Left atrial endocardium and prostacyclin.
In patients with rheumatic mitral stenosis, intracardiac thrombi are found mostly, for reasons still unknown, in the left atrium. We compared the release of PGI2 from the endocardium of the left atrium with that of the right ventricle and from the endothelium of the pulmonary arteries. Endocardial endothelial cells (EECs) were isolated from right ventricles (RV) and left atrial appendages (LAA) of porcine hearts, and vascular endothelial cells (VECs) from pulmonary arteries (PA) were obtained from the same animals. Cultured EEC and PA-VEC monolayers were placed in a pressure loading apparatus and incubated for 30 min under various pressures. After incubation, the supernatants were sampled and the 6-keto-PGF1 alpha contents measured. PGI2 release from LAA-EEC was much less than from RV-EEC or from PA-VEC. Moreover, transmural pressure did not enhance PGI2 release from LAA-EEC, although it did from RV-EEC and PA-EEC in a pressure-dependent manner. These results may explain why the left atrium is a common site for intracardiac thrombus formation in patients with mitral valve disease.
First Department of Surgery, Shimane Medical University, Japan.
S
S
Nosaka
M
M
Hashimoto
T
T
Sasaki
T
T
Hanada
M
M
Yamauchi
K
K
Nakayama
S
S
Masumura
K
K
Tamura
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000818:Animals; D002478:Cells, Cultured; D004699:Endocardium / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism*; D006325:Heart Atria / Q000378:metabolism*; D006352:Heart Ventricles / Q000378:metabolism; D006801:Humans; D008946:Mitral Valve Stenosis / Q000473:pathology; D011312:Pressure; D011651:Pulmonary Artery / Q000378:metabolism; D013552:Swine; D013927:Thrombosis / Q000473:pathology
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol