Velasco I T, Rocha-e-Silva M
Divisão de Experimentaçaõ, Hospital das Clínicas, Universidade de São Paulo, Brasil.
Braz J Med Biol Res. 1989;22(2):237-9.
Hypertonic saline resuscitation (HR, 7.5% NaCl, 4 ml/kg) effectively reverts severe hemorrhage, but a central neural component is probably involved in the survival response. This experiment examines the role of central angiotensinergic pathways in hemorrhage-hypertonic resuscitation interaction. Severely bled (43 +/- 2 ml/kg) pentobarbital-anesthetized dogs with chronically implanted cerebral ventricular cannulae were resuscitated with 4 ml/kg 7.5% NaCl, iv 10 min after intracerebroventricular injection of 0.5 ml normal saline (CT), 150 micrograms saralasin (in 0.5 ml saline, SR), or 10 mg captopril (in 0.5 ml saline, CP). All 10 SR-treated dogs died 2-6 h after HR. Their arterial pressure and cardiac index initially recovered to near pre-hemorrhage levels, but gradually decreased thereafter, base excess remaining at severe metabolic acidosis levels throughout. All CT- and 8/10 CP-treated dogs survived indefinitely, with near normal arterial pressure, cardiac index and base excess levels. It is therefore concluded that the inhibition of central angiotensinergic sites with the competitive antagonist saralasin effectively prevents survival after HR, whereas inhibition of angiotensin converting enzyme by captopril in cerebrospinal fluid is virtually ineffective.
高渗盐水复苏（HR，7.5%氯化钠，4毫升/千克）能有效逆转严重出血，但生存反应可能涉及中枢神经成分。本实验研究中枢血管紧张素能通路在出血-高渗复苏相互作用中的作用。对戊巴比妥麻醉、严重失血（43±2毫升/千克）且长期植入脑室插管的犬，在脑室内注射0.5毫升生理盐水（CT组）、150微克沙拉新（溶于0.5毫升生理盐水，SR组）或10毫克卡托普利（溶于0.5毫升生理盐水，CP组）10分钟后，静脉注射4毫升/千克7.5%氯化钠进行复苏。所有接受SR治疗的10只犬在高渗盐水复苏后2至6小时死亡。它们的动脉压和心脏指数最初恢复到接近出血前水平，但随后逐渐下降，碱剩余在整个过程中一直处于严重代谢性酸中毒水平。所有CT组和8/10的CP组犬均长期存活，动脉压、心脏指数和碱剩余水平接近正常。因此得出结论，用竞争性拮抗剂沙拉新抑制中枢血管紧张素能位点可有效阻止高渗盐水复苏后的生存，而脑脊液中卡托普利对血管紧张素转换酶的抑制实际上无效。
