Department of Anesthesiology, Huizhou Central People's Hospital, Huizhou, Guangdong 516001, China.
Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Comput Math Methods Med. 2022 Mar 20;2022:6267720. doi: 10.1155/2022/6267720. eCollection 2022.
Sufentanil is the most common drug in clinical practice for the treatment of ischemic heart disease. This study is to investigate the protective mechanism of sufentanil on rat myocardial ischemia-reperfusion (I/R) injury.
A rat I/R model was established by ligating the left anterior descending coronary artery. A total of 24 SD male rats were enrolled and divided randomly into the control group, I/R group, sufentanil group (SUF; 3 g/kg), and diltiazem group (DLZ; 20 mg/kg; positive control). The rat hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion. Subsequently, hemodynamics, pathological changes of myocardial tissue, serum biochemical parameters, oxidative stress factors, the level of serum inducible nitric oxide synthases (iNOS), interleukin-6 (IL-6), and other bioactive factors were analyzed in the rats.
Compared with the I/R group, sufentanil significantly improved cardiac action, myocardial fiber, and cardiomyocyte morphology and reduced inflammatory cell infiltration in rats in the SUF group. And the level of creatine kinase isoenzyme (CK-MB), troponin (cTn), lactate dehydrogenase (LDH), malondialdehyde (MDA), iNOS, and IL-6 was significantly declined in the serum of SUF group, while the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly activated in the myocardial tissues. In addition, sufentanil also significantly decreased the protein expression of GRP78, CHOP, Caspase 12, and ATF6 in the myocardial tissue of the SUF group.
Sufentanil has a significant protective activity on myocardial I/R injury in rats, the mechanism of which may be associated with the inhibition of endoplasmic reticulum stress and oxidative stress.
舒芬太尼是临床治疗缺血性心脏病最常用的药物。本研究旨在探讨舒芬太尼对大鼠心肌缺血再灌注（I/R）损伤的保护机制。
结扎大鼠左前降支冠状动脉建立大鼠 I/R 模型。共纳入 24 只雄性 SD 大鼠，随机分为对照组、I/R 组、舒芬太尼组（SUF；3μg/kg）和地尔硫卓组（DLZ；20mg/kg；阳性对照）。大鼠心脏缺血 30min 后再灌注 120min。随后，分析各组大鼠血流动力学、心肌组织病理变化、血清生化参数、氧化应激因子、血清诱导型一氧化氮合酶（iNOS）、白细胞介素-6（IL-6）等生物活性因子水平。
与 I/R 组相比，SUF 组大鼠心脏活动、心肌纤维和心肌细胞形态明显改善，炎性细胞浸润减少。SUF 组大鼠血清肌酸激酶同工酶（CK-MB）、肌钙蛋白（cTn）、乳酸脱氢酶（LDH）、丙二醛（MDA）、iNOS 和 IL-6 水平明显下降，心肌组织谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）活性明显升高。此外，SUF 组大鼠心肌组织 GRP78、CHOP、Caspase 12 和 ATF6 蛋白表达也明显下降。
舒芬太尼对大鼠心肌 I/R 损伤具有显著的保护作用，其机制可能与抑制内质网应激和氧化应激有关。
