![]() ![]() The tremor rat (TRM) (tm/tm), a single-gene mutant, is the parent strain of the spontaneously epileptic rat (SER: zi/zi, tm/tm) found in the Kyoto:Wistar colony that exhibits both absence-like and convulsive seizures without any external stimuli. ![]() The aim of this study is to explore the exact mechanism of epilepsy-induced NPE. A proven mechanism of seizure-induced NPE is the intense generalized vasoconstriction from the massive seizure-related outpouring of central sympathetic activity, which leads to an increase in pulmonary vascular resistance. NPE is found in many cases of epilepsy at autopsy. Both a rapid, transient, and severe sympathetic discharge and the release of vasoactive substances are thought to be involved in this process. Although several pathophysiological mechanisms have been proposed, the exact cascade leading to the development of NPE is unclear. It is characterized by marked pulmonary vascular congestion with perivascular edema, extravasation, and intra-alveolar accumulation of protein- rich edema fluid and intraalveolar hemorrhage. NPE develops rapidly following injury and significantly complicates the overall clinical status of the patient. The roles of central nervous system trigger zones, systemic sympathetic discharge, inflammation and anesthesia, and intracranial pressure in the etiopathogenesis of NPE have been considered in detail. ![]() It has been well known for almost 100 years, but its etiopathogenesis is still not completely understood. NPE is a life-threatening complication following central nervous system injury. ![]() The pulmonary conditions central apnea and NPE are among the most frequently implicated mechanisms in SUDEP cases. There are several pathophysiological events contributing to SUDEP, including central apnea, autonomic dysregulation of cerebral and cardiac blood flow, decreased heart rate variability (HRV), and neurogenic pulmonary edema (NPE). Sudden unexpected death in epilepsy (SUDEP) is defined as a sudden, unexpected, nontraumatic, witnessed or unwitnessed death and is a major clinical problem in epilepsy patients, especially those with chronic, uncontrolled epilepsy. Nervous system infections are the most important reason for seizures. Although most epilepsies are considered multifactorial diseases, some specific types are considered single-gene disorders. The mortality of patients with epilepsy is two to three times that of the general population. There are 50 million people with epilepsy worldwide 40 million live in developing countries. Thus, these findings suggest that pulmonary vascular remodeling and alveolar cell apoptosis might be involved in epilepsy-induced NPE and that the mitogen-activated protein kinase signal pathway was involved.Įpilepsy comprises a variety of neurological disorders characterized by recurrent seizures, and it affects 1–2 % of the population worldwide. In addition, the protein level of phosphorylated ERK (p-ERK) was found to be decreased while phosphorylated JNK and phosphorylated p38 were upregulated in TRM rats. Further study showed that cell apoptosis was mediated by increasing Bax, decreasing Bcl-2, and activating caspase-3. Moreover, pulmonary vascular remodeling including the deposition of collagen and medial thickening was also found in TRM rats. Also the occurrence of alveolar cell apoptosis was increased. We found the level of catecholamine was higher in TRM rats. We performed reverse-phase high-pressure liquid chromatography assay, H&E and Masson staining, TUNEL assay, and Western blot experiments to determine the role of seizures in NPE. In this study, we used the tremor rat (TRM: tm/tm) as an animal model of epilepsy to investigate the potential mechanisms of NPE under epileptic conditions. It is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. Neurogenic pulmonary edema (NPE) is found in many epilepsy patients at autopsy. ![]()
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