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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this investigation was to test the effects of glycine, a cytoprotectant in normothermic in vitro models of renal ischemia, in a model of hypothermic renal preservation injury. This study also probes possible physiological mechanisms of glycine protection during renal hypothermic ischemia-reperfusion injury. Canine kidneys were subjected to 48 h of hypothermic ischemia (4 degrees C) after intravascular flush with cold conventional Collins solution (G. H. Collins, M. B. Bravo-Shugarman, and P. I. Terasaki, Lancet 2: 1219-1223, 1969) and were subsequently revascularized for 1 h. After 1 h of reperfusion, glomerular filtration rate, urine production, and electrolyte excretion were dramatically higher when the Collins flush contained 5 mM glycine, compared with the 0 mM glycine controls. Renal tissue adenine nucleotides and glutathione levels progressively declined with graded cold ischemia times, and glycine had no effect on these levels. However, renal tissue ATP levels (but not glutathione) were significantly higher when kidneys were flushed with glycine, stored for 48 h, and reoxygenated in vitro for 1 h at 37 degrees C, compared with kidneys flushed without glycine. Analysis of CoA esters from ischemic renal tissue indicated altered production of only butyryl CoA after 48 and 72 h of cold ischemia, but no differences were detected in glycine or control kidneys. In conclusion, this study reports dramatic functional preservation with glycine in kidneys subjected to hypothermic ischemia and in vivo reperfusion. The mechanisms of these effects appear not to be attributable to the maintenance of cellular adenine nucleotide or glutathione levels nor to the scavenging of accumulated amphipathic acyl CoA esters.
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PMID:Protective effects of glycine during hypothermic renal ischemia-reperfusion injury. 195 15

We evaluated 1525 consecutive patients who had undergone thoracic or thoracoabdominal aortic surgery to ascertain the factors associated with the development of acute renal failure. Complete data were available in 1233 patients who were treated recently, and these were analyzed. Acute renal failure, severe enough to require dialysis, developed in 5.5% of this group (68/1233): 2.3% and 7%, respectively, for descending (9/391) and thoracoabdominal repairs (59/842). Of interest, on multivariate analysis, both renal artery endarterectomy for occlusive disease (p = 0.0006) and chronic dissection (p = 0.03) were associated with significantly less acute renal failure. On multivariate analysis, the significant independent predictors (p less than 0.05) of acute renal failure were preexistent renal dysfunction, evidence of diffuse atherosclerosis, the use of the pump bypass, and markers of hemodynamic instability. Contrary to earlier reports based on a smaller number of patients, we found that neither the use of pump bypass (7% acute renal failure), atriorenal bypass (8% acute renal failure), nor cold Ringer's lactate (3% acute renal failure) appeared to significantly avert the complication of acute renal failure. Indeed, pump bypass appeared to be deleterious (p = 0.0146) and perfusion with cold Ringer's lactate was not without risk. Furthermore, in a prospective evaluation of angiotensin converting enzyme blockers, we were unable to show that they afforded renal protection after transient renal ischemia. This study has clarified the clinical problems associated with acute renal failure and lays the foundation for future research.
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PMID:Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. 277 85

Acute tubular necrosis is a frequent occurrence following hypovolemic shock and human renal transplantation. Although this postischemic injury was originally thought to result from ischemia alone, it has recently been recognized that significant tissue injury can occur during the period of reperfusion. The demonstration of the oxygen free-radical-mediated postischemic reperfusion injury by Granger, Rutili, and McCord in ischemic cat intestine suggested that this mechanism might also be operative following renal ischemia. In the kidney, postischemic injury results in necrosis of the proximal renal tubule and accumulation of erythrocytes in the outer renal medulla. It has been proposed that the primary event leading to these pathologic changes is a free-radical-mediated injury to the endothelial cells in the inner stripe of the outer medulla. Experimental evidence in animals subjected to warm and cold ischemia supports a free-radical-mediated mechanism. The clinical significance of these findings is demonstrated in preclinical animal studies of renal transplantation in which approximately two-thirds of the injury following cold ischemia could be ablated by superoxide dismutase administered just prior to reperfusion or by allopurinol when administered both at the time of preservation and reperfusion or at the time of preservation alone.
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PMID:Free-radical-mediated postischemic reperfusion injury in the kidney. 329 86

