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作 者:严金川[1] 凌玲[1] 曹卫平 童加义[2] 刘乃丰[2]
机构地区:[1]镇江市第四人民医院 [2]南京铁道医学院,江苏南京210009
出 处:《中国病理生理杂志》2000年第7期615-618,共4页Chinese Journal of Pathophysiology
摘 要:目的 :从血流动力学及神经内分泌学两方面探讨左旋精氨酸 (L -Arg) -一氧化氮 (NO)通路对原发性高血压的影响。方法 :选择 2 4例高血压病人随机分为两组 ,一组静滴L -Arg ,一组静滴生理盐水 ,观察其血压、心率及心功能 ,同时检测血浆中NO、血管紧张素Ⅱ (AngⅡ )、内皮素 (ET)、血栓素A2 (TXA2 )以及前列环素(PGI2 )以探讨其降压机理。结果 :L -Arg治疗后 ,病人血压下降、心率增快 ,心输出量 (CO)、每搏输出量 (SV)、射血分数 (EF)增加 ,总外周阻力 (TPR)降低 ,血浆NO、PGI2 含量升高 ,ET、AngⅡ、TXA2 水平降低。静滴 80min时 ,随NO浓度降低CO、SV、EF也随之降低 ,而TPR又回升 ,血浆ET、AngⅡ发生相应变化 ,TXA2 、PGI2 无明显改变。结论 :L -Arg通过直接升高血浆NO水平引起血流动力学改变 ,通过间接反馈效应改变ET、AngⅡ水平 ,并可抑制血小板聚集。AIM and METHODS:To investigate the effect of L-arginine -nitric oxide pathway on patients with essential hypertension via hemodynamics and neuroendocrinology. 24 essential hypertension patients were randomly divided into two groups, group I was given L-Arg, and groups Ⅱ was given normal saline as control. Blood pressure, heart rate, heart funtion, nitric oxide, angiotensinⅡ, endothelin, thromboxane A 2 and prostacyline were measure in all patients. RESULTS: In group Ⅰ arterial pressure decreased, heart rate increased, cardial output, systolic volume and eject fraction increased, total peripheral resistance decreased. NO and PGI 2 levels were inceased. But at 80 min , with NO concentration decreased, SBP,DBP were increased, TPR, FT and AngⅡ were also increased. While HR, CO, SV and EF were decreased. However TXA 2 and PGI 2 showed not much change. CONCLUSION: Exogenous L-arginine produced a vasodilatory effect by increasing NO production ,caused the change of other hemodynamic function . It also indirectly changed plasma ET, AngⅡlevels by negative feed-back and suppressed the accumulation of platelet.
分 类 号:R544.102[医药卫生—心血管疾病]
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