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Eur J Cardiothorac Surg 2001;20:508-513
© 2001 Elsevier Science NL

Survival and graft function in a large animal lung transplant model after 30 h preservation and substitution of the nitric oxide pathway

^a Division of General Thoracic Surgery, University Hospital Zürich, Zürich, Switzerland
^b Division of General Thoracic Surgery, University Hospital Bern, Bern, Switzerland
^c Department of Anesthesiology, University Hospital Zürich, Zürich, Switzerland
^d Department of Internal Medicine, University Hospital Zürich, Zürich, Switzerland

Received 11 October 2000; received in revised form 2 May 2001; accepted 22 May 2001.

Corresponding author. Tel.: +41-31-632-2330; fax: +41-31-632-2327
e-mail: ralph.schmid{at}insel.ch

Objective: Substitution of the nitric oxide- (NO-) pathway improves early graft function following lung transplantation. We previously demonstrated that 8-Br-cGMP (second messenger of NO) to the flush solution and tetrahydrobiopterin (BH4, coenzyme of NO synthase) given as additive during reperfusion improve post-transplant graft function. In the present study, the combined treatment with 8-Br-cGMP and BH4 was evaluated. Methods: Unilateral left lung transplantation was performed in weight matched outbred pigs (24–31 kg). In group I, grafts were preserved for 30 h (n=5). 8-Br-cGMP (1 mg/kg) was added to the flush solution (Perfadex^TM, 1.5 l, 1°C) and BH4 (10 mg/kg/h) was given to the recipient for 5 h after reperfusion. In group II, lungs were transplanted after a preservation time of 30 h (n=3) and prostaglandin E₁ (250 g) was given into the pulmonary artery (PA) prior to flush. In all recipients 1 h after reperfusion the contralateral right PA and bronchus were ligated to assess graft function only. Survival time after reperfusion, extravascular lung water index (EVLWI), hemodynamic variables, and gas exchange (PaO₂) were assessed during a 12 h observation period. Results: All recipients in group I survived the 12 h assessment, whereas none of the group II animals survived more than 4 h after reperfusion with a rapid increase of EVLWI up to 24.8±6.7 ml/kg. In contrast, in group I EVLWI reached up to 8.9±1.5 ml/kg and returned to nearly normal levels at 12 h (6.1±0.8 ml/kg). In two animals of group I the gas exchange deteriorated slightly. The other three animals showed normal arterial oxygenation over the entire observation time. Conclusion: Our data indicate that the combined substitution of the NO pathway during preservation and reperfusion reduces ischemia/reperfusion injury substantially and that this treatment even allows lung transplantation after 30 h preservation in this model.

Key Words: Nitric oxide • Lung transplantation • Ischemia reperfusion injury

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