高渗盐水治疗犬严重失血性休克时血浆中血管紧张素Ⅱ/心钠素的变化

Changes of serum angiotensin Ⅱ /atrial natriuretic peptide in severe hemorrhagic shock dogs treated with hypertonic saline/dextran

本研究采用特异性的放免法测定 ７． ５％氯化钠／４． ２％右旋糖酐 ４０（ＨＳＤ）和 ０． ９％乳酸钠林格氏液（ＬＲ）治疗犬严重失血性休克前后血浆中血管紧张素 Ⅱ（ＡＧＴⅡ）和心钠素（ＡＮＰ）含量的变化，发现ＨＳＤ较ＬＲ能在快速提高平均动脉压（ＭＡＰ）的同时迅速恢复ＡＧＴⅡ／ＡＮＰ的平衡，及早地解除微血管痉挛，缩短缺血时间，减轻缺血再灌注损伤。本实验提示：ＨＳＤ快速恢复内源性损伤和抗损伤物质的平衡，可能是其抗休克的主要机制，而且高浓度Ｎａ＋刺激肾小管致密斑，抑制肾素分泌可能是ＨＳＤ抗休克的基本因素。

Twelve mongrel dogs, anesthetized with pento-barbital, were bled to a main atrial pressure (MAP) of 40 mmHg within 30 minutes and kept at this level for 30 minutes, then the changes of serum angiotensin Ⅱ (AGTⅡ ) /atrial natriuretic peptide (ANP) were observed before and after treatment with 7.5% NaCl/ 4. 2% dextran 40 (HSD) and lactate sodium ringer (LR). The results showed that AGT Ⅱ /ANP increased significantly during shock (from 72. 71 ± 18. 54 to 479. 31 ± 126. 25 n= 6 P<0. 001), and AGTⅡ /ANP was out of balance. At the begining of resuscitation, HSD elevated MAP rapidly,and produced a rapid dramatic reduction in AGTⅡ (479. 31 = 126. 25 vs 66. 13±22. 13 n＝6 P<0.001), and AGT Ⅱ / ANP also deccreased significantly at one hour after resuscitation compared with LR (P < 0. 05). The experiment showed that HSD can relieve microvascular spasm in time, improve microcirculation, shorten ischemia/reperfusion injury. The main mechaism is probably that HSD can rapidly recover the balance of endogenous injury and antiinjury factor, moreover, it is an essential element that high concentration of Na+ stimulates the macula densa, inhibiting renin secrete.