The effect of aprotinin on ischemia–reperfusion injury in an in situ normothermic ischemic lung model

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Abstract
Objectives: In the context of the physiopathology of damage due to ischemic preservation and reperfusion injury following preservation, we aimed to demonstrate the positive effects of the addition of aprotinin, a serine protease inhibitor, to low potassium dextran (LPD), used as a single-flush solution in normothermic ischemic animal models, on lung protection and the prevention of reperfusion injury. Methods: In the study, 21 New Zealand white rabbits were used as experimental subjects. The subjects were ventilated with the assistance of a manual mechanical ventilator at 30 breaths/min and 10 ml/kg tidal volume. Lung protection solution was supplied to the pulmonary artery via a catheter. After applying the solution, ischemia was carried out for 120 min. At the end of this period, reperfusion was carried out for 90 min. The subjects were divided into three groups of seven subjects each. In the control group, pulmonary perfusion solution was not employed, whereas in the second group LPD was employed, and in the third group LPD and aprotinin (LPD+A) were perfused. Blood gas analysis, bronchoalveolar lavage (BAL) fluid examination, tissue malondialdehyde (MDA) level analysis and morphological examinations were performed. Results: The LPD+A group showed the significantly highest levels of oxygenation at the 15th and 60th minutes of reperfusion (297±76.7 and 327±97.4 mmHg) in comparison to the LPD (157±20.6 and 170±53.6 mmHg) and control (64±8.4 and 59±7.2 mmHg) groups (PConclusions: It was observed that the addition of aprotinin to LPD solution as a pulmonary flush solution in an in situ normothermic ischemic lung model prevents reperfusion injury by means of various mechanisms and also protects the morphological, functional and biochemical integrity of the lung. In our view, therefore, the addition of aprotinin to lung protection solution will provide positive results in lung transplantation protocols.

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