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)

In order to investigate the role of the outer medulla in acute ischemic renal failure (Epstein FH, Balaban RS, Ross BD: Redox state of cytochrome aa3 in isolated perfused rat kidney. Am J Physiol 1982;243: F356-F363), the distribution of ATP in the in vivo porcine kidney and its relationship to Na transport and to ischemia was examined by using localized 31P magnetic resonance spectroscopy. Renal cortex (ATP) was higher than medulla. Reduction in Na transport produced by partial renal arterial occlusion ("hypofiltration"), resulted in a 13% increase in the ATP/Pi ratio of the whole kidney (from 2.61 +/- 0.26 to 2.96 +/- 0.27; P less than 0.03). This increase was accounted for by a statistically significant increase in (ATP) in the cortex, with medulla contributing to an insignificant extent. Further occlusion of the renal artery to reduce GFR to zero ("hypoperfusion") resulted in a 70% fall in ATP/Pi ratio. (ATP) was reduced most in the cortex, but pH fell equally in cortex and medulla. After release of arterial occlusion, cortical ATP recovered less completely than medulla ATP. Intracellular pH and Pi were restored in both cortex and medulla. It was concluded that cortex and medulla contribute equally to the pattern of disordered energy metabolism in acute renal failure. Sparing of ATP during hypofiltration may reflect the reduced energy requirements of active Na transport.
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PMID:Renal corticomedullary metabolite gradients during graded arterial occlusion: a localized 31P magnetic resonance spectroscopy study. 195 32

We have induced acute renal failure (ARF) in barbiturate anesthetized rabbits, through warm ischaemia of 30 or 60 min duration caused by transient bilateral occlusion of renal arteries. In this model we have monitored some renal performance parameters, before and 4 hours after reperfusion, aiming to characterize ARF in this animal species. Glomerular filtration rate (determined by the inulin clearance technique) was of 9.74 +/- 0.48 ml min-1 in 4 rabbits before injury and declined by 91% (60 min ischemia) during the first reperfusion hour. In 6 rabbits undergoing 30 min occlusion, pre-ARF values of 10.70 +/- 0.98 ml min-1 declined by 47%. In both groups no recovery was observed in the following hours. Tubular enzymes (alanine-amino-peptidase, AAP and N-acetyl-beta-glucosaminidase, NAG) were released into urines before injury at the rate of 1.11 +/- 0.18 and 1.32 +/- 0.41 mU min-1, respectively, in the 30 min model (3 animals/group). During ARF, maximal AAP output was five-fold increased (5.83 +/- 0.35 mU min-1), whereas NAG was unmodified. On the other hand, renal haemodynamics in 5 rabbits did not change after the ischaemic procedure: total renal blood flow (44 +/- 5 ml min-1) and renal vascular resistances (225 +/- 26 Pa ml-min) displayed less than 10% variations throughout the reperfusion period. We concluded that ARF in rabbits can be reliably and reproducibly monitored and that the pathogenesis of the disease, in our situation, is attributable mainly to tubular cell damage and not to impairment of the vascular component of renal performance.
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PMID:[Parameters of tubulo-glomerular function in anesthetized rabbits with acute kidney insufficiency]. 197 49

The purpose of this study was to better characterize renal adenine nucleotide pool responses to different forms of shock, contrast the changes to those found in other intra-abdominal organs (the liver and small intestine), and assess whether these changes are closely mimicked by those produced by renal arterial occlusion, the usual method used to study ischemic acute renal failure. Rats were subjected to hemorrhagic shock, septic shock, or cardiopulmonary shock of varying severities and durations. The liver consistently had the greatest energy depletion, followed by the kidney, and then the small intestine. However, only the kidney developed clear morphological damage (S3 brush border sloughing). Kidney adenylate pools were better preserved during septic shock and cardiopulmonary shock than during hemorrhagic shock despite comparable blood pressures. Only profound hemorrhagic shock (35-40 mm Hg for 25 minutes) decreased total adenylate pools (ATP + ADP + AMP). However, the degree of renal catabolite (nucleosides plus purine base) accumulation did not correlate with the amount of renal total adenine nucleotide depletion, partially because circulating catabolites contributed to intrarenal catabolite pools. Purine base/uric acid ratios differed among shocked organs, consistent with different degrees of xanthine oxidase activity (small intestine greater than liver greater than kidney). Renal morphological damage decreased during the immediate (0-30 minutes) postshock period, and the extent of this improvement was not altered by xanthine oxidase inhibition (oxypurinol), suggesting that the immediate postshock period is not one of serious oxidative injury. Shock, in comparison with renal arterial occlusion, caused only modest ATP loss/catabolite accumulation, very low purine base/uric acid ratios, and no immediate-reperfusion (0-30 minutes) resynthesis of the total adenylate pool. Thus, ischemia-induced renal adenylate changes may differ considerably, depending on the nature of the ischemic event.
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PMID:Adenine nucleotide changes in kidney, liver, and small intestine during different forms of ischemic injury. 198 61

