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      • KCI등재후보

        실험적 급성 허혈성 (虛血性) 신부전 (腎不全)에서 Ca++ - ATPase 의 발현양상과 칼슘길항제의 효과

        신종인(Jong In Shin),변현주(Hyoun Ju Byoun),이규백(Kyu Baik Lee),최태승(Tae Seung Choe),조원용(Won Yong Cho),김형규(Hyoung Kyu Kim) 대한내과학회 1991 대한내과학회지 Vol.41 No.1

        N/A Calcium has been implicated as a primary pathogenetic mediator of cellular injury under conditions of oxygen and substrate deprivation in the kidney such as ischemic acute renal failure (ARF). However, the role of Ca++-ATPase in ischemic ARF, one of the important intracellular calcium regulation machineries participating in calcium ion translocation is unclear. The authors evaluated the changes of Ca+-ATPase before and after renal ischemia. The experimental animals, cats, were divided into 3 groups. Group I (n=6) was ischemic ARF model by renal artery clamp for 60 minutes, Group II (n=5) was ischemic ARF with a verapamil pretreatment (5 ㎍/kg/ min), systemically, and Group III (n = 7) was the same as Group II but with nonsteroidal antiinflammatory drug pretreatment. The results were as followings: 1) In Group I, creatinine clearance was 10.79±7.19 ml/min/kg before clamp and decreased to 2.09±1.70 ml/min/kg, and Group II, 3.41±1.56 to 0.12±0.05 ml/min/kg, and in Group III, 6.8±5.6 to 0.8±0.7ml/min/kg, respectively. 2) Creatinine clearance decreased significantly in Group II, 96±2% compared with Group I, 61±30%. A reduction of creatinine clearance in Group III was 84±11%, not different significantly from the other groups. 3) A Ca++-ATPase of renal tubular cell in the preischemic period was almost negative. The luminal and posterobasal surface of the proxima1 tubule showed slightly increased Ca++-ATPase activities in the postischemic period but the difference of location and activity of Ca++-ATPase among each group was not significant. These results suggested that Ca++-ATPase was activated after ischemia to compensate for ischemic insults resulting in increased intracellular calcium. There were no benefits to protecing renal function from ischemia and therefore no effects on the location and activity of Ca++-ATPase by systemic pretreatment of verapamil for ischemic ARF.

      • KCI등재후보

        실험적 급성 허혈성 신부전에서 칼슘 길항제의 투여가 신기능과 뇨 Prostaglandin E2 의 배설에 미치는 영향

        조원용(Won Yong Cho),권현민(Hyoun Min Kwon),변현주(Hyoun Ju Byoun),구자룡(Ja Ryong Gu),이규백(Kyu Back Lee),김형규(Hyoung Kyu Kim),노정우(Jung Woo Noh) 대한내과학회 1991 대한내과학회지 Vol.40 No.5

        N/A It has been proposed that calcium entry from the external medium increases intracellular free calcium to toxic levels during ischemic acute renal failure (ARF) thereby converting cellular injury from a potentially reversible to an irreversible state. Because verapamil impedes calcium entrance into cells via voltage-dependednt slow calcium channels, it has been suggested that this agent may block calcium entry into the kidney cells. This study was designed to determine whether systemic verapamil pretreatment protects renal function in experimental ischemic ARF in cats and whether verapamil influences prostaglandin, a compensatory system for an acute insult of kidney. For these purpose, creatinine clearance and urinary PGE2 were measured in 18 cats before and after ischemia. The experimental animals were divided into 3 groups. Group I (n=6) was ischemic ARF model by renal artery clamping for 60 minutes. Group II (n=5) was ischemic ARF with systemic verapamil pretreatment (5 μg/kg/min), and Group III (n=7) was the same as Group II with nonsteroidal antiinflammatory drug pretreatment (20 μg/kg/min). The results were as follows: 1) In Group I, creatinine clearance was 10.79±7.19 before clamping and decreased to 2.09±1.70ml/min/ kg, in Group II, 3.41±1.56 to 0.12±0.05ml/min/kg; and in Group III, 6.30±5.50 to 0.80±0.70ml/min/kg. 2) Creatinine clearance decreased significantly in Group II (96±2%) compared with Group I (61±30%). 3) Urine PGE2 in the preischemic period of Group I was 346±175, Group II; 159±102, Group III; 137±91 ng/ ml increased to Group I 355±114, Group II; 471±346, Group III; 355±114 ng/ml in postischemic period. Urine PGE2 excretion was relatively low in Group II and Group III, compared with Group I but not significant statistically. From these findings, it was suggested that systemic verapamil pretreatment exerts no protective effect to ischemic ARF and that it may compromise the compensatory mechanism of the prostaglandin system in ischemic ARF.

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