Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 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 renal failure (ARF) remains a major clinical challenge, especially in the intensive care setting. Mortality of ARF combined with acute lung injury (ALI) is even higher and may reach 80%. Recent studies have suggested a remote effect of ARF on pulmonary homeostasis. However, it is unknown whether and to what extent ARF clinically affects pulmonary function, in particular oxygenation. For elucidation of the impact of ARF on aseptic ALI, a murine two-hit model that consists of acute uremia (AU) and subsequent ALI was developed. AU was induced by renal ischemia-reperfusion (inflammatory AU) or bilateral nephrectomy (noninflammatory AU). ALI was initiated by intratracheal HCl instillation and characterized by severe, PMN-dependent decrease in arterial partial pressure of O(2) (>70%) in nonuremic mice. Uremic mice, by contrast, showed a significant protection from ALI (decrease in arterial partial pressure of O(2) <40%); this was independent of the type of AU. Reconstitution experiments, in which uremic neutrophils were injected into nonuremic mice and vice versa, identified uremic neutrophils as the primary mediators. Between normal and uremic neutrophils, there were no differences in apoptosis or superoxide production. Pulmonary recruitment of uremic neutrophils, however, was significantly attenuated compared with that of normal neutrophils. This defect was associated with altered surface expression of L-selectin; sialyl Lewis(x), an L-selectin counterreceptor, previously was proved to be critical in aseptic ALI. In conclusion, it is shown that AU but not renal inflammation attenuates aseptic, neutrophil-dependent ALI and exerts an anti-inflammatory effect by attenuating pulmonary neutrophil recruitment.
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PMID:Acute uremia but not renal inflammation attenuates aseptic acute lung injury: a critical role for uremic neutrophils. 1703 12