Atrial and brain natriuretic peptide changes in an experimental model of intra-abdominal hypertension

Intra-abdominal hypertension (IAH) can have a profound impact on the cardiovascular system. We hypothesized that natriuretic peptides (Nt-pro-ANP and Nt-pro-BNP) are produced in response to the cardiovascular changes observed in an experimental model of IAH.

Eleven female pigs were enrolled in this study. Four experimental phases were created: a baseline phase for instrumentation (T1); two subsequent phases (T2 and T3), in which helium pneumoperitoneum was established at 20 and 35 mm Hg, respectively; and the final phase (T4), in which abdominal desufflation took place. Hemodynamic parameters and concentrations of Nt-pro-ANP and Nt-pro-BNP were measured.

Central venous pressure and pulmonary capillary wedge pressure increased significantly during the elevation of intra-abdominal pressure (IAP) and returned to baseline after abdominal desufflation. Right and left transmural pressures remained unaffected by the elevation of IAP. Cardiac output decreased in phases T2 and T3 and was restored to baseline levels after abdominal desufflation. Systemic and pulmonary vascular resistances increased significantly with IAH and decreased after abdominal desufflation. Nt-pro-ANP did not change significantly in comparison to baseline. Nt-pro-BNP increased significantly in comparison to baseline at T3 and T4. Peak Nt-pro-BNP levels at T3 (peak IAP) correlated positively with indices of afterload at this time point, that is, systemic vascular resistance and pulmonary vascular resistance (r(2) = 0.38, P = 0.042 and r(2) = 0.55, P = 0.009, respectively). A strong negative correlation between Nt-pro-BNP and cardiac output at T3 was also demonstrated (r(2) = 0.58, P = 0.006).

IAH resulted in cardiovascular compromise. The unchanged Nt-pro-ANP concentrations might reflect unaltered atrial stretch with IAH, despite the elevation of right atrial filling pressure. The significant increase of Nt-pro-BNP in response to high levels of IAP may reflect left ventricular strain and dysfunction due to the severe IAH and provide an alternative marker in the monitoring of IAH.