Pulmonary capillary pressure (Pcp) is the primary driving force determining the fluid flux across pulmonary capillary wall. Alterations of Pcp have been described in systemic inflammation, sepsis, ARDS, hypoxaemia and acute heart failure. The purpose of this study was to examine the Pcp alterations after lipopolysaccharide (LPS) intravenous administration in pigs. LPS has been administered (150μg/Kg BW) in the right atrium of 8 anesthetized and mechanical ventilated pigs (Group A) and the Pcp was calculated from pulmonary artery pressure tracings using the Gaar equation before, after LPS infusion and in 20min intervals for two hours. As control group served 8 pigs under similar conditions and normal saline administration (Group B). In group A significant increases of Pcp (p<0,01) have been observed directly after LPS infusion (baseline 7.23±0.9 to maximum 18.1±2.3 mmHg) which remained elevated until the end of the experiment. Group B showed no significant changes of Pcp at all. Comparison of A and B groups measurements revealed high significance (p<0,001) at all time intervals. Pulmonary Artery Occlusion Pressure showed no changes in both groups. Our study showed that endotoxin intravenous administration is significantly alterating the pulmonary capillary pressure in pigs under anesthesia and mechanical ventilation. On the contrary the pulmonary artery occlusion pressure was not been affected by the endotoxin administration during our observation. This finding may be important, because under specific circumstances such Pcp increases may lead to fluid extravasation and pulmonary oedema.