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控制肝硬化门脉高压继发食管静脉曲张破裂出血仍有困难.外科门脉分流术死亡率高,且有肝性脑病等副反应,仅限用于经选择的病例.加压素能降低门脉压,但有严重的心血管副反应,且需胃肠道外给药.长期口服非选择性β阻滞剂能降低静脉压,但对其防止再出血的效果仍有争论,且此法可降低肝脏灌注,使血氨浓度增加,肝性脑病恶化.体内、外实验都证明能降低动脉压,但钙拮抗剂对门脉循环和门脉压的作用仍未明确.已知门脉及肝静脉小枝周围纤维组织主要由兼具平滑肌和成纤维细胞的细胞成分组成,它们在门脉高压发生中可能起重要作用.而且证实,钙能介导肌成纤维细胞收缩,而钙拮抗剂能诱导放松并取消收缩作用.
Control of cirrhotic patients with portal hypertension secondary to esophageal variceal bleeding is still difficult.Patients with surgical portal bypass shunt high mortality and hepatic encephalopathy and other side effects, only for the selected cases.Vasin can reduce the door Pulse pressure but with severe cardiovascular side effects and parenteral administration. Long-term oral non-selective beta-blockers reduce venous pressure, but there is still debate about their rebleeding effect Reduce liver perfusion, so that increased blood ammonia concentration, worsening of hepatic encephalopathy in vivo and in vitro experiments have shown that arterial pressure can be reduced, but the effect of calcium antagonists on portal circulation and portal pressure is still not clear.It is known portal and liver Fibrous tissue around the venous twigs is composed mainly of cellular constituents of both smooth muscle and fibroblasts that may play an important role in portal hypertension and confirms that calcium mediates myofibroblastic contraction whereas calcium antagonists induce Relax and cancel the contraction.