Effects of ventricular unloading on apoptosis and atrophy of cardiac myocytes. J Surg Res 2004 Jul;120(1):119-26
Date
06/03/2004Pubmed ID
15172198DOI
10.1016/j.jss.2003.10.006Scopus ID
2-s2.0-2542486290 (requires institutional sign-in at Scopus site) 22 CitationsAbstract
BACKGROUND: Ventricular unloading decreases cardiac ventricular mass. This loss of ventricular mass can be due to either atrophy (a reversible process) or apoptosis (an irreversible process) of the cardiac myocytes. We investigated the effect of ventricular unloading on atrophy and apoptosis of cardiac myocytes, using working and nonworking transplant heart models in rats.
MATERIALS AND METHODS: ACI rats underwent heterotopic heart transplantation with two different techniques to create working and nonworking cardiac grafts. Cardiac grafts were harvested at different time points after transplantation. TUNEL, caspase-3 assay, and electron microscopy were used to assess the degree of apoptosis while cellular atrophy was estimated by calculation of the cytoplasmic index (CI = mean sectional cytoplasmic area/nucleus).
RESULTS: Ventricular mass reduction was more pronounced in nonworking than in working hearts (P < 0.05). Apoptotic index and caspase-3 activities increased in both groups, peaking at 3 days after transplantation, but were not significantly different between the two models. The cytoplasmic index was significantly lower in nonworking than in working grafts (P < 0.05).
CONCLUSIONS: These data suggest that cellular atrophy is the primary mechanism that accounts for myocardial weight reduction following ventricular unloading. The inference is that ventricular unloading by ventricular assist devices may not cause permanent loss of cardiac myocytes, thus allowing for functional recovery.
Author List
Schena S, Kurimoto Y, Fukada J, Tack I, Ruiz P, Pang M, Striker LJ, Aitouche A, Pham SMAuthor
Stefano Schena MD, PhD Associate Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsApoptosis
Atrophy
Heart Transplantation
Heart-Assist Devices
Male
Models, Animal
Myocytes, Cardiac
Organ Size
Rats
Rats, Inbred ACI
Ventricular Function