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  • Title: [Effect of propofol on protecting Rhesus macaques from reperfusion lung injury during hemorrhagic shock and resuscitation].
    Author: Song Q, Wang M, Huang X, Zhang H.
    Journal: Zhonghua Yi Xue Za Zhi; 2002 Sep 10; 82(17):1203-6. PubMed ID: 12475411.
    Abstract:
    OBJECTIVE: To investigate the protective efficacy of propofol against lung injury during hemorrhagic shock and resuscitation among Rhesus macaques. METHODS: 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. RESULTS: 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. CONCLUSION: Propofol remarkably relieves the lung injury occurring during hemorrhagic shock and resuscitation stage by ameliorating pulmonary circulation.
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