Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Naloxone HCl (Nx) improves cardiopulmonary performance, reverses cellular hypoxia, and stabilizes lysosomal membranes in shock states. However, no detailed study has yet explored its potential role in renal ischemia, which is inevitable in transplantation and surgical and nonsurgical conditions associated with hypotension and shock. This functional and microanatomical study was carried out on dogs subjected to renal warm ischemia with contralateral nephrectomy. Group I (control; N = 4) had bilateral renal dissection and right nephrectomy. Groups II-IV had their kidney pedicles cross-clamped for 60 min and then reperfused. Group II (N = 9) ischemic kidneys received no treatment. Group III (N = 6) kidneys were flushed with pure Nx HCl (2 mg/kg) during ischemia. Group IV (N = 6) dogs received one iv Nx bolus (2 mg/kg) before clamping and another dose before declamping. Biopsies for adenine nucleotides, histology, and ultrastructure were obtained before ischemia, before reflow, and 15 min and 7 days after reflow. Serum creatinine and blood urea nitrogen were measured daily. Ischemia induced significant renal dysfunction, which was reversed by systemic Nx. Nx offered a remarkable protection against postischemic structural damage. Seventy percent of Group II cortical sections showed grade 4 acute tubular necrosis (ATN), and severe residual damage after a week. Eighty-three percent of Group IV sections showed grade 1 ATN and no residual damage after a week. One week survival was 33% in Group II and 100% in Group IV. Nx can be useful in prevention of acute renal failure in clinical situations with arterial hypotension and shock.
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PMID:Naloxone in renal ischemia: a functional and microanatomical study. 358 32

Acute toxicity of ammonium metavanadate solutions in normal saline (pH 6.7) or 0.1 M Tris-HCl-NaCl buffers (pH 7.2 or pH 7.8) was studied in BALB/c mice at 20 mg V/kg. Animals receiving these solutions subcutaneously started to show severe clinical signs 10-15 min postinjection and high mortality rates (45-73%) during the first 3 d. Animals dying because of vanadium toxicity did so only within the first 3 d after injection. NH4VO3-treated animals showed a tendency to increase their liver and spleen weights as compared to those receiving control solutions. Severe necrosis in lymphoid tissues (thymus, spleen, lymph nodes, and Peyer's patch), pulmonary hemorrhage, and renal acute tubular necrosis were commonly demonstrated in vanadium-treated animals. Toxicity of NH4VO3 solution in 0.1 M Tris-HCl-NaCl buffer (pH 7.8) was greatly reduced upon acidification with HCl to pH 6.1 or following boiling for 15 min (final pH of 7.7). Acidification of the solution reduced the mortality rate to 20 from 68%; however, the clinical signs were still severe. Boiling of the solution reduced the mortality rate to zero and moderated the severity of the clinical signs.
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PMID:Acute toxicity of ammonium metavanadate in mice. 698 69