PARTIAL LIQUID VENTILATION (PLV) AND LUNG INJURY - IS PLV ABLE TO MODIFY PULMONARY VASCULAR-RESISTANCE

Introduction: Partial liquid ventilation (PLV) with perfluorocarbons c an be advantageous in treating lung injury. We studied this phenomenon in isolated piglet lungs devoid of systemic detractors by studying th e changes in pulmonary vascular resistance (PVR) after lung injury wit h and without PLV. The following questions were asked. (1) Does PLV al one affect PVR in the uninjured lung? (2) Does PLV prevent the increas e in-PVR associated with olelc acid-induced lung injury? (3) Does PLV modify the increase in PVR associated with oleic acid lung injury? (4) Are the prophylactic and therapeutic effects of PLV on the increased PVR associated with oleic acid-induced lung injury different? Methods: Neonatal piglet (3 to 4 kg) lungs were prepared without pulmonary isc hemia, hypoxia, or reperfusion injury for in situ study. Before pulmon ary Vascular isolation leg, aortic and ductus arteriosus ligation) the pulmonary artery (PA) and left atrium (LA) were cannulated and attach ed to a blood-primed perfusion circuit (flow 80 mL/kg/min). Pressure-l imited volume-cycled ventilation (FIO2, 0.21; TV, 15 mL/kg; PIP, 25 cm H2O) was accomplished via occlusive tracheostomy Blood gas parameters were monitored continuously and maintained within normal range (SpaO( 2), 75%; pH, 7.35 to 7.45; pCO(2), 35 to 45 torr). Pulmonary artery pr essure (P-pa), left atrial pressure (P-la) and pulmonary blood flow (Q (pa)) were recorded and PVR calculated (PVR = P-pa - P-la/Q(pa)). Afte r achieving a stable baseline with gas ventilation only, the animal pr eparations were assigned to one of the following four groups. In group 1 (n = 7) PLV was given alone, using endotracheally administered perf luorodecalin (15 mL/kg). In group 2 (Prophylactic, n = 7) PLV was give n prophylactically 60 minutes before lung injury induced by injecting oleic acid (OA) at 0.08 mL/kg into the pulmonary artery. In group 3 (T herapeutic, n = 8) PLV was given 60 minutes after OA-induced lung inju ry. P-PA, P-LA, and Q(PA) were measured and PVR was calculated In grou p 4 (n = 7) OA was given alone. Significance of differences between gr oups was obtained by repeated measures analysis of variance (ANOVA). R esults were expressed as mean +/- SEM (mm Hg/L/Kg). Results: Group I s howed baseline PVR of the normoxic gas ventilated animals was 127 +/- 19 mm Hg/L/kg. PVR 180 minutes after PLV administration was 160 +/- 15 mm Hg/L/kg (P = ns v baseline). In group 2 after OA infusion, PVR inc reased from 109 +/- 13 to 281 +/- 26 mm Hg/L/kg (P <.01 v baseline), a nd 60 minutes later, PVR decreased to 193 +/- 22 mm Hg/L/kg (P <.05 v GA). In group 3 PVR on gas ventilation, before lung injury, was 137 +/ - 28 mm Hg/L/kg. Sixty minutes after OA infusion, PVR increased to 314 +/- 23 mm Hg/L/kg (P <.01 v baseline). After 60 additional minutes of PLV, PVR decreased to 201 +/- 31 mm Hg/L/kg, (P <.05 v maximum). In g roup 4 baseline PVR was 96 +/- 16 mm Hg/L/kg. After 120 minutes of OA injection, PVR increased to 414 +/- 20 mm Hg/L/kg (P <.01 v baseline). Endpoint analysis of PVR at the conclusion of the recording interval showed no difference between group 2 and group 3 (P = not significant [ns]). Conclusions: (1) PLV does not significantly alter PVR in the un injured lung when given for 2 hours; (2) prophylactic administration o f PLV prevents the sustained increase in PVR known to be induced by OA injury; (3) PLV abates OA-induced elevation in PVR when given therape utically after injury; and (4) Prophylactic and therapeutic PLV have s imilar effects on PVR in the OA-injured lung. Copyright (C) 1997 by W. B. Saunders Company.