Effects of transient intracranial hypertension on lung fluid and protein exchange.

We determined whether a transient increase in intracranial pressure (Pic) increases lung vascular permeability and whether the increase occurs at a Pic threshold. Anesthetized sheep were prepared with lung lymph fistulas. Pic was increased by rapidly injecting 20-45 ml of freshly drawn autologous blood into the cisterna magna from a base line of 4.8 +/- 1.5 Torr to a peak mean value of either 142.0 +/- 17.6 Torr (group I, n = 5) or 70.3 +/- 3.5 Torr (group II, n = 5). Pic decreased to 34.6 +/- 2.2 Torr in group I and to 31.0 +/- 3.2 Torr in group II within 1 h and remained steady at these levels for the study. The Cushing response (i.e., marked systemic hypertension lasting 10-15 min) was elicited only in group I; changes in mean pulmonary arterial (Ppa) and mean pulmonary arterial wedge (Ppw) pressures during the first 15 min were small, pulmonary blood flow (QL) increased, and pulmonary vascular resistance (PVR) decreased only in the first 15 min after the intracisternal injection. In group II, Ppa and QL did not change significantly, but PVR increased after the increase in Pic. Both pulmonary lymph flow (Qlym) and transvascular protein clearance (CL) increased only in sheep with the Cushing response. In group III (n = 8) in which Qlym and CL increased after intracranial hypertension as in group I, the left atrial pressure was raised to increase the pulmonary capillary pressure (Pc) to determine the basis for the increases in Qlym and CL (i.e., whether vascular surface area or permeability increased). The increase in Pc produced a small increase and decrease in lymph-to-plasma protein concentration ratio, indicating that the transient increase in Pic did not increase endothelial permeability to proteins. The increases in Qlym and CL were due to increased pulmonary vascular surface area.