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Seth D. Blank
Joseph A. Lahorra
Robert S. McDonald
David F. Torchiana
Willard M. Daggett
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Ann Thorac Surg 1998;65:390-396
© 1998 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Superior Recovery of Hypertrophied Rat Myocardium After Cardioplegic Arrest

Seth D. Blank, MD, Joseph A. Lahorra, MD, Robert S. McDonald, MD, Alvin G. Denenberg, MS, James S. Titus, David F. Torchiana, MD, Willard M. Daggett, MD, Gillian A. Geffin, MB, BS

Departments of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA

Accepted for publication July 20, 1997.

Dr Daggett, Surgical Cardiovascular Unit, Massachusetts General Hospital BUL-119, Fruit St, Boston, MA 02114.

Background. Although cardioplegic protection of the hypertrophied heart remains a clinical challenge, we have previously observed enhanced recovery in rat hearts with pressure-overload hypertrophy induced by aortic banding. We investigated whether this unexpected result is found in other models of hypertrophy.

Methods. Hearts with hypertrophy induced by aortic banding or administration of desoxycorticosterone acetate were each compared with age-matched sham-operated and nonoperated controls. Spontaneously hypertensive rats and Wistar-Kyoto controls were also compared. We evaluated left ventricular isomyosin distribution by gel electrophoresis and recovery of isolated working rat hearts arrested at 8°C for 2 hours.

Results. The percentage of V3 isomyosin in hearts with hypertrophy from aortic banding or administration of desoxycorticosterone acetate was increased compared with the control groups. Recovery of aortic flow in all three groups of hypertrophied hearts was at least as good or better than their respective controls. There were no significant differences in ATP or glycogen between hypertrophied and control hearts before or after arrest.

Conclusions. Enhanced recovery of hypertrophied hearts is not specific to a single model. This level of recovery may be supported by induction of a "fetal genetic program," exemplified in the rat by the shift in isomyosin from predominantly V1 to the more efficient V3 isoform, which occurs in pressure-overloaded hearts.






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