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Summary:Purpose: To clarify the relationship of neuronal death to cellular responses, we studied neuronal death as well as reactions of glia and progenitor cells in the hippocampus of two rat models of epilepsy.Methods: Seizures were induced by either kainic acid (KA) administration or electrical kindling. Neuronal degeneration was assessed by in situ DNA fragmentation analysis. Reactions of glial cells were studied by immunohistochemistry. Progenitor cell division was evaluated using the bromodeoxyuridine (BrdU) labeling method.Results: DNA fragmentation and reactive microglia were observed in the CA1, CA3, and hilus region for 24 h to 4 weeks after KA injection, but not detected in the kindling model. Reactive astrocytes and enhancement of progenitor cell division were seen in both animal models. The number of BrdUpositive cells began to increase on day 3 after KA injection, peaked on day 5, and returned to baseline on day 10. After kindling, the number of BrdU-positive cells began to increase after five consecutive experience of stage I seizures.Conclusions: These observations show that neuronal degeneration is not necessary for triggering the upregulation. Microglial activation is closely related to the neuronal death process induced by KA.

BackgroundTension gastrothorax is a kind of obstructive shock with prolapse and distention of the stomach into the thoracic cavity. Progressive gastric distension leads to mediastinal shift, reduced venous return, decreased cardiac output, and ultimately cardiac arrest. Therefore, it is crucial to decompress the stomach distension for the initial resuscitation of tension gastrothorax.Case presentationA 75-year-old female was transported to our resuscitation bay due to motor vehicle crash. At the time of arrival to our hospital, the patient developed cardiac arrest. While undergoing cardiopulmonary resuscitation, an unstable pelvic ring was recognized, so we performed a resuscitative thoracotomy to control hemorrhage and to perform direct cardiac massage. Once we performed the thoracotomy, the stomach and omentum prolapsed out of the thoracotomy site and through the diaphragm rupture site and spontaneous circulation was recovered. Neither the descending aorta nor the heart was collapsed. Although we had continued the treatment for severe pelvic fracture (including blood transufusions), the patient died. Given that (1) the stomach prolapsed out of the body at the time of the thoracotomy; (2) at the same timing, spontaneous circulation returned; and (3) the descending aorta and heart did not collapse, we hypothesized that the main cause of the initial cardiac arrest was tension gastrothorax.ConclusionsRecognition of tension gastrothorax pathophysiology, which is a form of obstructive shock, makes it possible to manage this injury correctly.

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