title: Endoplasmic Reticulum Is Involved in Myocardial Injury in a Miniature Swine Model of Coronary Artery Stenosis Exposed to Acceleration-Associated Stress.
abstract: This study aimed to investigate the effects of myocardial injury in a minimally-invasive miniature swine model with different levels of coronary artery stenosis (CAS) and exposed to maximal tolerated +Gz. Proximal left anterior descending branch was ligated in 20 swine. Five swine underwent a sham operation. A trapezoid acceleration curve was used for +Gz stress. Pathological changes of myocardial tissue were detected by H&E staining. Apoptotic cardiomyocytes were detected by TUNEL. GRP78 and CHOP were investigated by immunohistochemistry and western blot. CAS models were successful in 18 animals.Compared with the sham-operated group (+8.00±0.71 Gz), the maximal tolerated +Gz values of the moderate stenosis (+6.00±0.89 Gz, P<0.05) and severe stenosis groups (+5.20±0.84 Gz, P<0.05) were decreased.Compared with sham animals (12.16±1.25%), after exposure to maximum +Gz, apoptotic cells of the moderate (43.53±8.42%, P<0.05) and severe stenosis group (60.50±9.35%, P<0.05) were increased, MDA content was increased (1.89 and 4.91 folds, respectively, P<0.05), and SOD activity was reduced (-13.66% and -21.71%, respectively). After exposure to maximum +Gz, GRP78 protein expression was low in the sham-operated (0.29±0.05) and mild stenosis groups (0.35±0.04), while expression was high in the moderate (0.72±0.04, P<0.05) and severe stenosis groups (0.65±0.07, P<0.05). CHOP protein expression was not observed in the sham-operated group, while expression was high in the moderate and severe stenosis groups. These results indicated that Under maximum exposure to +Gz stress, different levels of CAS led to different levels of myocardial injury. Endoplasmic reticulum response is involved in the apoptosis of cardiomyocytes after +Gz stress.
authors.affiliation: Department of Cardiology, General Hospital of Air Force, PLA, Beijing 100142, China.
authors.forename: Haitao
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing,Institute of Heart Lung and Blood Vessel Disease, Ministry of Education, Beijing 100029, China.
authors.forename: Meng
authors.initials: M
authors.lastname: Chai
authors.affiliation: General Hospital of Air Force, PLA, Beijing 100142, China.
authors.forename: Chaozhong
authors.initials: C
authors.lastname: Liu
authors.affiliation: Department of Cardiology, General Hospital of Air Force, PLA, Beijing 100142, China.
authors.forename: Jinjin
authors.initials: J
authors.lastname: Sun
authors.affiliation: Department of Cardiology, General Hospital of Air Force, PLA, Beijing 100142, China.
authors.forename: Congchun
authors.initials: C
authors.lastname: Huang
authors.affiliation: Department of Cardiology, General Hospital of Air Force, PLA, Beijing 100142, China.
authors.forename: Xinya
authors.initials: X
authors.lastname: Yu
authors.affiliation: Animal Experimental Center of Fuwai Hospital, National Heart Center of China, Beijing, 100037, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Tian
authors.affiliation: Department of Cardiology, General Hospital of Air Force, PLA, Beijing 100142, China.
authors.forename: Huilan
authors.initials: H
authors.lastname: Luo
mesh_terms: D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D023921:Coronary Stenosis / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D004721:Endoplasmic Reticulum / Q000502:physiology*; D005260:Female; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D013482:Superoxide Dismutase / Q000378:metabolism; D013552:Swine; D013556:Swine, Miniature
chemical_list: D008315:Malondialdehyde; D013482:Superoxide Dismutase