感染性休克左心室-动脉偶联关系变化的实验观察

Variations of left ventricular-arterial coupling in septic shock

目的探讨感染性休克左心室一动脉偶联关系的变化及机制。方法通过静脉注射内毒素建立感染性休克兔模型，随机分为2组，假手术组（s组，n=6），内毒素组（E组，n=6）；分别在0h点（手术完成后30min），2h点（注射内毒素或生理盐水后1h）和4h点（注射内毒素或生理盐水后3h），行超声检查及血流动力学监测，记录各血流动力学指标。结果E组2h点左心室收缩末弹性（Ees）低于0h点，（75．7±5．2）mmHg／ml比（90．8±7．2）mmHg／ml；4h点Ees低于2h点，（58．5±3．6）mmHg／ml比（75．7±5．2）mmHg／ml；差异均有统计学意义（均P〈0．05）。E组2h点和4h点左心室舒张末容积（LVDV）均小于0h点，（3．3±0．2）ml比（3．6±0．3）ml和（3．3±0．2）m1比（3．6±0．3）ml；4h点左心室顺应性（Ced）低于0h和2h点，（0．6±0．1）ml／mmHg比（0．7±0．1）ml／mmHg和（0．64-0．1）ml／mmHg比（0．8±0．1）mL／mmHg，差异均有统计学意义（均P〈0．05）。E组2h和4h点有效动脉弹性（Ea）均低于0h点，（41．4±2．9）mmHg／ml比（50．5±3．2）mmHg／ml和（40．1±2．7）比（50．5±3．2）mmHg／ml，差异均有统计学意义（均P〈0．05）。E组4h点Ea／Ees高于0h和2h点，（0．7±0．1）比（0．6±0．1）和（0．7±0．1）比（0．6±0．1），差异均有统计学意义（均P〈0．05）；Ea／Ees2h点与0h点差异无统计学意义，（0．6±0．1）比（0．6±0．1），P〉0．05。结论感染性休克代偿期左心室一动脉偶联关系无显著变化，感染休克失代偿期偶联不匹配，主要与心肌收缩功能相对心室后负荷降低更显著有关，可能与心脏舒张功能障碍有关。

Objective To explore the variations of left ventrieular-arterial coupling and elucidate its mechanisms in septic shock. Methods Septic shock rabbits were established by an intravenous injection of endotoxin. A total of 12 rabbits were divided randomly into sham operation group （S, n = 6） and endotoxin injection group （ E, n = 6）. Ultrasonic echoeardiography and hemodynamic monitoring were conducted at 0 h （30-rain post-operation） , 2 h （ 1-hour after endotoxin or saline injection） and 4 h （3-hour after endotoxin or saline injection） and the relative hemodynamie indices were recorded. Results （ 1 ） In E group, end- systolic elastanee （Ees） at 2 h was lower than that at 0 h（75.72 ±5. 16 vs 90. 77 ±7. 17 mm Hg/ml） and Ees at4 hwaslower than that at2 h （58.45 ±3.63 vs75.72±5.16 mm Hg/ml, P〈0.05）. （2） In E group, left ventrieular diastolic volume （LVDV） at 2 h and 4 h were both lower than that at 0 h （3.26 ± 0. 21 vs 3.58 ±0. 25 ml, 3.27 ±0. 19 vs 3.58 ±0. 25 ml）. And left ventricular end diastolic compliance （Ced） at 4 h were lower than that at 0 h and 2 h （0. 61 ±0. 05 vs 0. 74 ±0. 07 ml/mm Hg, 0. 61 _＋0. 05 vs 0.75±0.08 ml/mm Hg, P〈0.05）. （3） In E group, Ea at 2 h and 4 h was lower than that at 0 h （41.35 ±2. 87 vs 50.46 ±3.22 mm Hg/ml,40. 13 ±2. 68 vs 50. 46 ±3.22 mm Hg/ml, P 〈0. 05）. （4）In E group, Ea/Ees at 4 h was higher than that at 0 h and 4 h （0. 70 ±0. 07 vs 0. 57 ±0. 06, 0. 70 ±0. 07 vs 0. 56 ±0. 05, P 〈0. 05）. And Ea/Ees at 2 h had no significant difference with that at 0 h （0. 56 ±0. 05 vs 0. 57 ± 0. 06, P 〈 0. 05）. Conclusion During compensatory stage of septic shock, left ventricular-arterial coupling shows no significant variation. However, during decompensatory stage of septic shock, there is significant left ventricular-arterial decoupling. The main reason for decoupling lies in that the decrease of left myocardial contractility is more significant than that of left ventricular afterload. And ventricular diastolic dysfunction may also participate.