Effects of propofol on myocardial ischemia-reperfusion injury in rats with type-2 diabetes mellitus

Abstract

Abstract. The current study aimed to examine the effects of propofol on myocardial ischemia-reperfusion injury (MIRI) in rats with type-2 diabetes mellitus (T2DM) and to assess the role of inflammatory mediators. Fifty healthy male adult Sprague-Dawley rats were randomly divided into the sham, ischemia-reperfusion (IR), IR plus low, middle and high-dose (6, 12 and 24 mg/kg/h, intravenous) propofol groups. The rats of all the groups were fed a high-sugar and high-fat diet for 8 weeks and streptozotocin (30 mg/kg, intraperitoneally) was used to establish the T2DM model. Apart from the sham group rats, MIRI was induced by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for 2 h. Heart rate (HR), left ventricular systolic pressure (LVSP), and the rate of left ventricular pressure increase in early systole (± dp/dt max ) were recorded. Levels of cardiac troponin T (cTnT), nitric oxide (NO), endothelin-1 (ET-1), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were also measured. Myocardial lesions were observed under light microscopy and scanning electron microscopy. Compared with levels prior to arterial occlusion, HR, LVSP, and ± dp/dt max were significantly reduced (P<0.05) following occlusion for 30 min and reper fusion for 2 h. The administration of propofol ameliorated the cardiac function of rats as reflected by the increase in HR, LVSP and ± dp/dt max . In addition, the administration of propofol increased the serum NO concentration, and reduced ET-1 and cTnT levels, as well as levels of inflammatory mediators including IL-1β, IL-6 and TNF-α. Thus, propofol exerts protective effects against MIRI in T2DM rats by increasing NO and reducing ET-1 and the inflammatory mediators.

The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice

“…The underlying radio-protective mechanisms were explored further, and consistent with previous studies, 7,17,18 propofol decreased the ROS levels in LSKs and HPCs. It has been reported that propofol can alleviate transplanted liver damage 15 through the Nrf2 pathways.…”

“…8 Propofol can also decrease ROS levels in a myocardial ischemia-reperfusion injury model in vitro and alleviate myocardial injury caused by postreperfusion. 17,18 Moreover, propofol attenuates intestinal ischemia-reperfusion injury by scavenging ROS, 7 improves Parkinson's disease by activating antioxidant enzyme activity, and inhibits lipid peroxidation in heart, liver, kidney, and lung tissue. 19 In summary, the anti-oxidative effect of propofol protects against a variety of tissue damage caused by oxidative stress.…”

An increasing electromechanical window is a predictive marker of ventricular fibrillation in anesthetized rabbit with ischemic heart

“…These results indicate that the model of acute myocardial ischemia performed by coronaries ligation was successfully established. Similar results were found in previous works of rabbits and other species [ 2 , 4 , 29 , 39 ].…”

Propofol induces nuclear localization of Nrf2 under conditions of oxidative stress in cardiac H9c2 cells

“…These results suggest that propofol-induced Nrf2/HO-1 expression is increased in the early stage of reperfusion at penumbra region. Wang et al reported that administration of propofol ameliorated the cardiac function of rats at 2 h after reperfusion [ 23 ]. It is presumed that the expression of Nrf2 and its downstream enzyme including HO-1 are elevated in the early reperfusion stage and contribute to restoration of cardiac function.…”