室间隔缺损合并重度肺动脉高压患者围术期肺损伤的临床研究

目的　探讨室间隔缺损合并重度肺动脉高压患者围术期肺损伤的发生机制。方法　对31例先心病室间隔缺损直视修补术患者分组 (非肺动脉高压 16例 ,重度肺动脉高压 15例 )进行临床研究 ,在麻醉后 (AA) ,体外循环停止 (OEC) ,体外循环后 1h(PEC1)、6h(PEC6 )、2 4h(PEC2 4 )、4 8h(PEC4 8)、72h(PEC72 )对血栓素B2 (TXB2 )和 6 酮 前列腺素F1α(6 keto PGF1α)、丙二醛 (MDA)、IL 6、IL 8的变化进行研究 ,并结合体外循环前、后肺病理改变对肺损伤程度进行分析。结果　重度肺高压组 6 keto PGF1α与TXB2 的比值 (P/T)在OEC时下降至最低 ,于PECl时丙二醛 (MDA) (7 3μmol/L± 0 9μmol/L)和IL 6 (0 5 0ng/L± 0 19ng/L)达到最高峰 ,在PEC6时IL 8(183ng/L± 6 3ng/L)明显增高。肺动脉压在PECl～PEC6时变化最大。TXB2 与全肺阻力呈正相关性 (γ =0 2 83,P <0 0 5 ) ,呼吸指数(RI)与全肺阻力呈正相关性 (γ =0 4 0 3,P <0 0 5 ) ,RI与MDA呈正相关性 (γ =0 .5 90 8,P <0 0 5 )。体外循环后肺病理改变有明显的血管内皮细胞脱落、炎症细胞浸润、肺血管的白细胞栓塞和肺泡上皮细胞的脱落及肺泡内出血。结论　室间隔缺损合并重度肺动脉高压患者体液因素变化及肺病理改变是引起围术期严重肺损伤的机制之一

Perioperative lung injury in ventricular septal defect with severe pulmonary hypertension,a clinical study of 31 cases

OBJECTIVE: To investigate the mechanism of perioperative lung injury in patients of ventricular septal defect (VSD) with severe pulmonary hypertension. METHOD: The thromboxane B(2) (TXB(2)), 6-keto-prostagladin F(1 alpha) (6-keto-PGF(1 alpha)), malonyldiadehyde (MDA), interleukin-6 (IL-6), and IL-8, and blood pressure, pulmonary arterial pressure (PAP) and total pulmonary pressure (TPR) in thirty-one patients of VSD, 16 cases without pulmonary hypertension and 15 cases with severe pulmonary hypertension, were examined after anesthesia (AA), over extracorporeal circulation (OEC), and 1 hour (PEC1), 6 hours (PEC6), 24 hours (PEC24), 48 hours (PEC48), and 72 hours (PEC72) post extracorporeal circulation. The respiratory index (RI) and ratio of 6-keto-PGF(1alpha) and TXB(2) (P/T) were calculated. Before and after extracorporeal circulation, pulmonary tissues were taken to be examined by light microscopy and electron microscopy. RESULT: In the cases with severe pulmonary hypertension the P/T was 0.81 +/- 0.26 after anesthesia, then decreased 0.65 +/- 0.28 over extracorporeal circulation, and reached its lowest value (0.51 +/- 0.32) 1 hour post extracorporeal circulation. MDA was 2.4 micromol/L +/- 0.6 micromol/L after anesthesia, then increased, was 7.0 micromol/L +/- 1.7 micromol/L OEC, and reached its peak value (7.3 micromol/L +/- 0.9 micromol/L) PEC1. IL-6 was 0.27 ng/L +/- 0.12 ng/L after anesthesia, then increased, and reached its peak value (0.50 ng/L +/- 0.19 ng/L) PEC1. IL-8 was 7.5 ng/L +/- 1.5 ng/L after anesthesia, then increased, was 152 ng/L +/- 50 ng/L PEC1, and reached its peak (183 ng/L +/- 63 ng/L) PEC6. TXB(2) was 251 ng/L +/- 44 ng/L after anesthesia, then increased, and reached its peak (967 ng/L +/- 145 ng/L) at PEC1. The PAP was 72.1 +/- 18.8 mm Hg after anesthesia, 55 mm Hg +/- 15.3 mm Hg OPC, and 7.4 +/- 2.1 at PEC1, then decreased, and was 53 mm Hg +/- 15 mm Hg at PEC72. The total pulmonary resistance (TPR) was 10.6 +/- 2.9 mm Hg x min(-1) x L(-1) after anesthesia, then increased, and reached its peak (15.0 +/- 3.9 mm Hg x min(-1) x L(-1) at PEC6. Respiratory index (RI) was 0.88 +/- 0.23, then increased, and reached its peak (2.35 +/- 0.72) at PEC6. TXB(2) and RI were positively correlated with pulmonary vascular resistance (gamma = 0.283, P < 0.05; gamma = 0.403, P < 0.05). RI was positively correlated with MDA (gamma = 0.403, P < 0.05). Morphologic studies revealed discontinuities in the endothelial cell lining of pulmonary capillaries, infiltration of inflammatory cells, plugging of pulmonary capillaries with neutrophils, and intraalveolar hemorrhage. CONCLUSION: During the perioperative period, the pulmonary damage, which leads to pulmonary hypertensive crisis, is more severe among the cases of VSD with severe pulmonary hypertension than among the case without pulmonary hypertension.