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  • Title: Prostanoid release after lung transplantation.
    Author: Kimblad PO, Gréen K, Sjöberg T, Steen S.
    Journal: J Heart Lung Transplant; 1996 Oct; 15(10):999-1004. PubMed ID: 8913917.
    Abstract:
    BACKGROUND: Increased pulmonary vascular resistance is frequently seen after lung transplantation. Thromboxane A2 is a potent vasoconstrictor of pulmonary arteries. Thromboxane-elicited vasoconstriction can ben counteracted by prostacyclin. The effects of lung transplantation on the biosynthesis of these substances were investigated. METHODS: Pulmonary artery flush perfusion with a low-potassium dextran glucose solution was performed in six donor pigs. After a 24-hour storage period, the left lung was transplanted into a recipient, followed by right pneumonectomy, making the recipient's survival entirely dependent on the transplanted lung. A sham operation (bilateral thoracotomy, right pneumonectomy) ws done in six pigs. the urine contents of the stable thromboxane A2 metabolite 2,3-dinor-thromboxane B2 and the stable prostacyclin metabolite 2,3-dinor-6-keto-protaglandin F1 alpha were measured with a gas chromatography-mass spectrometry method. RESULTS: One to four hours after reperfusion, thromboxane A2 production reached its maximum in both groups: it ws fivefold the basal value in the transplanted group, but only twofold in the sham-operated group, the difference being significant (p < 0.005). Twenty to twenty-four hours after reperfusion, thromboxane A2 production had stabilized at about twofold the basal value in both the transplanted and in the sham-operated group. Four to eight hours after reperfusion, prostacyclin production reached 15 times the basal value in the transplanted group and twofold in the sham-operated group, the difference being significant (p < 0.05). Twenty to twenty-four hours after reperfusion, prostacyclin production was 18-fold the basal value in the transplanted group and sevenfold in the sham-operated group. No correlation was found between the thromboxane or prostacyclin production and the pulmonary vascular resistance or the mean pulmonary arterial pressure. CONCLUSIONS: The thromboxane A2 production increased fivefold after lung transplantation, with a concomitant 15-fold increase in prostacyclin synthesis, which might have counteracted the vasoconstrictor effect of thromboxane.
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