A murine model of ischemic cardiomyopathy induced by repetitive ischemia and reperfusion. 2004

O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
Section of Cardiovascular Sciences and DeBakey Heart Center, Baylor College of Medicine, and The Methodist Hospital, Houston, TX, USA. Oliver.Dewald@ukb.uni-bonn.de.

BACKGROUND Repetitive brief myocardial ischemia has been implicated in the pathogenesis of the ventricular dysfunction associated with ischemic cardiomyopathy and myocardial hibernation. In this study we examine the effects of repetitive ischemia and reperfusion (I/R) on murine myocardium. METHODS C57/BL6 mice underwent daily 15 min left anterior descending coronary occlusions followed by reperfusion. After 3, 5, 7, 14, 21 and 28 days, echocardiographic studies were performed, and hearts of I/R and sham-operated animals were processed for histological examination. RESULTS Histological studies showed no evidence of myocardial necrosis in the ischemic region. Quantitative assessment of collagen revealed a marked persistent interstitial deposition of collagen after seven days I/R in the anterior left ventricular wall (sham 4.6 +/- 2.0 %, I/R 21.5 +/- 6.5 %, p < 0.05). Echocardiographic studies showed persistent regional anterior wall dysfunction in I/R animals. Histological evaluation showed absence of neovessel formation. After discontinuation of the I/R protocol, fibrosis and regional ventricular dysfunction decreased within 60 days. CONCLUSIONS Repetitive brief murine myocardial I/R induces reversible fibrotic remodeling and ventricular dysfunction, without myocardial infarction and necrosis, and may play a role in the pathogenesis of ischemic cardiomyopathy and myocardial hibernation.

UI MeSH Term Description Entries
D008810 Mice, Inbred C57BL One of the first INBRED MOUSE STRAINS to be sequenced. This strain is commonly used as genetic background for transgenic mouse models. Refractory to many tumors, this strain is also preferred model for studying role of genetic variations in development of diseases. Mice, C57BL,Mouse, C57BL,Mouse, Inbred C57BL,C57BL Mice,C57BL Mice, Inbred,C57BL Mouse,C57BL Mouse, Inbred,Inbred C57BL Mice,Inbred C57BL Mouse
D009206 Myocardium The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow. Muscle, Cardiac,Muscle, Heart,Cardiac Muscle,Myocardia,Cardiac Muscles,Heart Muscle,Heart Muscles,Muscles, Cardiac,Muscles, Heart
D009336 Necrosis The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D005260 Female Females
D005355 Fibrosis Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. Cirrhosis,Fibroses
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D015427 Reperfusion Injury Adverse functional, metabolic, or structural changes in tissues that result from the restoration of blood flow to the tissue (REPERFUSION) following ISCHEMIA. Ischemia-Reperfusion Injury,Injury, Ischemia-Reperfusion,Injury, Reperfusion,Reperfusion Damage,Damage, Reperfusion,Injury, Ischemia Reperfusion,Ischemia Reperfusion Injury,Ischemia-Reperfusion Injuries,Reperfusion Damages,Reperfusion Injuries
D017202 Myocardial Ischemia A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION). Heart Disease, Ischemic,Ischemia, Myocardial,Ischemic Heart Disease,Disease, Ischemic Heart,Diseases, Ischemic Heart,Heart Diseases, Ischemic,Ischemias, Myocardial,Ischemic Heart Diseases,Myocardial Ischemias
D017682 Myocardial Stunning Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity. Hibernation, Myocardial,Myocardial Hibernation,Stunned Myocardium,Myocardium, Stunned,Stunning, Myocardial

Related Publications

O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
May 2007, Circulation journal : official journal of the Japanese Circulation Society,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
December 1995, The American journal of physiology,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
September 2014, JACC. Cardiovascular imaging,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
January 2018, Methods in molecular biology (Clifton, N.J.),
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
February 1988, Revista espanola de cardiologia,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
May 2016, Journal of visualized experiments : JoVE,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
July 2012, Journal of visualized experiments : JoVE,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
February 2016, Experimental and therapeutic medicine,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
June 1998, The Journal of thoracic and cardiovascular surgery,
O Dewald, and N G Frangogiannis, and M P Zoerlein, and G D Duerr, and G Taffet, and L H Michael, and A Welz, and M L Entman
September 2019, American journal of physiology. Renal physiology,
Copied contents to your clipboard!