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Ann Thorac Surg 1998;65:719-723
© 1998 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Granulocyte Elastase Release and Pulmonary Hemodynamics in Patients With Atrial Septal Defect

First Department of Surgery, Yamaguchi University School of Medicine, Yamaguchi, Japan

Accepted for publication September 15, 1997.

Dr Gohra, First Department of Surgery, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi 755, Japan.

Background. In patients with increased pulmonary artery pressure, the pulmonary vascular endothelium is morphologically and functionally abnormal and may be vulnerable to neutrophil-mediated injury induced by cardiopulmonary bypass (CPB). We investigated the relation between levels of granulocyte elastase (GEL), interleukin-6, or interleukin-8 after CPB and preoperative pulmonary hemodynamics or changes in pulmonary function after the operation.

Methods. We measured plasma levels of GEL, interleukin-6, and interleukin-8 before and after CPB in patients who underwent closure of an atrial septal defect. Preoperative and postoperative respiratory index were evaluated. Preoperative pulmonary hemodynamics were determined within 1 month before the operation.

Results. The level of GEL rose significantly after CPB from baseline (164.8 ± 81.3 versus 819.4 ± 320.3 µg/L; p < 0.01). Levels of interleukin-6 and interleukin-8 showed no significant changes after CPB. Peak level of GEL was significantly correlated with preoperative systolic pulmonary artery pressure (r = 0.76; p = 0.017), mean pulmonary artery pressure (r = 0.75; p = 0.021) and pulmonary-to-systemic arterial pressure ratio (r = 0.77; p = 0.016), but not with the hemodynamic variables for pulmonary blood flow or pulmonary resistance. Moreover, the value of (postoperative respiratory index - preoperative respiratory index)/preoperative respiratory index was positively correlated with the peak level of GEL (r = 0.72; p = 0.030).

Conclusions. The increase in GEL level after CPB is proportional to the increase in preoperative pulmonary artery pressure, which may cause the accordant pulmonary vascular damage.

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