A conglomeration of preclinical models related to myocardial infarction

Abstract

Cardiovascular diseases are the main source of death and morbidity in developed and developing nations. Animal models are required to propel our understanding of the pathogenesis, increase our knowledge, disease progress, and mechanism behind cardiovascular disorder, providing new approaches focused to improve the diagnostic and the treatment of these pathological conditions and additionally to test various therapeutic ways to deal with tissue regeneration and re-establish heart working following damage. A perfect model framework ought to be reasonable, effectively controlled, reproducible, and physiologically illustrative of human disease, show cardinal signs and pathology that resembles after the human ailment and ethically stable. The decision of selection of animal model should be considered precisely since it influences exploratory results and whether results of the research can be sensibly matched with the human. In this way, no specific technique splendidly reproduces the human disease, and relying upon the model, extra cost burden, resources, infrastructure and the necessity for technical hands, should also be kept under consideration. Here we have discussed and compiled various methods of inducing myocardial infarction in animals, basically by surgery, chemicals and through genetic modification, this may benefit the researchers in getting a complied data regarding various methods through which they can induce myocardial infarction in animals.

Effectual Endeavors of Silk Protein Sericin against Isoproterenol Induced Cardiac Toxicity and Hypertrophy in Wistar Rats

“…A nomenclature was performed for all different experimental groups and the codes were written on the cages. Animals were fed with rodent specific pellet diet (Dayal animal feed) and normal drinking water ad libitum during this study [ 7 ].…”

“…Isoproterenol, produces highly cytotoxic free radicals which are used to stimulate peroxidation of membrane phospholipids leading to severe damage to the membrane of the myocardium resulting in an infarct-like necrosis of the cardiac tissue in experimental animal. ISO-induced myocardial necrosis establishes a well-standardized model for the reason that the pathophysiological changes in cardiac muscle of experimental animals are analogous to that perceived in human myocardial infarction or necrosis [ 7 ].…”

D-limonene (5 (one-methyl-four-[1-methylethenyl]) cyclohexane) diminishes CCl4-induced cardiac toxicity by alleviating oxidative stress, inflammatory and cardiac markers

“…CCl 4 is used as a chemical agent to induce myocardial infarction/cardiotoxicity. It mimics the pathology close to humans by producing free radicals, a rate-limiting process in cellular peroxidative damage [ 17 ]. These free radicals and other related oxidative species cause oxidative stress, which produces significant interrelated changes in cellular metabolism, thus increasing the calcium level inside the cell, which further causes damage to the permeability and transport of ions through the membrane and destroys the cells by LPO.…”

“…These free radicals and other related oxidative species cause oxidative stress, which produces significant interrelated changes in cellular metabolism, thus increasing the calcium level inside the cell, which further causes damage to the permeability and transport of ions through the membrane and destroys the cells by LPO. This model has been seen to elevate lactate dehydrogenase (LDH), creatine kinase (CK), and malondialdehyde (MDA) levels and alleviate the level of antioxidant enzyme armoury, which includes SOD, CAT, and GPx levels in the heart, indicating that the heart can be targeted by CCl 4 [ 17 , 18 ]. It has also been reported that the release of ROS can lead to myocardial ischaemia with subsequent cell injury and mitochondrial dysfunction.…”