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本文对30例急性心肌梗塞(AMI)患者用随机分组法观察了卡托普利治疗前后外周血淋巴细胞β受体密度(Bmax)、平衡解离常数(Kd)、血浆去甲肾上腺素(NE)、血浆肾素活性(PRA)、血管紧张素Ⅱ(AⅡ)及醛固酮(Ald)的变化.结果显示:①AMI组Bmax较对照组明显下降,NE、PRA、AⅡ及Ald则明显升高(P<0.05);②心功能为NYHAⅢ～Ⅳ级的AMI患者,其Bmax较I～Ⅱ级者低,而 NE、PRA、AⅡ及Ald均较高(P<0.05);③治疗2周后,卡托普利组Bmax较非卡托普利组升高(p<0.05);PRA、AⅡ及Ald在治疗后1周时,卡托普利组较非卡托普利组下降(p<0.05);2周时,两组间无明显差异(P>0.05);NE在治疗后1周及2周时,两组间均无显著差异(P>0.05).表明:AMI时β受体出现下行调节,且与心功能损害程度有关,交感神经系统和肾素血管紧张素-醛固酮系统被激活.卡托普利可明显逆转β受体的下行调节.
In this study, 30 patients with acute myocardial infarction (AMI) were randomized to observe the effects of captopril on peripheral blood lymphocyte beta receptor density (Bmax), equilibrium dissociation constant (Kd), plasma norepinephrine (NE ), Plasma renin activity (PRA), angiotensin Ⅱ (AⅡ) and aldosterone (Ald) .The results showed that: (1) Bmax in AMI group was significantly lower than that in control group, but NE, PRA, AⅡ and Ald were significantly increased <0.05). ② The AMI patients with NYHA Ⅲ ~ Ⅳ cardiac function had lower Bmax than those with I ~ Ⅱ and NE, PRA, AⅡ and Ald (all P <0.05); ③ After 2 weeks of treatment, Captopril group was higher than non-captopril group (p <0.05); Captopril group was lower than non-Captopril group (p <0.05) at 1 week after treatment with PRA, AII and Ald, There was no significant difference between the two groups at 2 weeks (P> 0.05); NE at 1 week and 2 weeks after treatment showed no significant difference between the two groups (P> 0.05) Regulation, and the degree of cardiac dysfunction, the sympathetic nervous system and the renin-angiotensin-aldosterone system is activated.Captopril can reverse the β receptor down regulation.