Song Qing, Wang Mingjun, Huang Xiaoming, Zhang Hong
Department of Anesthesia, General Hospital of People's Liberation Army, Beijing 100853, China.
Zhonghua Yi Xue Za Zhi. 2002 Sep 10;82(17):1203-6.
To investigate the protective efficacy of propofol against lung injury during hemorrhagic shock and resuscitation among Rhesus macaques.
Two healthy rhesus monkeys (Rhesus macaques) were killed and their lungs were taken out as samples of normal lung. Two healthy rhesus monkeys were made animal models of hemorrhagic shock and then were killed with their lungs taken out as samples of hemorrhagic shock lung. Another 12 healthy rhesus monkeys were randomly divided into two groups of six animals: propofol group (administered with propofol to a plasma concentration of 8 mg/L by target control infusion with computer before hemorrhagic shock) and control group. The monkeys were bled through the right femoral vein till the mean arterial pressure remained at the shock level of 40 mm Hg +/- 5 mm Hg. Two hours later, the total amount of bled blood and normal saline of the volume 2 times the volume of blood loss were reinfused into the animals quickly. Another 2 hours later hemodynamic parameters were measured, and blood samples were taken for measurement of malondialdehyde (MDA), superoxidedismutase (SOD) and lactate before bleeding, two hours after shock appeared, and 2 hours after resuscitation. The monkeys were killed 2 hours after resuscitation; their lungs were taken for pathologic examination and determination of water-to-dry weight ratio.
The lungs of the 2 normal rhesus monkeys were normal with the W/D of 5.545 +/- 0.191. There is not remarkable change in the lung constitution of the 2 shock rhesus monkeys with a W/D ratio of 5.655 +/- 0.474. The mean pulmonary arterial pressure (MPA) and pulmonary vascular resistance index (PVRI) of the control group 2 hours after hemorrhagic shock and 2 hours after resuscitation were 17.00 +/- 4.42 and 22.83 +/- 5.11 respectively, both significantly higher than those of the propofol group (10.83 +/- 2.71 and 18.66 +/- 3.38, both P < 0.05). The pulmonary vascular resistance index (PVRI) of the control group 2 hours after hemorrhagic shock and 2 hours after resuscitation were 458.67 +/- 91.92 and 260.17 +/- 57.85 respectively, both significantly higher than those of the propofol group (258.67 +/- 63.02 and 159.17 +/- 47.98 respectively, both P < 0.05). The W/D ratio of the control group 2 hours after resuscitation was significantly higher than that of the propofol group (P < 0.05). The pulmonary edema of the control group was more serious than that of the propofol group by light microscopy and electron microscopy.
Propofol remarkably relieves the lung injury occurring during hemorrhagic shock and resuscitation stage by ameliorating pulmonary circulation.
探讨丙泊酚对恒河猴失血性休克及复苏过程中肺损伤的保护作用。
处死2只健康恒河猴，取出其肺作为正常肺组织样本。将2只健康恒河猴制成失血性休克动物模型，然后处死并取出肺作为失血性休克肺组织样本。另外12只健康恒河猴随机分为两组，每组6只：丙泊酚组（在失血性休克前通过计算机靶控输注给予丙泊酚，使血浆浓度达到8mg/L）和对照组。通过右股静脉放血，直至平均动脉压维持在40mmHg±5mmHg的休克水平。2小时后，将放出的全血量及2倍失血量的生理盐水快速回输到动物体内。再过2小时后测量血流动力学参数，并在放血前、休克出现后2小时及复苏后2小时采集血样，测定丙二醛（MDA）、超氧化物歧化酶（SOD）和乳酸水平。复苏后2小时处死动物，取出肺组织进行病理检查并测定湿干重比。
2只正常恒河猴的肺组织正常，湿干重比为5.545±0.191。2只休克恒河猴的肺组织构成无明显变化，湿干重比为5.655±0.474。对照组在失血性休克后2小时及复苏后2小时的平均肺动脉压（MPA）和肺血管阻力指数（PVRI）分别为17.00±4.42和22.83±5.11，均显著高于丙泊酚组（10.83±2.71和18.66±3.38，P均<0.05）。对照组在失血性休克后2小时及复苏后2小时的肺血管阻力指数（PVRI）分别为458.67±91.92和260.17±57.85，均显著高于丙泊酚组（分别为258.67±63.02和159.17±47.98，P均<0.05）。复苏后2小时对照组的湿干重比显著高于丙泊酚组（P<0.05）。光镜和电镜下对照组的肺水肿比丙泊酚组更严重。
丙泊酚通过改善肺循环显著减轻失血性休克及复苏阶段发生的肺损伤。
