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)

A 52-year-old male suffered from acute viral myocarditis with severe cardiogenic shock. On his admission, he underwent the inotropic and IABP supports, and subsequently was treated effectively by V-A bypass, which was continued for 35 hours. But he died in the period of 69 hours after V-A bypass from extended bowel necrosis and septic shock. The small and large intestinal mucosal necrosis, hemorrhagic hepatic necrosis and acute tubular necrosis were confirmed at necropsy. It is well known that the nonocclusive mesenteric vascular spasm is concerned strongly in their pathogenesis, after prolonged severe cardiogenic shock.
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PMID:[Nonocclusive intestinal necrosis after the successful veno-arterial bypass]. 195 43

The experiments were made to determine whether alpha-adrenergic blockade would reverse the vascular spasm in kidney grafts exposed to a warm ischaemia time of 30 min and 24 hr cold storage. Total vascular resistance per unit kidney mass, hematocrit, urinary flow, plasma and urine concentrations of creatinine, [Na+] and [K+], blood gases, renal O2 consumption and acid-base balance were studied in 21 anaesthetized dogs before and after kidney transplantation and administration of the blocking agent. Seven dogs were used to evaluate the effects of warm and cold ischemic stress on graft circulation and function without blockade (group 1). In the remaining dogs the blockade was induced by infusion of phentolamine (100 micrograms/kg/min) over 20 min. Controlled normal level of blood pressure was maintained throughout the experiments by infusion of 10% dextran 40 in saline (group 2) or by blood transfusion (group 3). Despite of interruption of neural pathways phentolamine induced a marked decrease in graft vascular resistance ranging from 89.2% +/- 5.9 (group 2) to 78.5% +/- 6.7 (group 3) in relation to the difference between the resistances before and after transplantation. In contrast, the decrease in vascular resistance of untreated grafts amounted only to 10.7% +/- 7.8 within a recirculation period of 4 1/2 hours. The increased renal blood flow following the blockade was associated with a considerable rise in urine flow and urinary excretion of creatinine, [Na+] and [K+] and a significant decrease in their plasma levels. The reduced O2 utilization by the grafts and the metabolic acidosis remained unchanged. These results indicate that phentolamine caused an effective suppression of vasoconstriction in kidney grafts exposed to warm ischemia and cold storage reflecting the intensive sympathetic activity under these conditions. Although the recovery of ischemic damaged tubular cells in this way was not acutely effected, the pharmacological enhancement of the cortical and medullary blood supply in the early posttransplant period may be helpful for overcoming the acute tubular necrosis and for preventing the development of hypertension due to the augmented release of vasodepressive medullary hormones.
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PMID:[Hemodynamic effects of an alpha-adrenergic blockade following experimental kidney transplantation]. 637 12

Pathological changes in the organs and tissues of beach-stranded, net-caught or captive small odontocete cetaceans (whales and dolphins) are reported. These changes include contraction band necrosis of cardiac and smooth muscles, smooth muscle spasm, ischemic injury to the intestinal mucosa (especially the mucosa of the small intestine) and acute tubular necrosis (ATN) of the proximal tubules of the nephron. Spastic contraction of terminal bronchiolar muscular sphincters was also observed. The changes are consistent with multi-systemic injury caused by massive release of endogenous catecholamines or vasospasm leading to ischemic injury, followed by reperfusion and reperfusion injury. The histopathological findings suggest that the reflex response of an odontocete to any major perceived threat (the "alarm reaction") is to activate the physiological adaptations to diving or escape to an extreme or pathological level, resulting, if greatly prolonged, in widespread ischemic injury to tissues. These observations may explain why these species die abruptly from handling or transportation and why the mortality of highly stressed beach-stranded animals is very high.
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PMID:Histopathology of the alarm reaction in small odontocetes. 1855 67

Reflex anuria (RA) was defined by Hull as cessation of urine output from both kidneys due to irritation or trauma to one kidney or its ureter, or severely painful stimuli to other organs. This is not a common concept among urologists or nephrologists even though it has been proposed for more than half a century. The phenomenon has not been thoroughly understood. But intrarenal arteriolar spasm and ureteral spasm have gained wide acceptance as the mechanisms of RA. The present review summarized papers published up to now on RA, in order to depict the general profile of the disease and to further elucidate the pathogenesis of RA. A classification system of RA was proposed as neurovascular reflex, ureterorenal reflex, radiated renovascular reflex, renoureteral reflex, ureteroureteral reflex and radiated ureteral reflex, based on the two assumed mechanisms and the stimulus' origins. All these types except renoureteral reflex had gained supporting evidence from animal experiments and/or clinical case reports. RA is a diagnosis of exclusion, only being considered after ruling out common and tangible etiologies such as ureteral calculi, acute tubular necrosis, renal vascular occlusion, hypovolemia, infection, etc. If the diagnosis has been established, treatment plan should be directed toward the mechanisms more than the causative factors. Abnormalities of the autonomic nerve system and congenital urogenital malformations incline people to RA. In summary, RA is a cessation of urine production caused by stimuli on kidney, ureter or other organs, through a mechanism of reflex spasm of intrarenal arterioles or ureters, leading to acute renal failure. It is a functional rather than parenchymal disease.
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PMID:Reflex anuria: an old concept with new evidence. 2397 16