The pulmonary microvascular hydrostatic or effective capillary pressure (PCPeff) is the principal determinant of the rate of edema formation [1,2]. Since scarce data are available only on the natural development PCPeff, of independently from vasoactive treatment, we investigated the time course of both PCPeff 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, PCPeff 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 . The contribution of the venous resistance to the pressure drop over the pulmonary vascular bed was calculated as PVRven=(PCPeff-PAOP)/(MPAP-PAOP) .
Early endotoxemia results in a pronounced increase of PCPeff 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 . The later normalization of both PCPeff and PVRven may be due to increased NO formation .
D Vasilev is supported by the Deutscher Akademischer Austauschdienst.