大鼠脓毒性休克时肝α_1-肾上腺素能受体的变化及其机制  

Studies on Changes and its Mechanisms of Hepatocellular Sarcolemmal α1 -AR during Rat Septic Shock

作　　者：杨和平[1] 高爱国 董林旺[1] 常英姿[1] 吴立玲[1] 唐朝枢[1] 

机构地区：[1]北京医科大学心血管基础研究所休克研究室

出　　处：《基础医学与临床》1997年第2期108-114,共7页Basic and Clinical Medicine

摘　　要：在结扎和刺穿盲肠诱导的大鼠脓毒性休克模型上，发现休克大鼠发生两种代谢变化：早期（９ｈ）高代谢（高血糖）和晚期（１８ｈ）低代谢（低血搪）。３Ｈ－哌唑结合试验显示：早期脓毒性休克时，肝细胞质膜α_１－肾上腺素能受体〔α_１－ＡＲ）最大结合容量增加３５％。晚期休克时下降３０％。Ｎｏｒｔｈｅｒｎｂｌｏｔｔｉｎｇ、核ｒｕｎｏｆｆ测定显示：早期脓毒性休克大鼠α_１ｂ－肾上腺素能受体（α_１ｂ－ＡＲ）ｍＲＮＡ转录水平比对照组增加３４．７％，其ｍＲＮＡ合成相对比率增加５１．３％；晚期脓毒性休克大鼠α_１－ＡＲｍＲＮＡ转录水平比对照组降低２８．１％，其ｍＲＮＡ合成相对比率减少２４．９％，而ｍＲＮＡ半衰期无明显改变。提示脓毒性休克时α_１－ＡＲ的上调和下调的时相性变化也发生于转录水平。On the rat septic shock model induced by cecum ligation and puncture ,we found that there exists two types of metabolic changes , high and low metabolism ( high and low blood glucose ) during earlier ( ES , 9h ) and later stage (LS , 18h ) during septic shock process. 3H-prazosin binding ( Vmax ) of hepatocellular sarcolemmal α1-AR increased 3 5% and decreased 3 0% during ES and LS respectively. During ES , transcription level of α1-AR mRNA increased 3 4. 7% , relative rates of the mRNA synthesis increased 51.3% , while the α1-AR mRNA halflife did not change compared with control. The above data suggest that phasic changes of α1-AR up and down regulation were paralled with transcription level during septic shock. The changes of hepatocellular sarcolemmal ,α1 -AR may be one of the important mechanisins of glucose metabolec disturbance during septic shock.

关 键 词：脓毒性休克 肝脏 肾上腺素能受体 受体 基因表达 

分 类 号：R631.402[医药卫生—外科学]