Perfluorochemical (PFC) liquids are biologically inert and nonbiotransformable substances that, when used as breathing medium, may be transported across the lung epithelium in small quantities, distributed throughout the body, and ultimately vapourized through the lungs and transpired through the skin. To further evaluate the uptake, biodistribution and elimination of a PFC liquid (perfluorodecalin) in the neonatal population, arterial blood, tissue and expired gas samples were obtained from preterm lambs (105-114 days gestation). Two groups of premature lambs were studied: Group I (n = 4) lambs were liquid ventilated from birth for 1 h and killed without exposure to gas ventilation (GV) and Group II (n = 5) lambs were liquid ventilated for 1 h followed by up to 2 h of GV. Samples were analysed by electron-capture gas chromatography and data were expressed in nl of PFC/ml of blood or gas and nl of PFC/gm tissue. During liquid ventilation and subsequent GV, PFC blood levels significantly increased (P < 0.001) from baseline control levels (0.007 +/- 0.001 SE nl PFC/ml blood) to a high of 2.95 +/- 1.03 SE nl PFC/ml blood. Perfluorochemical levels measured in expired gas (Group II) demonstrated a rapid decrease as a function of time of GV. Tissue levels of PFC indicated that uptake of PFC in Group I was significantly different (P < 0.001) than baseline levels and organ dependent; the highest levels were in the lungs (221 +/- 26.2 SE nl PFC/g tissue) and the lowest in the liver (2.24 +/- 1.6 SE nl PFC/g tissue). Comparison of tissue levels of PFC between groups indicated a 34.8% mean decrease across organs in Group II compared with Group I. These data indicate that PFC uptake and elimination is organ dependent and that PFC liquids can be eliminated through the lungs upon return to GV. Sustained PFC blood levels may be related to residual PFC in the organs and lung as well as regional variation in ventilation-perfusion matching upon return to GV.

Cardiac output and pulmonary blood flow do not change significantly during PLV and therefore do not appear to contribute to improved gas exchange. This stable cardiac performance occurs at lower wall stress and thereby more advantageous energetic conditions.