[Protective effect of Shenmai injection on lung injury induced by cardiac pulmonary bypass].

Objective: To observe the protective effect of Shenmai Injection (SMI) on acute lung injury (ALI) induced by cardiac pulmonary bypass (CPB).

Methods: Thirty patients, scheduled to receive cardiac valve replacement by CPB for the first time, were equally randomized into 2 groups, the treated group and the control group. Cardiac valve replacement was performed under extracorporeal circulation after general anaesthesia. SMI 0.6 mL/kg was given to the treated group by adding in 250 mL physiological saline for intravenous dripping at the time between intubation under anaesthesia and CPB, while 250 mL physiological saline was given to the control group alone. Blood-gas analysis was performed with blood withdrawal from the radial artery to record PaO2, PaCO2, fraction of inspired oxygen (FiO2), by them the alveolar-arterial difference of partial oxygen pressure [P(A-a) DO2] was calculated, and the respiratory index (RI), the blood concentrations of soluble intercellular adhesion molelue-1 (sICAM-1), endothelin-1 (ET-1) and nitric oxide (NO) were measured at various time points, i.e. before anesthesia induction, 0.5 h, 2 h, 6 h and 24 h after ending CPB.

Results: All indices wer not significantly different between the two groups before operation (P > 0.05). After CPB, P(A-a) DO2 and RI were gradually elevated and reached the peak at 2 h after ending CPB, the increment in the treated group was lower than that in the control group (P < 0.05 or P < 0.01). Compared with the P(A-a) DO2 before anesthesia induction, P (A-a) DO2 at 0.5-24 h was statistically different (P < 0.05 or P < 0.01). Compared with the RI before anesthesia induction, RI at 2-24 h was statistically different (P < 0.05 or P < 0.01). Blood concentrations of sICAM-1 gradually raised after CPB, and reached the peak at 2 h after ending CPB, showed a higher level at 0.5-6 h after ending CPB as compared with that before anesthesia induction (P < 0.05 or P < 0.01). Blood ET-1 showed a figure of increasing as sICAM did (P < 0.05 or P < 0.01), and with a lower degree at 0.5-2 h after ending CPB in the treated group (P < 0. 01). Blood NO obviously reduced after CPB, it was lower at 0.5-24 h after ending CPB than at that before anesthesia induction (P < 0.01), and the decrement was lesser in the treated group (P < 0.05 or P < 0.01).

Conclusion: SMI can attenuate the acute lung injury after CPB by way of inhibiting vascular endothelial cell adhesion with inflammatory cells, antagonizing lipid peroxidation, and improving the ventilation and oxygenation function of lung.