动物造模 z-bio 2022-07-11 269

　　Objective: To investigate the changes of cardiac electrophysiology and cardiac function after amputation in rats and their relationship with endothelial nitric oxide synthase/nitric oxide (eNOS/NO) pathway.

　　Methods: The left hind limb trauma model was established, and the rats were divided into normal group (anesthesia only), amputation control group, amputation 0.25h, amputation 0.5h, amputation 0.75h, amputation 1.5h, 12 in each group. Electrocardiogram (ECG) The changes of heart rate, QT interval and PR interval of rats were detected; left ventricular ejection fraction (LVEF) and left ventricular short-axis shortening rate (LVFS) were detected by ultrasound; The highest rate of increase in left ventricular pressure (+dp/dtmax), the highest rate of decrease in left ventricular pressure (-dp/dtmax); kits to detect malondialdehyde (MDA), superoxide dismutase (SOD) in serum and myocardial tissue ), nitric oxide (NO), myeloperoxidase (MPO), tumor necrosis factor-ɑ (TNF-ɑ) and interleukin-6 (IL-6) levels; hematoxylin-eosin staining (HE) The morphological changes of myocardial tissue were observed by staining; the apoptosis of myocardial tissue was observed by TUNEL staining; eNOS, B-lymphoma-2 protein (Bcl-2) and Bcl-2 in myocardial tissue were detected by Western blotting. Associated X protein (Bax) protein expression.

　　Results: Compared with the normal group, the heart rate increased at 0.5h and 0.75h after amputation, the QT interval decreased, LVSP, +dp/dmax, -dp/dmax, LVEF, LVFS decreased, MPO, MDA, TNF-ɑ, IL -6 increased, SOD decreased, cell arrangement was loose and necrotic, accompanied by a large number of inflammatory cell infiltration; myocardial cell apoptosis index increased, myocardial tissue Bcl-2 protein expression decreased, Bax protein expression increased, NO level, eNOS The protein expression decreased in a time-dependent manner, and the difference was significant (P<0.05); compared with 0.75h after amputation, heart rate decreased at 1.5h, QT interval, PR interval increased, LVSP, +dp/dmax, - dp/dmax, LVEF, LVFS increased, MPO, MDA, SOD, TNF-ɑ, IL-6 decreased, and the degree of myocardial pathological damage was alleviated; myocardial apoptosis index decreased, Bcl-2 protein expression increased, Bax protein increased. The expression decreased, the level of NO and the expression of eNOS protein increased, and the difference was significant (P<0.05).

　　Conclusion: Amputation trauma can cause ischemic ECG changes, impaired cardiac function, excessive oxidative stress, and inflammatory injury in rats, and the mechanism may be related to the inhibition of eNOS/NO pathway.