Aerosolized PGE 1 , PGI 2 and nitroprusside protect against vascular leakage in lung ischaemia-reperfusion
2001; European Respiratory Society; Volume: 18; Issue: 1 Linguagem: Inglês
10.1183/09031936.01.00070001
ISSN1399-3003
AutoresHartwig Schütte, Alexander Löckinger, Werner Seeger, Friedrich Grimminger,
Tópico(s)Cardiac Ischemia and Reperfusion
ResumoHigh permeability oedema is an important feature in lung injury secondary to ischaemia-reperfusion. This study investigated the influence of aerosolized prostaglandin E 1 (PGE 1 ), prostaglandin I 2 (PGI 2 ) and the nitric oxide (NO)-donor, sodium nitroprusside (SNP) on microvascular barrier function in pulmonary ischaemia-reperfusion. Buffer-perfused rabbit lungs were exposed to 180 or 210 min of warm ischaemia while maintaining anoxic ventilation and a positive intravascular pressure. Reperfusion provoked a transient, mostly precapillary elevation of vascular resistance, followed by a severe increase of the capillary filtration coefficient (Kfc) versus nonischaemic controls (3.17±0.34 versus 0.85±0.05 cm 3 s −1 ·cmH 2 O −1 ·g −1 ·10 −4 after 30 min of reperfusion), and progressive oedema formation. Short-term aerosolization of SNP, PGE 1 or PGI 2 at the beginning of ischaemia largely suppressed the Kfc increase (1.36±0.22, 1.32±0.23 and 1.32±0.22 cm 3 ·s −1 ·cmH 2 O −1 ·g −1 ·10 −4 , respectively) and oedema formation. In contrast, application prior to reperfusion was much less effective, with some reduction of Kfc increase by PGI 2 and SNP and no effect of PGE 1 (1.79±0.31, 2.2±0.53 and 3.2±0.05 cm 3 ·s −1 ·cmH 2 O −1 ·g −1 ·10 −4 , respectively). Haemodynamics, including microvascular pressure, were only marginally affected by the chosen doses of aerosolized vasodilators. It is concluded that short-term aerosolization of prostaglandin E 1 , prostaglandin I 2 and sodium nitroprusside at the onset of ischaemia is highly effective in maintaining endothelial barrier properties in pulmonary ischaemia-reperfusion. This effect is apparently attributable to nonvasodilatory mechanisms exerted by these agents. Alveolar deposition of prostaglandins and/or nitric oxide donors by the aerosol technique may offer pulmonary protection in ischaemia-reperfusion injury.
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