To estimate the renal ischemia-protective effect of saralasin, model studies were performed on rats and dogs. Acute ischemic renal failure was induced in rats by clamping off the vascular pedicle for 90 minutes. When the drug was prophylactically administered before the ischemia episode, a premature increase in post-ischemic plasma urea level and a shortening of survival time of the animals were observed compared with the untreated control. Following auto-transplantation of 24-hour cold-stored dog kidneys, the infusion of saralasin failed to improve renal blood flow (MRBF), glomerular filtration rate (KrCl) and fractional sodium excretion (FENa). On the other hand, the angiotensin blockade with captopril led to an increase in MRBF which was associated, however, with significant decreases in KrCl and FENa. This discrepancy was suggested to be due to a predominant postglomerular vasodilation. The results show that the application of saralasin before renal ischemia may aggravate the loss of renal function whilst the post-ischemic administration of the drug has no substantial effect on the acute failure of transplanted kidneys.
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PMID:[Experimental studies on the modifiability of ischemic acute renal failure by saralasin]. 391 17

The aims of this study were (1) to investigate the effect of R 75231, a nucleoside transport inhibitor, on renin-angiotensin release after renal ischemia-reperfusion and (2) to establish a possible protective effect of this drug on renal function. We used a canine model for auto- transplantation of kidneys that had been subjected to 30 min of warm ischemia and subsequently to 24h of cold storage in HTK preservation solution, with immediate contralateral nephrectomy. R 75231 was injected intravenously into six dogs in two equal portions of 0.05 mg/kg both 30 min and 10 min before reanastomosis was established. Another six dogs were used as a control group. At 2 weeks post-transplantation, five out of six dogs in the R 75231 group and one out of six in the control group were still alive. Starting on day 4, serum creatinine was lower in the R 75231 group than in the control group (p < 0.005). In contrast to the control group, an inversion of the median preischemia adenosine/inosine ratio was observed in the R 75231 group after reperfusion (0.4 preischemia vs 4.0 after 60 min of reperfusion). Reperfusion of the graft resulted in an immediate increase in renin, angiotensin I, and angiotensin II venous blood levels in the control group. In the R 75231 group, renin, angiotension I, and angiotensin II levels were significantly lower. We conclude that administration of R 75231 before reperfusion has a protective effect on post-transplant function of kidneys that have been subjected to prolonged warm ischemia. This effect may, at least in part, be ascribed to inhibition of the breakdown and disposal of endogenous adenosine which, in turn, inhibits the excessive stimulation of the renin-angiotensin system in the early phase of reperfusion.
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PMID:Protection of canine renal grafts by renin-angiotensin inhibition through nucleoside transport blockade. 762 81

The present study was designed to determine whether beta-2 integrin-mediated leukocyte adherence to the endothelium is involved in renal ischemia-reperfusion damage and to evaluate the therapeutic intervention potency of monoclonal antibody (mAb) 6.5 E, directed against the leukocyte CD18 adhesion molecule. To answer these questions, we used a clinically relevant canine model for the autotransplantation of kidneys that had been subjected to 30 min of normothermic ischemia, followed by 24 h of cold storage preservation. Intravital fluorescence microscopy of capsular microvessels showed that substantial leukocyte adherence occurred after renal ischemia and reperfusion. Leukocyte adherence was observed in both arterioles and venules, but predominantly in the latter. Reperfusion of the graft resulted in a statistically significant reduction of the venular red blood cell velocity (RBCV). Moreover, the venular diameter increased. No significant changes in the arteriolar RBCV or in the arteriolar diameter were observed. Administration of mAb 6.5 E, 1 h before reperfusion, inhibited leukocyte adherence to the renal microvascular endothelium, resulting in an improved venular flow 2 h after reperfusion. However, we observed no beneficial effect of mAb 6.5 E pretreatment on post-transplant graft function and survival. We conclude that leukocyte adherence does not play a critical role in the development of renal injury following reperfusion of kidneys that have been subjected to prolonged warm and cold ischemia.
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PMID:Inhibition of CD18-dependent leukocyte adherence by mAb 6.5 E does not prevent ischemia-reperfusion injury as seen in grafted kidneys. 776 94

Tandem scanning confocal microscopy (TSCM) permits the noninvasive microscopic viewing of unstained, living, solid organs in real time. This article provides an overview of recent studies conducted by the author and other scientists, using TSCM and demonstrating its advantages in evaluating the histopathology of uriniferous tubules associated with normothermic renal ischemia, the nephrotic syndrome, and extracorporeal cold-storage preservation of kidneys.
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PMID:The histopathology of kidney uriniferous tubules as revealed by noninvasive confocal vital microscopy. 803 17

