The pulmonary microvascular hydrostatic or effective capillary pressure (PCP_eff) is the principal determinant of the rate of edema formation [1,2]. Since scarce data are available only on the natural development PCP_eff, of independently from vasoactive treatment, we investigated the time course of both PCP_eff and the longitudinal distribution of pulmonary vascular resistance during long-term hyperdynamic porcine endotoxemia.

Over 9 h anesthetized and ventilated pigs received continuous intravenous endotoxin (ETX, n=7) or placebo (Sham, n=5). Hydroxyethylstarch was infused to maintain MAP > 65 mmHg together with a sustained 30–50% increase in cardiac output. Mean (MPAP) and pulmonary artery occluded (PAOP) pressures were recorded before and 3, 6, and 9 h after the start of ETX. After signal filtering via a low-pass filter, PCP_eff was derived from a bi-exponential fit to the post-occlusion pressure decay curve, back-extrapolating the slower part to the instant of occlusion determined by simultaneously recording the balloon pressure [1]. The contribution of the venous resistance to the pressure drop over the pulmonary vascular bed was calculated as PVR_ven=(PCP_eff-PAOP)/(MPAP-PAOP) [1].

See Table.

Early endotoxemia results in a pronounced increase of PCP_eff both due to increased downstream (i.e.left atrial) pressure as well as increased contribution of the postcapillary pressure drop. Hypoxia and/or early mediator release (i.e. thromboxane) probably assume importance in this context [1]. The later normalization of both PCP_eff and PVR_ven may be due to increased NO formation [3].