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作 者:袁媛[1] 张诗海[2] 姚尚龙[2] 王贤东[1] 王冬[1]
机构地区:[1]甘肃省人民医院麻醉科,兰州市730030 [2]华中科技大学同济医学院附属协和医院麻醉科
出 处:《中华麻醉学杂志》2008年第6期530-533,共4页Chinese Journal of Anesthesiology
基 金:国家自然科学基金资助项目(30271255)
摘 要:目的观察异丙酚对急性和慢性代谢性酸中毒大鼠红细胞内pH(pHi)的影响。方法Wistar大鼠,雌雄不拘。第一部分采用静脉输注HCl的方法制备急性代谢性酸中毒模型,模型制备成功的40只大鼠随机分为4组(n=10):10%脂肪乳10ml·kg^-1·h^-1组(F组)、碳酸酐酶(CA)抑制剂乙酰唑胺20mg·kg^-1·h^-1组(Z组)、异丙酚10mg·kg^-1·h^-1组(P1组)和异丙酚20mg·kg^-1·h^-1组(P2组)。第二部分采用管饲NH4Cl的方法制备慢性代谢性酸中毒模型,模型制备成功的40只大鼠随机分为4组(n=10),处理情况同第一部分。分别于给药前、给药1、3、6h时采集动脉血样,测定红细胞pHi、CA活性及钠氢交换体-1(NHE-1)活性。结果第一部分与F组比较,Z组CA活性降低(P〈0.05或0.01),P1组和B组pHi、CA活性及NHE-1活性差异无统计学意义(P〉0.05)。第二部分与F组比较,Z组、P1组和P2组pHi和CA活性降低(P〈0.05或0.01);与Z组比较,P1组和P2组phi和CA活性降低(P〈0.05或0.01),NHE-1活性差异无统计学意义(P〉0.05)。结论静脉输注异丙酚10、20mg·kg^-1·h^-1可导致慢性代谢性酸中毒大鼠红细胞pHi降低,其机制与抑制CA活性有关;而对急性代谢性酸中毒大鼠红细胞pHi无影响。Objective To investigate the effect of propofol on erythroeyte intraeellular pH (pHi) in rats with acute or chronic metabolic acidosis. Methods Adult Wistar rats of both sexes weighing 290-330 g were used in this study. In the first part, acute metabolic acidosis was induced by 0. 15 mol/L HCl (4 mmol/kg) infusion via tail vein for4 h and then forty rats were randomly divided into 4 groups (n = 10): eontrol group (F) 10% fat emulsion 10 ml·kg^-1·h^-1 , aeetazolamide 20 mg·kg^-1·h^-1 group (Z), propofol 10 mg·kg^-1·h^-1 group (P1) and propofol 20 rag" kg- l. h - 1 group ( P2 ). In the seeond part, ehronie metabolie aeidosis was indueed by drinking water containing NH4 Cl 0.28 mol/L (535 mg/kg) for 5 days and then forty rats were randomly divided into 4 groups ( n = 10) receiving the same drugs respeetively as that of the first part. Blood samples were taken from femoral artery immediately before and at 1, 3 and 6 h during drug administration for determination of carbonic anhydrase (CA) activity, pHi and sodium-hydrogen exchanger-1 (NHE-1) aetivity. Results In the first part, eompared with group F, CA aetivity was signifieantly deereased after drug administration in group Z (P 〈 0.05 or 0.01), while there was no significant differenee in pHi and CA and NHE-1 activity after drug administration in group P1 and P2 (P 〉 0.05). In the seeond part, pHi and CA aetivity were signifieantly decreased after drug administration in group Z, P1 and P2 than in group F (P 〈 0.05 or 0.01 ); pHi and CA activity were significantly decreased after drug administration in group PI and P2 than in group Z, while there was no significant difference in NHE-1 activity after drug administration between group Z, P1 and P2 ( P 〉 0.05 ). Conclusion pHi can be decreased by infusion of propofol at 10 and 20 mg·kg^-1·h^-1 in rats with chronic metabolic acidosis by inhibition of CA, but is not affected by propofol infusion in rats with acute metabolic acidosis.
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