title: The mechanism of neurogenic pulmonary edema in epilepsy.
abstract: Neurogenic pulmonary edema (NPE) is found in many epilepsy patients at autopsy. It is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. 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. 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. We found the level of catecholamine was higher in TRM rats. Also the occurrence of alveolar cell apoptosis was increased. Moreover, pulmonary vascular remodeling including the deposition of collagen and medial thickening was also found in TRM rats. Further study showed that cell apoptosis was mediated by increasing Bax, decreasing Bcl-2, and activating caspase-3. 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. 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.
authors.affiliation: Department of Respiratory Medicine, The Fifth Clinical College of Harbin Medical University, Daqing, 163316, Heilongjiang, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhao
authors.forename: Guijun
authors.initials: G
authors.lastname: Lin
authors.forename: Mumu
authors.initials: M
authors.lastname: Shi
authors.forename: Jingquan
authors.initials: J
authors.lastname: Gao
authors.forename: Yanming
authors.initials: Y
authors.lastname: Wang
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Wang
authors.forename: Hongli
authors.initials: H
authors.lastname: Sun
authors.forename: Yonggang
authors.initials: Y
authors.lastname: Cao
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D015897:Comorbidity; D004195:Disease Models, Animal; D004827:Epilepsy / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005260:Female; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000473:pathology; D011654:Pulmonary Edema / Q000453:epidemiology* / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D011922:Rats, Mutant Strains; D015398:Signal Transduction / Q000502:physiology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D048049:Extracellular Signal-Regulated MAP Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D053148:Caspase 3