An animal model was established to study the effects of elevated intra-abdominal pressure (IAP) on systemic and renal hemodynamics during laparoscopy. In a pilot study in five dogs, we simultaneously recorded carotid artery blood flow (CABF), carotid artery blood pressure (CABP), inferior vena caval pressure (IVCP), renal parenchymal blood now, and IAP. The renal parenchymal blood now was measured by a laser Doppler flowmetry (LDF) needle probe and the renal artery blood flow by an ultrasonic Doppler probe, both placed through laparotomy. The reliability and reproducibility of these two measurements at different renal perfusion pressures were documented. The established method was then used to assess the effects of increased IAP on renal hemodynamics during laparoscopy in six pigs. Pneumoperitoneum was achieved by insufflating the abdominal cavity with air. The LDF needle probe was inserted into the renal parenchyma laparoscopically. An increase in IAP from 0 to 40 mm Hg did not influence CABP. However, significant decreases in CABF were seen from 190.8 +/- 59.5 mL/min at 0 mm Hg IAP to 169 +/- 43.6 mL/min at 15 mm Hg. The CABF decreased in a linear fashion as IAP was increasing (correlation coefficient R = 0.976). Renal cortical blood flow (RCBF) decreased from 50.1 +/- 17.7 mL/min per 100 g at 0 mm Hg to IAP to 21.2 +/- 9.6 mL/min per 100 g of tissue at 15 mm Hg. There was an exponential correlation between IAP and RCBF (R = 0.897). Renal medullary blood flow (RMBF) demonstrated two patterns: an increase from 8.8 +/- 3.3 mL/min per 100 g at 0 mm Hg IAP to 25.0 +/- 15.1 mL/min per 100 g of tissue at 20 mm Hg and then a drop to 15.3 +/- 4.2 mL/min per 100 g at 40 mm Hg IAP. Elevation of the IVCP by occlusion of the intrathoracic IVC resulted in a minimal influence on the renal parenchymal perfusion. Manual compression over the left ventricle decreased equally CABF and RCBF. Thus, three factors contribute to the renal hemodynamic changes under elevated IAP: the local compressing effect of the pneumoperitoneum, decreased cardiac output, and impaired venous return. A shunting mechanism within the parenchymal vasculature may be the explanation for the hemodynamic changes in the renal medullary region. Finally, because elevation of the IVCP and decreased cardiac output produced only mild effects on renal parenchymal perfusion, the local compressing effect is likely to be the most important factor affecting renal hemodynamics during pneumoperitoneum.