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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
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.
實驗的 急性 虛血性 腎不全에서 Ca^(++)-ATPase의 發現 樣相과 칼슘 길항제의 效果
신종인,김형규,홍순국 고려대학교 의과대학 1990 고려대 의대 잡지 Vol.27 No.1
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, a role of Ca^(++)-ATPase, one of the important intracellular calcium regulating machineries participating in the calcium ion translocation is unclear in ischemic ARF. The author evaluated the change of Ca^(++)-ATPase and influence of verapamil, well known calcium channel blocker, on Ca^(++) -ATPase before and after renal ischemia. The experimental animals, cats 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 ischemic ARF with verapamil and piroxicam pretreatment. The results were as follows. 1) Creatinine clearance before and after clamp were 10.79±1.79 and 2.09±1.70ml/ min/kg in group I , 3.41±1.56 and 0.12±0.05ml/min/kg in group Ⅱ and 6.8±5.6 and 0.8±0.7ml/min/kg in group Ⅲ, respectively. 2) Creatinine clearance decreased significantly in group Ⅱ, 96±2% compard with group Ⅰ 61±30 %. A reduction rate of creatinine clearance in group Ⅲ , 84±11 % was not different significantly from other groups. 3) A Ca^(++) - ATPase of renal tubular cell before clamp was almost negative. Luminal and posterobasal surface of proximal tubule showed slightly increased Ca^(++) - ATPase activities after clamp but the difference of location and activity of Ca^(++) - ATPase among each group was not significant. These results suggested that Ca^(++) - ATPase were activated after ischemia to compensate ischemic insults which resulted in a increased intracellular calcium. There were no benefits to protect renal function from ischemia and seems no effects on the location and activity of Ca^(++)- ATPase by systemic pretreatment of verapamil for ischemic ARF.