The effects of transmural pressure on prostacyclin release from porcine endocardial endothelial cells – comparison with vascular endothelial cells |
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| Authors: | S. Nosaka Michio Hashimoto Tetsuya Sasaki Kwansong Ku Yuhei Saitoh Masanobu Yamauchi Yoko Tanabe Toshio Nakaki Keiichi Hishikawa Sumio Masumura Kengo Nakayama Katsuhiro Tamura |
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| Affiliation: | (1) First Department of Surgery, Shimane Medical University, 89-1, Enya-cho, Izumo, Shimane 693, Japan, JP;(2) Department of Physiology, Shimane Medical University, 89-1 Enya-cho, Izumo, Shimane 693, Japan, JP;(3) Department of Pharmacology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan, JP;(4) Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Toyko 160, Japan, JP |
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| Abstract: | We assessed the effects of pressure on the release of prostacyclin (PGI2) from cultured endocardial endothelial cells (EECs) and vascular endothelial cells (VECs). EECs were harvested from the right ventricle (RV) and left ventricle (LV) of porcine hearts, and VECs from pulmonary artery (PA), aorta (Ao) and coronary artery (CA). Confluent EECs and VECs were incubated for 30 min under various pressures (0, 50, 100, 150 mmHg) and PGI2 release from each cell was measured. Pressure-induced PGI2 release from LV-EECs was larger than that from RV-EECs. Pressure also increased PGI2 release from both PA- and Ao-VECs, but not from CA-VECs. These findings suggest that endocardium can produce PGI2 in response to pressure and PGI2 released into the coronary blood from the ventricle may play an important role in the prevention of myocardial ischemia. Received: 13 August 1996 / Received after revision: 13 December 1996 / Accepted: 17 January 1997 |
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| Keywords: | Prostacyclin (PGI2) Endocardial endothelial cell (EEC) Vascular endothelial cell (VEC) Pressure |
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