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Eur J Cardiothorac Surg 2004;25:523-529
© 2004 Elsevier Science NL

Ultrastructural changes in pneumocyte type II cells following traumatic brain injury in rats

^a Department of Thoracic Surgery, Ankara Numune Education and Research Hospital, Ankara, Turkey
^b Department of Neurosurgery, Ankara Numune Education and Research Hospital, Ankara, Turkey
^c Department of Anatomy, Faculty of Medicine, Hacettepe University, Ankara, Turkey
^d Department of Biochemistry, Faculty of Medicine, Hacettepe University, Ankara, Turkey

Received 23 July 2003; received in revised form 4 October 2003; accepted 15 December 2003.

^* Corresponding author. Address: Asagiovecler Mh. 79.Sk. 8/3 Dikmen, Cankaya, Ankara, Turkey. Tel.: +90-312-482-72-79; fax: +90-312-310-34-60
e-mail: erseyda{at}yahoo.com

Objective: We aimed to demonstrate the time-dependent ultrastructural changes in pneumocyte type II cells following brain injury, and to propose an electron microscopic scoring model for the damage. Methods: Forty Wistar-Albino female rats weighing 170–200 g were used. The rats were allocated into five groups. The first group was the control and the second was the craniotomy without trauma. The others were trauma groups. Weight-drop method was used for achieving head trauma. Samples were obtained from the right and left pulmonary lobes at 2-, 8-, and 24-h intervals after transcardiac perfusion. An electron microscopic scoring model was used to reveal the changes. Results: There were no ultrastructural pathological findings pointing to lung injury in any rat of the control groups. There was intense intracellular oedema in type II pneumocyte and interstitial oedema in the adjacent tissue in trauma groups. Oedema in mitochondria and dilatation in both smooth endoplasmic reticulum and Golgi apparatus was more evident in the 8- and 24-h trauma groups. The chromatin dispersion was disintegrated in the nucleus in all trauma groups. Scores of all trauma groups were significantly different from the controls (P<0.05). All trauma groups were different from each other at significant levels (P<0.05 for each trauma groups). Conclusions: The data suggested that ultrastructural damage is obvious at 2 h and deteriorates with time. The electron microscopic scoring model worked well in depicting the traumatic changes, which were supported by lipid peroxidation. Further experiments are needed to determine the exact outcome after brain death model.

Key Words: Brain • Trauma • Animal model • Electron microscopy • Lung • Pneumocyte type II cells

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