A Novel and Efficient Model of Coronary Artery Ligation and Myocardial Infarction in the Mouse

Abstract

Rationale: Coronary artery ligation to induce myocardial infarction (MI) in mice is typically performed by an invasive and time-consuming approach that requires ventilation and chest opening (classic method), often resulting in extensive tissue damage and high mortality. We developed a novel and rapid surgical method to induce MI that does not require ventilation.Objective: The purpose of this study was to develop and comprehensively describe this method and directly compare it to the classic method. Key Words: myocardial ischemia Ⅲ myocardial ischemia/reperfusion injury Ⅲ cardiac injury Ⅲ cardiac dysfunction Ⅲ mouse model C ardiovascular disease represents the leading cause of morbidity and death in developed countries. Coronary heart disease, which is the single largest cause of cardiovascular disease, is the narrowing of arteries over time caused by atherosclerotic plaques or the acute occlusion of the coronary artery by thrombosis, both of which lead to possible myocardial infarction (MI) and the eventual development of heart failure. 1,2 Protection from coronary heart disease-induced damage of the myocardium during myocardial ischemia/ reperfusion (I/R) injury has been a target of investigation for the development of innovative cardioprotective therapies. [3][4][5][6][7] The increase in the availability of various types of genetically manipulated mice has brought about the need for more efficient ways to induce myocardial damage for both molecular mechanistic studies and potentially therapeutic interventions. Two of the most common models used by researchers are permanent left main descending coronary artery (LCA) occlusion to induce a MI and also temporary coronary artery occlusion to induce I/R injury. 8,9 The I/R model is generally used to examine the short-term consequences of ischemic injury, whereas the MI model is usually used to investigate myocardial changes such as remodeling that occur over an extended period of time. Although a variety of surgical manipulations have been used during the past decade to induce the ischemic event, ligation of the LCA is still the most commonly practiced method. 3,9 -11 However, most investigators still use a method requiring ventilation and wide opening the chest (referred to as the classic method), which can cause extensive tissue damage, high surgical-related death and can also be quite time consuming for most surgeons. [12][13][14][15] Over the last few years, we have developed a new MI approach in mice that does not require ventilation. 11,16 -18 Complete characterization and description of this model has Original Methods and Results:

Postinfarction Hearts Are Protected by Premature Senescent Cardiomyocytes Via GATA4‐Dependent CCN1 Secretion

“…Eight‐ to 12‐week‐old male littermate mice were used in the study and randomization was performed. Experimental AMI was produced by ligation of the left anterior descending coronary artery as described previously 19. All animal experimental procedures were performed under the Guide for the Care and Use of Laboratory Animals and were approved by the Institutional Animal Care and Use Committee of Shandong University 20…”

Aging might increase myocardial ischemia / reperfusion-induced apoptosis in humans and rats

“…Left ventricular (LV) function was continuously monitored via a Millar Mikro-Tip catheter pressure transducer inserted into the LV via left carotid artery as previously described (Gao et al 2010). Left ventricular end diastolic pressure (LVDEP), left ventricular systolic pressure (LVSP), and rate of rise of left ventricular pressure (±dp/dt) were derived by computer algorithms (Chengdu Instrument Co., Chengdu, China).…”

Use of bone mesenchymal stem cells to treat rats with acute liver failure

“…Subsequently, the cells that adhere to the blood vessel endothelium, permeate the vessel walls to access the target tissue. With the help of SDF-1α, the secretion of more MMP-9, NO, and VEGF promote the mobilization of stem cells (Tang et al, 2007;Kuang et al, 2008;Gao et al, 2010;Huang et al, 2010;Takamiya et al, 2011). These paracrine factors, especially VEGF, are important for maintaining or improving normal vascular endothelial function.…”