Tempol Reduces Warm Ischemic Damage of Lung Functions In Non‐Heart‐Beating Donors if Added Pre‐arrestly but Doesn’t Have any Protective Effect on Ischemia – Reperfusion Injury

Abstract

Lungs retrieved from non-heart-beating donors (NHBD) may alleviate the critical shortage of suitable organs for transplantation. We tested the role of cell permeable reactive oxygen species scavenger – Tempol – in protection of warm ischemic and reperfusion injury of lung functions in experimental model of NHBD. We measured perfusion pressure, weight gain and arterio - venous difference in O2 partial pressure in Salt solution + Ficol perfused lungs isolated from Wistar rats in following two experiments: A Experimental rats underwent the protocol of NHBD lung harvesting: 1 hour of warm ischemia after pentobarbital euthanasia followed with 90 min of cold ischemia (12°C). Under these conditions we compared room-air ventilated rats with non-ventilated during warm ischemia and we were interested in possible protective effect of Tempol (100mg/kg) added pre-arrestly. In controls, lungs were harvested immediately after euthanasia. B We used the same protocol as in A and observed the effect of Tempol added into perfusate at the beginning of reperfusion of NHBD lungs. Ventilation during warm ischemia deteriorates lung functions by the effect of reactive oxygen species. This mechanism was in part A inhibited by pre-arrest administration of Tempol, which prevented development of lung edema and improved oxygen transport ability. In part B Tempol added into the perfusate deteriorated lung functions by causing pulmonary edema. This could be caused by Tempol-mediated inhibition of hypoxic pulmonary vasoconstriction Supported by GAUK 45/2005/C