Comparison between endocardial and great vessel endothelial cells: morphology, growth, and prostaglandin release.

Abstract

The release of vasoactive mediators by vascular (VEC) and endocardial endothelial cells (EEC) has not been directly compared. In this study, in vitro morphological and cell growth characteristics and the rate of prostanoid release were compared in cultured sheep endothelial cells from great vessels (VEC; pulmonary artery and aorta) and endocardium (EEC; right and left ventricles) harvested from the same animals. Morphologically, in flasks, VEC demonstrated the classic cobblestone pattern, whereas EEC developed numerous cytoplasmic interdigitations and overlaps. Rate of cell proliferation was greater for EEC than for VEC (P < 0.05): doubling time was shorter for EEC (34 +/- 3 h) than for VEC (45 +/- 5 h). Under static (no-flow) conditions, in response to arachidonic acid and calcium ionophore A-23187, the rate of prostacyclin (PGI2) and prostaglandin E2 release by VEC and EEC was not different. In contrast, in response to flow and acute hypoxia (O2 tension = 35 Torr), the rate of PGI2 release was greater in EEC than in VEC (P < 0.0001). After 2 h of perfusion, the rate of PGI2 release was 19-fold greater for EEC than for VEC during normoxia and 34-fold greater during hypoxia. Thus our study showed anatomic site of origin-dependent heterogeneity in prostanoid release between VEC and EEC. Endocardial endothelium is a greater source of PGI2 than great vessel endothelium; in vivo, endocardial endothelial PGI2 may inhibit local platelet aggregation and modulate downstream vascular tone.