Experimental pulmonary hypertension induced by constriction of the pulmonary arteries resulting in rupture or extraordinary dilatation of the right ventricle after administration of a little amount of Na2EDTA

Summary Our earlier studies on the hypocalcemic condition have focused on the histological distortion of the organ structure with the removal of the calcium ion from the molecular structure of acid mucopolysaccharides (AMPs); resulting in the sol-gel diversion of the matrix. Bivalent cationic materials including calcium are related not only to function but also to structural alteration of the living organism ( Yamaguchi et al. 1978, 1981, 1982, 1985, 1991). The ionic shift from the structural phase to the functional phase induced a number of morphological distortions of the various organs. In the present paper, starting our research from a different experimental viewpoint, we decreased the Na 2 EDTA dose used to prevent the conventional typical tetanic shock which sometimes results in animal death. We expected this decreased dose to induce mild constriction of muscle cells. In our experiment, administration of a small amount of Na 2 EDTA intraperitoneally provoked animal death after 10 days to two weeks over a two-month period. In the initial phase of 10 days to two weeks, rupture of the right ventricular wall along the septum occurred at an anterior angle with moderate right ventricular dilatation and a remarkably thin ventricular wall. Characteristic of these cases was elastosis between the medial smooth muscle cells of the main pulmonary arteries accompanied by a severe degree of constriction. On the other hand, demonstrated in the delayed cases of between more than two weeks to two months there was severe dilatation of the right ventricular lumina with paper-like thinness of the wall. In these cases, the main pulmonary arteries showed rather slight constriction with scarce elastosis. Conversely, the peripheral pulmonary arteries showed extraordinary constriction with marked vacuolar formation in the media where red blood cells could hardly pass through. These results confirmed that actual constriction at various sites of the pulmonary arteries, resulting in extraordinary pulmonary hypertension basically plays an essential role in the provocation of these changes. Also considering the effects on the heart, depending on the constriction site of the pulmonary arteries, alternatives could include rupture or not.