Effect of platelet activating factor (PAF) on pulmonary circulation in isolated rabbit lung.

Platelet activating factor (PAF) has been implicated in the pathophysiology of acute lung injury. The aim of this work is to study the effect of PAF on isolated and perfused rabbit lungs with blood and with a blood-free solution. 24 isolated and perfused rabbit lungs have been used: 8 control preparations (CP), 4 vehicles preparations (VP), 8 PAF preparations (PP) to which we administered PAF (1 microg/Kg of rabbit weight) and 4 acellular preparations (AP) with the same dose of PAF as in PP but dissolved in BSA-Krebs buffer solution. In the preparations pulmonary artery pressure (Ppa), airway pressure (Paw), left atria pressure (Pla) and fluid filtration rate (FFR) were registered. Ppa resulted in a significant difference in AP vs PP, with a value of 21 cm of water (CI 95%: 12-26) vs 205.1 cm of water (CI 95%: 141.3 - 271) respectively. A increase in FFR was observed in PP but it did not occur in AP, the difference being statistically significant: 5.515 g/min (CI 95 %: 2.425 - 8.865) vs 0.049 g/min (CI 95%: 0.008 - 0.32) respectively. Paw was statistically different in PP vs AP, with a value of 14.3 cm of water (CI 95%: 11.57 - 16.7) vs 8.5 cm of water (CI 95%: 8-9) respectively. These results suggest that PAF does not have a direct effect on the endothelium or smooth muscle in the production of lung edema.

Effect of Fenoterol on PAF-induced lung edema in isolated and perfused rabbit lungs.

We have studied the effects of fenoterol on PAF-induced response in pulmonary circulation. We used 28 isolated and perfused rabbit lungs preparations: eight control preparations (CP), four vehicles preparations (VP), eight PAF preparations (PP) with two doses of PAF, one called low dose (LD = 0.5 microg/kg of weight) and the other high dose (HD = 1 microg/kg of weight) and eight Fenoterol preparations (FP) which we administered 0.05 mg of Fenoterol for 15 min, followed by a LD and HD of PAF. FP prevented elevation of pulmonary artery pressure (Ppa) as compared to PP, at LD of PAF: 12.615 (CI 95%: 8.57-20.885) versus 83.705 (CI 95%: 50.55-114.3) cm of water; and at HD of PAF: 19.38 (CI 95%: 11.235-28.94) versus 205.1 (CI 95%: 141.3-271) cm of water respectively. FP prevented the increase in fluid filtration rate (FFR) observed in PP at both doses of PAF LD: 0.765 (CI 95%: 0.07-3.385) versus 0.01 (CI 95%: -0.05-0.005) g/min; HD: 5.515 (CI 95%: 2.425-8.865) versus 0.03 (CI 95%: 0-0.33) g/min. Our results suggest that PAF has a vasoconstrictor effect that produces lung edema and this effect is inhibited by fenoterol.

[Effect of the administration of furosemide on the fluid filtration rate and in pulmonary artery pressure in isolated lungs of rabbits]. / Efecto de la administración de furosemida en la tasa de filtracion de liquido y en la presión de la arteria pulmonar en el pulmón aislado de conejo.

To study the possible effects of Furosemide at the lung level, two groups of isolated rabbit lung preparation were studied. An experimental group underwent a pulmonary hydrostatic oedema when the pressure of the left auricle (PAI) was increased from 0.45 +/- 0.74 t0 11.8 +/- 2.9 cm of H2O, with that increase in PAI we obtained an increase of 0.457 +/- 0.51 g/min in FFR (Fluid Filtration Rate), during this stable and sustained oedema, a 2 mg/Kg dosis of Furosemide was injected every 10 minutes and the possible changes in PAP, PAI, PVA, TFL, PaO2, PaCO2 and pH was observed, but no changes were observed in these parameters during the Furosemide infusion, and the same effect was observed in the control group were the preparations were maintained in basal conditions and without oedema. These results suggests that the Furosemide hat not a direct cardio-pulmonary effects, and the only possible effects could be by increasing diuresis at renal level.