论文部分内容阅读
心房排钠肽(Atrial natriuretic peptide,ANP)存在于哺乳动物心房和心室,促进排钠和扩张血管,有时抑制肾素-血管紧张素-醛固酮轴,可使血管内液体转移至血管外。充血性心力衰竭患者,血浆ANP水平明显增加,可能属于一种代偿机理。目前已能合成ANP,供充血性心力衰竭患者临床应用,以降低心脏负荷、促进排钠。据证明,快速静注ANP50～200μg,使动脉压稍许下
Atrial natriuretic peptide (ANP) is present in the mammalian atria and ventricles and promotes the release of sodium and dilates blood vessels, sometimes inhibiting the renin-angiotensin-aldosterone axis, allowing the transvascular fluid to migrate extravascularly. Patients with congestive heart failure, plasma ANP levels increased significantly, may belong to a compensatory mechanism. ANP has been synthesized for clinical use in patients with congestive heart failure to reduce cardiac load and promote sodium efflux. It has been demonstrated that rapid intravenous injection of ANP50 ~ 200μg, arterial pressure slightly