An experimental study on how brain-dead state affects the lung morphology of Ba-Ma mini pigs and the mechanism / 中华器官移植杂志

ABSTRACT

Objective To investigate the change of lung morphology and the mechanism in the brain-dead state. Methods Ten Ba-Ma mini pigs were randomized into 2 groups brain-dead group (group B, n=5) and control group (group C, n=5). Brain-dead model was established in group B by increasing intracranial pressure in a modified, slow and intermittent way, and brain-dead state maintained for 24 h by respiration and circulation support. The serum TNF-?, IL-1?, and IL-6 were determined at 3, 6 12, 18 and 24 h after the initial confirmation of brain death. Lung tissues were taken at 24 h. The alterations of lung tissues were observed by HE staining, and the expression of PKC-? detected by immunohistochemistry. PKC-? mRNA at each time point was detected by RT-PCR. The microstructure of hepatic tissues was observed under an electron microscope. Results (1) Under the light microscopy, broadened lung alveolar septum, edematous, extravasate in the alveolar congestive capillary vessel, infiltration of lymphocyte were observed. Under the election microscopy, cytoplasm edema, swollen mitochondria of the type-Ⅱ epithelial cells, partial membrane dissolution of mitochondria were observed and the microtomentum disappeared. No obvious morphological injury was observed under light microscopy and election microscopy. (2) Compared with control group, the serum IL-1?, IL-6 and TNF-? in brain-dead group began to increase at 3 h after brain death, and become more and more higher when the maintained state was prolonged. The expression of PKC-? and PKC-? mRNA in brain-dead group was increased at 24 h in the lung tissue. Conclusion Brain death may evoke lung morphological injury and increase the level of inflammatory mediators; After brain death the levels of PKC-? mRNA transcription and protein translation is increased. The activation of PKC-? and the alteration of inflammatory mediators are supposed to be one of the mechanisms of the lung injury.