7 healthy pigs, anesthetized with ketamine/azaperon/thiopen tone and ventilated with O2/N2O by volume control, underwent anterior resection of the descending colon by laparoscopic view. During operation a pneumoperitoneum by inflating CO2 to an abdominal pressure of 14 mm Hg was installed Immediately (+2 min) after the onset of insufflation, both systemic and pulmonary arterial pressure increased. However, pulmonary artery pressure started to decrease after 10 min. whereas systemic arterial pressure remained elevated until the end of the experimental protocol. Left ventricular (LV) pressure and LV dp/dt increased in parallel with the systemic arterial pressure. Peak inspiratory pressure and central venous pressure increased in parallel with the abdominal pressure. Blood gas analysis of arterial and pulmonary blood demonstrated increased pCO2 associated with mild acidosis. Arterial pO2 did not change significantly indicating that the decreased pulmonal distensibility did not endanger the oxygenation. Pulmonary pO2 and pulmonary O2 saturation increased early (+10 min) after start of insufflation and were stable during the 2 h of observation indicating either increased cardiac output or decreased O2 extraction. We conclude that the sharp initial rise of both arterial pressures could be the effect of a mechanical action, whereas sustained hemodynamic alterations would involve complex regulatory mechanisms like an increase of sympathetic activity, baroreceptor control, or a response to acidosis. The acute and, in the systemic circulation, stable increase of ventricular afterload should be considered in patients with underlying cardiac diseases such as ischemic heart disease or valvular dysfunction or in patients taking drugs which interfere with normal compensatory processes.