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机构地区:[1]军事医学科学院基础医学研究所,北京100850
出 处:《生理学报》1992年第1期39-44,共6页Acta Physiologica Sinica
基 金:国家自然科学基金
摘 要:本文观察了热应激对大鼠肺组织细胞膜中β-受体Bmax,磷脂酶A_2(PLA_2)活性,磷脂酰胆碱(PC),磷脂酰丝氨酸(PS)含量的影响及膜流动性的改变。测得正常大鼠肺中β-受体的B_(max),PLA_2活性,PC和PS值分别为479±94fmol/mg蛋白,78.5±8.2U,53.5±9.7mg/g湿重和425.1±68.1μg/g湿重;在热应激使肛温达42℃并持续15min时,β-受体B_(max)减少43%;PLA_2活性增加83%,PC和PS分别减少50%和47%;测流动性结果表明,热应激使红细胞和肺组织细胞膜流动性都明显减弱。作者认为这些变化之间的关系是:β-受体B_(max)的减少可能是热应激时激活了肺组织细胞膜中的PLA_2,加速了PC和PS等的分解代谢,使膜液晶态改变的结果。To explore the relationship between the change of β-adrenoceptor and themetabolism of phospholipids in lung tissue from acute heat stressed rats, the B_(max)of β-adrenoceptors, the activity of phospholipase A_2 (PLA_2), the content ofphosphatidylcholine (PC) and phosphatidylserine (PS), and membrane fluidityin lung tissue of normal and heatstressed rats. were investigated. The relevantparameter values mentioned above were 479±94 fmol / mg protein, 78.5±8.2U, 53.5±1.7 mg /g· wet. w. and 425.1±68.1 μg/g·wet. w. respectively. Wher-eas in the hear stressed rats with rectal temperature raised to 42℃ for 15 min, theB_(max) of β-adrenoceptor was decreased by 43% (P<0.01), the activity of PLA_2increased by 83% (P<0.01), the contents of PC and PS decreased by 50% and47%(P<0.01) respectively. A lower membrane fluidity in lung tissue for heatstressed rats was also demonstrated. The results suggest that the decreased binding sites of β-adrenoceptor in lungtissue of rat during hyperthermia may be contributed to the activation of PLA_2,which then accelerated the catabolism of phospholipids such as PC and PS in thecell plasma membrane, with a consequent alteration of membrane fluidity
分 类 号:R329.25[医药卫生—人体解剖和组织胚胎学]
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