gentamicin group. Cortical gentamicin levels were elevated in the ischemia plus gentamicin group, despite similar plasma gentamicin half-lives. However, the elevation in cortical gentamicin levels was dissociated from the enhanced nephrotoxicity seen following mild ischemic injury. Taken together these data indicate that mild renal ischemia, occurring prior to gentamicin administration, greatly enhanced gentamicin nephrotoxicity with the greatest damage occurring to S3 cells.
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PMID:Mild ischemia predisposes the S3 segment to gentamicin toxicity. 223 88

Acute renal failure after contrast media injection has been recognized for at least 35 years but the exact mechanism responsible for the renal injury remains an enigma. The clinical characteristics of contrast-induced nephropathy (CAN) are well-known although more recently the nonoliguric presentation has occurred at an increased frequency--in 70 to 90% of cases. For nonoliguric presentation of CAN, one can expect an asymptomatic increase in serum creatinine, the mean peak occurring at 4.2 days. If oliguric, the fractional excretion of sodium will be less than 1% and resistant to either fluid challenge or loop diuretics. Preexisting renal insufficiency, with or without diabetes mellitus, increases the risk of CAN 6- to 10-fold but recovery is expected, with less than 10% of all patients requiring dialytic support. Despite the growing body of published reports, the lack of a suitable animal model to evaluate various proposed mechanisms of renal injury has compromised our ability to devise a technique for preventing CAN. A popular scheme has been proposed to describe the possible sequence by which ischemia or nephrotoxins, or both, induce acute renal failure. In particular, a vascular mechanism (i.e., ischemia), is an appealing explanation for CAN since acute changes in renal hemodynamics after contrast media injection have been confirmed by several animal experiments. Unlike other vascular beds in which contrast media induce acute vasoconstriction followed by vasodilatation, the initial effect on the renal circulation is acute vasodilatation, followed by progressive vasoconstriction, increasing renal vascular resistance and a concomitant decrease in both renal blood flow and glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental contrast-associated nephropathy and its clinical implications. 223 94

The effect of the calcium blocker S-(+)-methyl 4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitro-phenyl)thieno[2,3-b]pyridine- 5-carboxylate (S-312-d) on ischemic acute renal failure (ARF) was studied in rats. Ischemic ARF was induced by temporary (30-60 min) clamping of the left kidney 2 weeks after contralateral right nephrectomy. Plasma creatinine, creatinine clearance, urinary osmolality and fractional excretion of sodium were used to test the effectiveness of the drug. S-312-d (0.01-0.1 mg/kg b.wt. i.v.) administration before ischemia offered dose-dependent protection against the functional impairment induced by ischemia. This effect was accompanied by an increase in the survival rate of ischemic rats. S-312-d given after ischemia was not effective. The renal cortical edema induced by ischemia was significantly reduced by pretreatment with S-312-d. The increase in renal tissue calcium content observed after ischemia was also suppressed by S-312-d. Comparison with other established calcium blockers indicated S-312-d to be a good candidate for protection against ischemic ARF. These findings indicate that S-312-d may be clinically useful against renal ischemia.
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PMID:Protective effect of a novel calcium blocker, S-312-d, on ischemic acute renal failure in rat. 224 38


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