Experiments were conducted in anesthetized cats to determine if spinal neuronal responses to activation of renal receptors are tonically modulated by descending spinal pathways. Eighty-seven thoracolumbar spinal neurons with renal and somatic input were tested for responses to occlusion of the renal vein, renal artery, and ureter before, during, and after cooling the spinal cord rostral to the recording site. Cooling increased the number of neurons that responded as well as the magnitude of the responses to renal vein (RVO), renal artery (RAO), and ureteral occlusion (UO). RVO increased cell activity of 21 neurons from 12.5 +/- 2.7 to 31.7 +/- 6.0 spikes/s during cooling. UO increased cell activity of 24 neurons from 9.0 +/- 2.1 before cooling to 25.0 +/- 4.9 spikes/s during cooling. Cold block increased the magnitude of both types of responses to RAO that were due to mechanical deformation of the renal artery and prolonged renal ischemia. These data show that the majority of spinal neuronal responses to renal receptor stimulation are modulated by tonic inhibitory influences. Thus these results provide a mechanism by which the brain may control spinal circuitry that underlies reflexes of renal origin.
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PMID:Tonic descending modulation of spinal neuronal responses to activation of renal receptors. 828 69

The effects of hypothermic ischemia utilizing Euro-Collins flush on renal tissue long-chain activated fatty acid content was studied in dogs. Also, the ability of the simple amino acid glycine to complex these acyl thioesters was also investigated. Renal inner cortex was found to contain (in increasing amounts) myristoyl-, palmitoleoyl-, palmitoyl-, arachidonyl-, and oleoyl-coenzyme A throughout the 3 days of cold ischemia. Although the amounts of individual long-chain acyl-CoA compounds varied considerably, the concentrations were not found to differ significantly with increasing ischemia times. The presence of 5 mM of glycine in the flush also did not influence the amount or species of long-chain acyl-CoA esters in renal tissue during cold ischemia. Ischemic renal tissue content of most long-chain acyl-CoA compounds was reduced by about 50% when the tissue underwent in vitro reperfusion with 37 degrees C O2-saturated media. Glycine included in the flush storage solution did not alter acyl-CoA levels in tissue undergoing hypothermic ischemia and short-term in vitro reperfusion with O2-saturated buffer. In conclusion, long-chain acyl-CoA thioesters are present during hypothermic renal ischemia and the levels of most of these species are reduced during in vitro reperfusion after ischemia. The quality and production mass of these metabolites appears to be unaltered by progressive hypothermic ischemia times. Finally, the protective effects of glycine in this model of renal organ preservation injury are not associated with reductions of renal tissue long-chain activated fatty acids.
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PMID:Long-chain acyl-coenzyme A thioesters and renal hypothermic ischemic injury: effects of glycine flush. 844 Jan 27

Midaortic syndrome (MAS) is a well-recognized but rare cause of renovascular hypertension (RVH). Several techniques have been described to treat RVH caused by MAS. The authors recently treated two children with MAS and RVH. In both patients the right kidney had two renal arteries. A 13-year-old boy presented with severe headaches, pain in his lower extremities with exertion, and marked hypertension (blood pressure, 170/110). An aortogram demonstrated 70% narrowing of his abdominal aorta from the suprarenal region to 5 cm above the iliac bifurcation. There was significant stenosis of the celiac axis, superior mesenteric artery, and left renal artery. The right kidney had two renal arteries, and the upper pole artery was stenotic at its origin. A 10-year-old girl, known to have hypertension for several years had an aortogram that demonstrated 70% narrowing of the abdominal aorta from the suprarenal region to 3 cm above the iliac bifurcation. There was involvement of the left renal artery at its orifice. She also had two renal arteries to the right kidney with the right upper pole artery being stenotic at its origin and in the mid-portion of the vessel. Aortic reconstruction was accomplished with a polytetrafluoroehtylene (PTFE) bypass graft in each case. The first case also involved patch angioplasty of the celiac axis. In both cases, the right kidney was autotransplanted. It was removed intraoperatively, cold perfused, and the two renal arteries reconstructed followed by transplantation to the right iliac vessels. In both cases the left renal artery was reimplanted into the PTFE graft. Both patients had uncomplicated postoperative courses. The 13-year-old boy had evidence of renal ischemia in a portion of the lower pole of the autotransplanted kidney by DTPA scan. He has mild hypertension controlled with antihypertensive medication. The 10-year-old girl has a normal DTPA scan and is normotensive. MAS is a rare and challenging congenital vascular anomaly that causes RVH. In the presence of double renal arteries the technique of autotransplantation with cold perfusion and "bench" vascular reconstruction reduces the warm ischemia time and should produce satisfactory results.
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PMID:Renal autotransplantation for renovascular hypertension caused by midaortic syndrome. 904 31


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