Meeting Abstract

P2.77  Tuesday, Jan. 5  Python model of pathological cardiac hypertrophy REAVES PIERCE, Holland*; RIQUELME, Cecilia A.; LEINWAND, Leslie A; SECOR, Stephen M.; University of Alabama; University of Colorado; University of Colorado; University of Alabama hipierce@crimson.ua.edu

Cardiac hypertrophy is a physiologic/morphologic response to volume (‘physiological hypertrophy’) or pressure (‘pathological hypertrophy’) overload. Burmese pythons experience with feeding physiological cardiac hypertrophy, evident by a 20-30% increase in heart mass. Because pathological cardiac hypertrophy characterizes human heart disease and failure, mammalian models of pathological cardiac hypertrophy have been developed using transverse aortic constriction to generate chronic pressure overload. We modified this procedure for the python by completely ligating the left systemic artery, thereby forcing all cardiac output through the right systemic arch. This procedure has not resulted in any mortality and ligated pythons are active and feeding for many months. Compared to hearts of fasted, non-ligated snakes, ligation has generated a 20% increase in ventricular mass within one month, a level of increase observed for similar-size non-ligated pythons (500 – 550g) digesting rodent meals. When exposed to the combination of ligation and meal digestion, pythons responded with a 32% increase in ventricular mass. A morphological characteristic of pathological cardiac hypertrophy for mammals is an increase in interstitial connective tissue content. Using Masson’s trichrome staining we observed a slight increase in the presence of fibrotic tissue for hearts from ligated snakes. In addition to exhibiting physiological cardiac hypertrophy during digestion, pythons potentially respond to pressure overload with pathological hypertrophy and hence increase their utility as a model to explore the signaling and cellular mechanisms of cardiac hypertrophy.