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1 The Division of Cardiology, University of Utah, Salt Lake City, UT, USA
2 The Division of Endocrinology, Metabolism and Diabetes, University of Utah, Salt Lake City, UT, USA; The Division of Cardiology, University of Utah, Salt Lake City, UT, USA
3 The Division of Endocrinology, Metabolism and Diabetes, University of Utah, Salt Lake City, UT, USA; The Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT, USA
4 The Division of Cardiology, Salt Lake City Veterans Affairs Medical Center, Salt Lake City, UT, USA; The Division of Cardiology, University of Utah, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: sheldon.litwin{at}hsc.utah.edu.
We have developed a minimally invasive method for producing left ventricular pressure-overload in mice. Using this technique we quickly and reproducibly banded the transverse aorta with low surgical morbidity and mortality. Minimally invasive transverse aortic banding (MTAB) acutely and chronically increased left ventricular (LV) systolic pressure, increased heart weight/body weight and induced myocardial fibrosis. We used this technique to determine whether reduced insulin signaling in the heart altered the cardiac response to pressure-overload. Mice with cardiac myocyte restricted knock out of the insulin receptor (CIRKO) have smaller hearts than wild type (WT) controls. Four weeks after MTAB, WT and CIRKO mice had comparably increased LV systolic pressure, increased cardiac mass and induction of mRNA for 
-myosin heavy chain and atrial natriuretic factor. However, CIRKO hearts were more dilated, had depressed left ventricular systolic function by echocardiography and had greater interstitial fibrosis than WT. Expression of connective tissue growth factor was increased in banded CIRKO hearts compared to WT. Thus, lack of insulin signaling in the heart accelerates the transition to a more decompensated state during cardiac pressure-overload. The use of the MTAB approach should facilitate the study of the pathophysiology and treatment of pressure-overload hypertrophy.
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