TY - JOUR
T1 - Rat infarct model of myocardial infarction and heart failure
AU - Goldman, Steven
AU - Raya, Thomas E.
N1 - Funding Information:
Supported by grants from the Veterans Administration, the National Institute of Health (RO 1 HL-48163), Arizona Disease Control Research Commission (82-0697), and the Arizona Affiliate of the American Heart Association. Manuscript received September 13, 1994; revised manuscript received November 8, 1994; accepted November 8, 1994. Reprint requests: Dr. Steven Goldman, Cardiology Section, lllC, Tucson VA Medical Center, Tucson, AZ 85723.
PY - 1995/3
Y1 - 1995/3
N2 - This review outlines the development and current use of the rat coronary artery ligation model of heart failure. The techniques to ligate the left coronary artery and to obtain morphologic/hemodynamic measurements are described. The authors show how the pathology seen in this model relates to clinical ischemic heart disease. An effort is made throughout the review to relate the changes that occur in this model to clinically relevant observations. For example, the progression to heart failure in these rats is similar to what happens when a patient sustains a large myocardial infarction, survives, but goes on to develop heart failure without another ischemic insult. In both rats and people with large infarctions, the noninfarcted myocardium, even though not damaged at the time of the infarct, cannot compensate sufficiently to prevent the eventual development of heart failure. In addition to being a good approximation of human disease, the responses to pharmacologic interventions, like angiotensin converting enzyme inhibitors, in rats has proved useful in predicting what will happen in humans given the same treatment. More recent data on the molecular control of ventricular remodeling emphasizes how this model will provide important information in the study of integrated physiology by examining biochemical, pharmacologic, and physiologic changes in the same tissue.
AB - This review outlines the development and current use of the rat coronary artery ligation model of heart failure. The techniques to ligate the left coronary artery and to obtain morphologic/hemodynamic measurements are described. The authors show how the pathology seen in this model relates to clinical ischemic heart disease. An effort is made throughout the review to relate the changes that occur in this model to clinically relevant observations. For example, the progression to heart failure in these rats is similar to what happens when a patient sustains a large myocardial infarction, survives, but goes on to develop heart failure without another ischemic insult. In both rats and people with large infarctions, the noninfarcted myocardium, even though not damaged at the time of the infarct, cannot compensate sufficiently to prevent the eventual development of heart failure. In addition to being a good approximation of human disease, the responses to pharmacologic interventions, like angiotensin converting enzyme inhibitors, in rats has proved useful in predicting what will happen in humans given the same treatment. More recent data on the molecular control of ventricular remodeling emphasizes how this model will provide important information in the study of integrated physiology by examining biochemical, pharmacologic, and physiologic changes in the same tissue.
KW - congestive heart failure
KW - coronary artery ligation
KW - ventricular remodeling after infarction
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U2 - 10.1016/1071-9164(95)90019-5
DO - 10.1016/1071-9164(95)90019-5
M3 - Review article
C2 - 9420647
AN - SCOPUS:0029257791
SN - 1071-9164
VL - 1
SP - 169
EP - 177
JO - Journal of cardiac failure
JF - Journal of cardiac failure
IS - 2
ER -