RESUMEN
BACKGROUND: Predicting the important role of intercellular adhesion molecule-1 expression on the acute ischemia-reperfusion injury, we set out to demonstrate it by assessing the degree of expression of ICAM-1 after warm ischemia-reperfusion in canine unilateral lung ischemia model. MATERIAL AND METHOD: Left unilateral lung ischemia was induced by clamping the left hilum for 100 minutes in seven adult mongrel dogs. After reperfusion, various hemodynamic parameters and blood gases were analyzed for 4 hours, while intermittently clamping the right hilum in order to allow observation of the injured left lung function. The pulmonary venous blood was collected serially to measure TNF-alpha and cICAM-1 level. After 4 hours of reperfusion, the lung tissue was biopsied to assess ICAM-1 expression, and to measure tissue malondialdehyde(MDA) and ATP level. RESULT: The parameters including arterial oxygen partial pressure, pulmonary vascular resistance and tissue MDA and ATP level suggested severe lung damage. Serum TNF-alpha level was 8.76+/-2.37 ng/ml at 60 minutes after reperfusion and decreased thereafter. The cICAM-1 level showed no change after the reperfusion during the experiment. The tissue ICAM-1 expression was confirmed in 5 dogs. CONCLUSION: The increase of TNF-alpha level and expression of tissue ICAM-1 were demonstrated after ischemia reperfusion injury in canine lung model. However, the difference in expression time of each component suggested that the blockage against ICAM-1 should be performed within 4 hours, and the blockage of TNF-alpha should be done within 60 minutes to achieve prevention of acute ischemia-reperfusion injury.
Asunto(s)
Adulto , Animales , Perros , Humanos , Adenosina Trifosfato , Constricción , Gases , Hemodinámica , Molécula 1 de Adhesión Intercelular , Isquemia , Pulmón , Preservación de Órganos , Oxígeno , Presión Parcial , Reperfusión , Daño por Reperfusión , Factor de Necrosis Tumoral alfa , Resistencia VascularRESUMEN
Reexpansion Pulmonary edema is the iatrogenic complication which develops in a lung that has been rapidly reinflated after varied period of collapse secondary to a pneumothorax or a pleural effusion of large volume. Its incidence is relatively low, but can sometimes lead to death. The prevention of this disease is known well, but the definite treatment method has not been known in severe case although there have been conventional ventilator therapy and some medications in mild case. Asynchronous differential lung ventilation is a new therapeutic modelity which is applied independently to bilateral lungs in respiratory failure patients secondary to ventilation-perfusion mismatch, preoperatively, intraoperatively or postoperatively. By asynchronous differential lung ventilation, we successfully treated a severe reexpansion pulmonary edema in 29 year old male patient. Therefore we suggest that asynchronous differential lung ventilation is the treatment of choice for severe reexpansion pulmonary edema.