The role of tissue reperfusion in the reexpansion injury of the lungs

Abstract

Objective: The aim was to discuss the balance between free radical damage and body defense mechanisms that occurred in reexpansed pulmonary tissue and to evaluate the relationship between the changes in the pulmonary circulation and the mentioned balance.

Methods: Twenty male Wistar Albino rats were used for these study results. Pneumothorax was created in the left hemithorax by percutaneous route in all the rats. After 7 days, the first group (n = 10) had a sternotomy under ketamine anesthesia. Following invasive measurement of pulmonary artery pressure, tissue samples were obtained from the lower lobes of the right and left lungs before reexpansion occurred. Tracheotomies were opened in the second group (n = 10) with a 16 gauge cannula. Following sternotomy, invasive mean pulmonary artery pressure measurements were obtained by the support of non-invasive cardiac monitorization. The lungs were aerated with 4 cmH(2)O oxygen and fixed volume support and 1 h of reexpansion was obtained. Invasive mean pulmonary artery pressure measurements were repeated after reexpansion and tissue samples were obtained from the lower lobes of left and right lungs. Nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured in tissue samples, surfactant staining and light microscopic evaluations were performed.

Results: At the end of the reexpansion, there was a decrease in mean pulmonary artery pressure (P < 0.01), MDA (P < 0.01) and SOD (P < 0.05) levels and an increase in NO (P < 0.05) levels. Under the light microscopic examination, in the samples that were provided with reexpansion, the alveolo-capillary membrane was thickened due to increasing edema, increase in the number of lymphocytes and return of the neutrophil leukocytes to the area. There was no significant difference between the groups in terms of surfactant staining.

Conclusion: The tissue reperfusion that is achieved with the restoration of blood flow during the reexpansion of collapsed lungs, can be the initial pathology in the chain of events that result in reexpansion injury.