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T Kamiyama

Publications and source records attributed to T Kamiyama.

200 records · Page 12Linked to original sources

Effects of N-(2-mercaptopropionyl)-glycine on postischemic contractile function in ischemic/reperfused hearts. Dissociation of thiobarbiturate-reacting substance formation and contractile dysfunction.

The present study was undertaken to determine whether N-(2-mercaptopropionyl)-glycine, a membrane-permeable antioxidant agent, improves the ischemia/reperfusion-induced cardiac contractile dysfunction. Rat isolated hearts were subjected to a 35 min global ischemia, followed by a 60 min reperfusion. Ischemia/reperfusion did not result in the recovery of postischemic left ventricular developed pressure. Reperfusion markedly increased the content of the thiobarbiturate-reacting substance in the myocardium. Treatment of the perfused heart with 1 mM of N-(2-mercaptopropionyl)-glycine, either during a 30 min pre-ischemia or during a 30 min pre-ischemia and the first 10 min of reperfusion, resulted in an appreciable recovery of the postischemic left ventricular developed pressure and an attenuation of the increase in thiobarbiturate-reacting substance content. When hearts were treated with the same concentration of the agent only during the first 10 min of reperfusion, the cardiac contractile function was not improved during reperfusion despite the increase in thiobarbiturate-reacting substance content of the reperfused myocardium. These results suggest that the increase in thiobarbiturate-reacting substance content during reperfusion is independent of the postischemic contractile failure.

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Enhanced renal susceptibility to ischemia-reperfusion injury in the rat with obstructive jaundice.

BACKGROUND/AIMS: To investigate the susceptibility of kidneys to ischemia-reperfusion injury under obstructive jaundice. MATERIALS AND METHODS: Bile ducts of male rats were ligated for five days, right kidneys were removed, and vascular clamps were placed across left renal arteries for 30 minutes. RESULTS: Twenty-four hours later, ischemia-reperfusion produced renal injury in jaundiced rats as shown by increased serum creatinine and urea nitrogen levels. Histological observation showed tubular damages. These changes were minimal after ischemia-reperfusion in control rats. Renal thiobarbituric acid reactive substance contents were increased after bile duct ligation, which did not change after ischemia-reperfusion. On the other hand, ischemia-reperfusion produced a significant increase in renal thiobarbituric acid reactive substance contents in control rats. Renal glutathione contents were increased two fold after bile duct ligation and they were significantly decreased by ischemia-reperfusion. CONCLUSIONS: Kidneys in obstructive jaundice appear to be susceptible to ischemia-reperfusion injury. Although protective roles of GSH is suggested, the role of oxygen radicals in this type of renal injury remains to be further elucidated.

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