A forty-two years old male underwent an aortic arch replacement for an emergency treatment of dissecting aortic aneurysm (DeBakey type I). Separate cardiopulmonary bypass was used with main arterial inflow cannula inserted to right femoral artery. After the operation, ischemia of the right lower extremity led to acute renal failure due to myonephropathic-metabolic syndrome. Peritoneal dialysis, hemodialysis, and continuous arterio-venous hemofiltration were performed. Renal failure improved gradually. At the diuretic phase serum calcium concentration began to rise. Inspite of large amount of fluid and furosemide injection it became higher and finally reached to 20 mg/dl level. Calcitonin injection (320 mu/day) was very effective. In 2 months after surgery serum creatinine and calcium concentrations went down to normal range. Abnormalities in calcium metabolism are frequent in rhabdomyolysis-induced acute renal failure. However, it is rare to encounter such a remarkable hypercalcemia as seen in this patient. When treating MNMS we should pay attention to the changes of serum calcium concentration.
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PMID:[Dissecting aortic aneurysm associated with myonephropathic-metabolic syndrome and hypercalcemia]. 202 21

12 patients underwent resection of a thoraco-abdominal aortic aneurysm. There were 10 men and 2 women, ranging in age from 54-78 years (mean 65). Aortic arteriosclerosis was the primary etiology in 11, and Behcet's disease in the other 1. Most patients (7/12) presented with Type 3 aneurysm, extending from the distal descending thoracic aorta to the distal abdominal aorta; none had aortic dissection. 11 were operated on for symptoms related to the aneurysm: 3 of these had a contained rupture. The risk factors were chronic obstructive pulmonary disease in 10, hypertension (10), diffuse arteriosclerosis (8), ischemic heart disease (6), chronic renal failure (5) and cerebrovascular accident (1). The surgical technique in 11 was graft inclusion and visceral vessel reattachment. The main complication was acute renal failure, seen in 3 patients. None had spinal ischemia. Operative mortality was 33%. Of the 4 who died, 2 had myocardial infarction and 2 uncontrolled intraoperative bleeding. According to the literature the major complications are spinal cord ischemia and renal failure.
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PMID:[Surgery for thoraco-abdominal aortic aneurysm]. 206 16

The effect of treatment of rats with ginsenosides (extracted from Panax ginseng) on transport of p-aminohippurate (PAH) in renal cortical slices was studied for an in vitro reflection of PAH secretion in the proximal tubules in the kidney. The treatment of rats with ginsenosides stimulated PAH accumulation in the slices and tended to prevent the decrease in PAH accumulation in incubated slices from the rats with acute renal failure caused by cisplatin or ischemia followed by reperfusion. Ginsenoside treatment affected other biochemical responses in renal cortical slices, with a decrease in adenosine triphosphate level and an increase in potassium level. The latter may lead to the stimulation of PAH transport in the slices, but additional information on the cellular action of ginsenosides is needed for this conclusion. It may be that the stimulatory effect of ginsenosides on PAH accumulation in the slices counterbalances the decrease in PAH accumulation in the slices from rats with acute renal failure.
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PMID:Stimulation of p-aminohippurate transport in renal cortical slices prepared from rats treated with ginsenosides. 207 46

