Twenty-six pigs were subjected to 120 min CPB (90 min cardioplegic cardiac arrest, 30 min reperfusion). Left ventricular (LV) power during ejection (= CO × AoP/ejection time) was calculated. Blood samples (before CPB, at 90 min, 120 min CPB and every 30 min until 5 h after CPB) were analyzed for the receptor antagonist IL-1ra, leukocytes, the leukocyte neutral proteinase inhibitor (LNPI to assess leukocyte activation), and plasma protein concentration (PP). Half-life of intravenously injected Evans Blue and intravascular protein content (IVP) were measured before and 3.5 h after CPB. Histologic samples of the LV-wall and septum were assessed for leukocyte infiltration.LV-power was markedly reduced after CPB. Leukocytes, LNPI and IL-1ra were significantly upregulated following CPB and a marked leukocyte infiltration to the subendocardium of the LV was present 5 h after CPB. PP was reduced by the crystalloid primed CPB, it increased after CPB, but did not reach the pre-CPB level. IVP was reduced after CPB. Half-life of intravenously injected Evans Blue was not affected by CPB.In the present model CPB was followed by depression of left ventricular function and a systemic inflammatory response. An increase in microvascular permeability to plasma proteins, however, was absent after 120 min of CPB including 90 min of myocardial ischemia. Fluid shift from the intra- to extravascular compartment occurred due to an increased microvascular effective filtration pressure. This is a result of reduced plasma colloid osmotic pressure due to hemodilution and, in part, to protein loss to the foreign surfaces of the CPB-system.