丙泊酚对老年患者外周血淋巴细胞β1肾上腺素能受体脱敏的影响

Effect of propofol on desensitization of peripheral lymphocytic β1 adrenergic receptor in eldly patients

目的观察丙泊酚单次静脉给药对老年患者外周血淋巴细胞β1肾上腺素能受体脱敏的影响,探讨丙泊酚循环抑制机制。方法选择拟全麻下行择期手术治疗的老年患者30例,随机分为3组(n=10)。低剂量组(L组):丙泊酚1.0 mg/kg,高剂量组(H组):丙泊酚2.0 mg/kg,对照组(C组):生理盐水。全麻诱导前,静脉单次注药。给药前后3 min,记录SBP、DBP和HR变化,同时抽取外周静脉抗凝血各15 mL,Boyum法分离淋巴细胞,免疫印迹法分别检测总蛋白、胞膜和胞浆蛋白中的β1肾上腺素能受体表达,放免法检测异丙肾上腺素刺激的淋巴细胞内cAMP含量。结果与C组比较,L组和H组给药后均可引起SBP、DBP、淋巴细胞内cAMP含量及胞膜β1肾上腺素能受体蛋白水平降低(P<0.05或P<0.01),胞浆β1肾上腺素能受体蛋白水平增加(P<0.05或P<0.01);与L组比较,H组的指标变化明显(P<0.05)。组间两两比较,淋巴细胞总蛋白中β1肾上腺素能受体水平变化均无显著差别(P>0.05)。结论丙泊酚单次静脉给药可引起老年患者外周血淋巴细胞β1肾上腺素能受体脱敏,且呈剂量依赖性,与促进β1肾上腺素能受体由胞膜内化进入胞浆有关;β1肾上腺素能受体脱敏可能是丙泊酚的循环抑制机制之一。

Objective To evaluate the effect of propofol on the desensitization of peripheral lymphocytic β1 adrenergic receptor （ β1- AR） in eldly patients. Methods Thirty eldly patients were recruited and classified into three groups （n = 10） ： low dose group （group L）, high dose group （group H） and control group （group C）. 1.0 mg/kg propofol was given to group L, 2.0 mg/kg propofol was given to group H and normal saline was given to group C through intravenous injection. The systolic blood pressure （ SBP）, diastolic blood pressure （DBP） and heart rate （HR） before and after injection were recorded. The lymphocytes were isolated. The expressions of β1-AR in total protein, cytomembrane and cytoplasm were detected by western blot respectively. Isoproterenol-stimulated cAMP products in lymphocytes were measured by radioimmunoassay. Results SBP, DBP, cAMP product and β1-AR level in lymphocytic cytomembrane in group L and group H were lower than those in group C （P 〈 0. 05 ）. On the contrary, β1-AR protein level in lymphocytic cytoplasm in group L and group H was significantly higher than that in group C （ P 〈 0.05 ）. No significant differences in β1-AR level in total protein was detected between the three groups （P 〉 0.05）. Conclusion Intravenous injection of propofol to elderly patients can induce the desensitization of peripheral lymphocytic β1- AR in a dose-dependent manner. β1-adrenergic signal transduction in peripheral lymphocyte was decreased through internalizing β1-AR into cytoplasm and inhibiting cAMP production, which could be a contributory factor of cardiac vascular inhibition.