The acute occlusion of the popliteal artery involves: 1. A regional disease: muscular ischaemia with an increase of capillary permeability and oedema. The recovery of the circulation brings with it the formation of free radicals. 2. Sometimes, a general and metabolic illness complicates the muscular ischaemia. It associates to varying degrees: hypovolemic shock, metabolic troubles, acute renal failure, disseminated intravascular coagulation, infection. It can compromise the vital prognosis. The reanimation which completes the surgical treatment includes two stages: 1. The prehospital stage when the first imperative is to commit the patient to the vascular surgeon's care as soon as possible and in the best hemodynamic conditions. 2. The hospital stage when the therapeutic objectives are represented by: a) the treatment of hypovolemia; b) the curing of acute renal failure (bicarbonates 2 mmol.kg-1, hypertonic mannitol 1 g.kg-1; c) fight against infection; d) Heparin: 1 to 2 mg.kg-1 (if there is no counterindication); e) hyperbaric oxygen treatment in some situations. Despite the progress of reanimation, the initially intended amputation is subject to discussion in the following circumstances: crushing which in fact accomplishes an amputation, prolonged and complete ischemia lasting more than 10 to 12 hours, severe I.V.D.C., associated serious lesions (cranial traumatism, pelvis crushing).
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PMID:[The physiopathology and medical treatment of acute traumatic occlusion of the popliteal artery. The point of view of the anesthesiologist-resuscitator]. 220 22

The concentration of 18 alpha-amino acids (AAs) in plasma and renal cortical cell water were measured 3 or 24 hr after 1 hr of unilateral renal artery clamping or 24 or 48 hr after 15 mg/kg body weight HgCl2 injection sc as a test of epithelial integrity. Cellular glycine (Gly), hydroxyproline (Hpr), ornithine (Orn), phenylalanine (Phe), serine (Ser), and tryptophan (Trp) concentrations were depressed 24 hr after HgCl2 (p less than 0.05), but the remaining 12 AAs were not distinguishable from control despite the presence of severe renal failure. ARginine (Arg), glutamic acid (Glu), and valine (Val) also were decreased (P less than 0.05) 24 hr later, but concentrations of half of all measured AAs were still normal. Cellular alanine (Ala), Arg, Glu, Gly, Phe, and Ser concentrations were decreased 3 hr after ischemia, p less than 0.05, but 12 AAs were unchanged and only Arg, Phe, Ser, and threonine (Thr) were reduced 24 hr after ischemia was reversed. Concentrations of even the most affected AAs remained notably higher than in plasma in both forms of acute renal failure (ARF). Total loss of AAs from a small proportion of tubular cells would be hidden by essentially normal concentrations in the rest, and such losses may well have occurred. Unless cellular AAs in ARF are almost completely bound, however, the well-maintained cell:plasma AA concentration ratios indicate that cellular energetics were adequate for AA uptake and that epithelial permeability to AAs in the vast majority of cells was not greatly disturbed. Such findings suggest that most of the epithelium, although seriously damaged, had remained viable.
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PMID:Renal epithelial amino acid concentrations in mercury-induced and postischemic acute renal failure. 221 14

Trapping of red blood cells (RBCs) in renal medulla vasculature in postischemic acute renal failure (ARF) was found to depend upon the length of the ischemic period. Thus trapping occurred after 45 minutes but not 25 minutes of ischemia. By prior hemodilution to a hematocrit (hct) of 30%, RBC trapping after 45 minutes of ischemia could be completely prevented. Likewise hemo-concentration (hct = 60%) before 25 minutes of ischemia resulted in extensive RBC trapping. By increasing or decreasing the hct, the contribution of RBC trapping to the functional defects and decrease in renal blood flow that follows minor (25 min) and more substantial (45 min) ischemia was investigated. Renal blood flow (RBF) was measured by microspheres, and vascular and tubular pressure by the micropuncture technique. Glomerular filtration rate (GFR) was estimated from inulin clearance, and tubular function from urine osmolality and sodium and potassium excretion. It was found that postischemic RBF was not correlated to RBC trapping but depended on the length of ischemia. After both 25 and 45 minutes of ischemia tubular obstructions occurred in the proximal tubules and/or loops of Henle, causing an increase in proximal tubular pressure. These obstructions were dependent on the length of ischemia but not on RBC trapping. After hemoconcentration and 25 minutes of ischemia there was an increment in distal tubular pressure, indicating that abundant RBC trapping may contribute to an increase in tubular pressure by compression of medullary tubules and thereby reduce GFR. When the damage was more severe other factors came into play and the contribution of RBC trapping to the decrease in GFR was minimal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephron function in the early phase of ischemic renal failure. Significance of erythrocyte trapping. 223 85

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


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