Pulmonary artery perfusion does not improve brain natriuretic peptide (BNP) levels in suine experimental research

Assess if the main pulmonary artery controlled perfusion over cardiopulmonary bypass (CPB) modifies BNP levels expressed by the ventricular myocardium.

Experimental research involving 32 pigs, divided into two groups according to CPB strategy--group I (cardioplegia) and group II (beating heart). Both groups were allocated into three subgroups according to lung perfusion strategy--subgroup A (control: no lung perfusion), subgroup B (lung perfusion with arterial blood) and subgroup C (lung perfusion with venous blood). In subgroups B and C, lung was perfused for 30 minutes, using preoperative mean pulmonary artery pressure (MPAP) as perfusion pressure, which was monitored through manometer. MPAP and pulmonary vascular resistance (PVR) were measured after coming off CPB using Swan-Ganz catheter. At preoperative time and 30 minutes after lung perfusion, specimens were taken from the right ventricular myocardium aiming to assess brain natriuretic peptide (BNP) and histologic pattern. Immunohistochemical and hematoxylin-eosin techniques were used to determine, respectively, BNP expression and inflammatory myocardial lesions.

In animals submitted to controlled lung perfusion, there was a postoperative reduction of MPAP (P = 0.03) and PVR (P = 0.005).There was no differences among subgroups within the group, I (P = 0.228) and subgroups within group II (P = 0.325) as to postoperative BNP expression. There were no differences among subgroups with and without lung perfusion as to postoperative inflammatory lesions (P > 0.05).

Main pulmonary artery controlled perfusion for 30 minutes did not yield substantial modifications in BNP expression and histologic pattern of the right ventricular myocardium.