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Right arrow Lung - transplantation

Ann Thorac Surg 2006;82:465-471
© 2006 The Society of Thoracic Surgeons

Original Articles: General Thoracic

Protective Effect of a Nebulized ß2-Adrenoreceptor Agonist in Warm Ischemic–Reperfused Rat Lungs

Fengshi Chen, MDa, Takayuki Nakamura, MDb, Takuji Fujinaga, MDa, Jitian Zhang, MDa, Hiroshi Hamakawa, MDa, Mitsugu Omasa, MDa, Hiroaki Sakai, MDa, Nobuharu Hanaoka, MDa, Toru Bando, MDa, Hiromi Wada, MDa,*, Tatsuo Fukuse, MDa

a Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan
b Department of Experimental Therapeutic, Translational Research Center, Kyoto University Hospital, Kyoto, Japan

Accepted for publication January 3, 2006.

* Address correspondence to Dr Wada, Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin, Kyoto 606-8507, Japan. (Email: wadah{at}kuhp.kyoto-u.ac.jp).

BACKGROUND: It seems inevitable that non–beating-heart donors will be utilized to resolve the shortage of donors for clinical lung transplantation. The control of warm ischemia-reperfusion injury is crucial in manipulating non–beating-heart donors. We hypothesized that nebulization of a ß2-adrenoreceptor agonist, salmeterol xinafoate (SLM), during warm ischemia would increase lung tissue cyclic adenosine monophosphate (cAMP) levels, resulting in lung protection.

METHODS: Two studies were conducted. The first investigated the effect of SLM nebulization during ischemia on pulmonary ischemia-reperfusion injury, using an isolated rat lung-perfusion model. The heart-lung block was excised with cannulation of the pulmonary artery and vein, exposed to 55 minutes of ischemia at 37°C, and subsequently reperfused for 60 minutes. Several parameters were measured during reperfusion. In the second study, to measure changes in lung tissue cAMP levels during warm ischemia with or without SLM nebulization, rat lungs were harvested and exposed to 60 minutes of warm ischemia with ventilation.

RESULTS: Salmeterol xinafoate nebulization significantly decreased the pulmonary shunt fraction, airway resistance, and pulmonary vascular resistance. It also inhibited pulmonary edema throughout the reperfusion period. Lung tissue cAMP was effectively maintained by SLM nebulization at the end of reperfusion. Myeloperoxidase activity in the lungs was decreased significantly by SLM nebulization. Lung tissue cAMP levels decreased during the 60 minutes of warm ischemia, but increased with SLM nebulization (p < 0.01).

CONCLUSIONS: Our results confirmed that SLM nebulization during warm ischemia maintained lung tissue cAMP levels, resulting in the alleviation of pulmonary warm ischemia-reperfusion injury.




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