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1 Dept of Internal Medicine, Justus-Liebig University, Giessen, Germany, and 2 Dept of Anesthesiology and Critical Care Medicine, Leopold-Franzens University, Innsbruck, Austria
CORRESPONDENCE: H. Schütte, Dept of Internal Medicine, Justus-Liebig University, Klinikstrasse 36, 35385, Giessen, Germany. Fax: 49 6419942509
Keywords: nitroprusside, prostaglandin E1, prostaglandin I2, pulmonary oedema, reperfusion injury
Received: August 2, 2000
Accepted March 12, 2001
This work was supported by the Deutsche Forschungsgemeinschaft, Sonderforschungsbereich 547 "Kardiopulmonales Gefäßsystem"
High permeability oedema is an important feature in lung injury secondary to ischaemia-reperfusion. This study investigated the influence of aerosolized prostaglandin E1 (PGE1), prostaglandin I2 (PGI2) 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 cm3 s–1·cmH2O–1·g–1·10–4 after 30 min of reperfusion), and progressive oedema formation. Short-term aerosolization of SNP, PGE1 or PGI2 at the beginning of ischaemia largely suppressed the Kfc increase (1.36±0.22, 1.32±0.23 and 1.32±0.22 cm3·s–1·cmH2O–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 PGI2 and SNP and no effect of PGE1 (1.79±0.31, 2.2±0.53 and 3.2±0.05 cm3·s–1·cmH2O–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 E1, prostaglandin I2 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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