Ultrastructural observation in clinical and experimental myocardial infarction, with reference to pathogenesis.

Electron microscopic investigation was carried out to confirm our hypothesis, derived from a large number of macroscopic and light-microscopic observations, that impairment of the peripheral circulation of the myocardium, and not the presence of coronary thrombi, plays the fundamental role in the development of acute myocardial infarction. The peripheral coronary vessels of 5 human hearts obtained at autopsy showed severe histolytic impairment of the endothelial cells and of the tunica media muscle cells, even though no myocardial necrosis was observed either macroscopically or microscopically. An additional experimental study using 12 rabbits was performed to ascertain the induction of myocardial necrosis without coronary occlusion, by intravenous administration of either epinephrine or endotoxin alone or a combination of both. One-third of the epinephrine group and all of the combined treatment group developed myocardial necrosis. The intramyocardial vessels of these rabbits showed similar hystolytic changes to those observed in human cases. These findings support our concept that derangement of the peripheral circulation precedes the development of a coronary thrombus in cases of acute myocardial infarction.

[Healing of operative cardiac wounds].

Healing process of operative cardiac wounds was studied histopathologically in 14 patients who died 28 hours to 5 years after the operation of cardiac valve replacement. Repair of wounds in aorta and free wall of atrium was characterized by production of neointima and proliferation of collagen fiber at adventitia of aorta or epicardium of heart. Adhesion with granulation tissue at left ventricular venting wounds was observed in the case of 18th post-operative day. Reticulofibrosis of surrounding intracardiac muscle played an important role in development of granulation tissue. Cicatrix with collagen fiber was appeared from one month after the operation. In spite of attenuation of ventricular scar, aneurysmal bulging could not be observed. The basic healing pattern of wound in atrial septum was production and thickening of neointima. Granulation tissue rarely developed at the septum. Adhesion between sutured edges of atrial septal endocardium could not be observed and the dead space there remained over a period of 7 months after the operation. These findings indicated the continuous presence of unexpected weakness of the sutured septum until sufficient thickening of neointima had developed.

Immune complex-mediated glomerulonephritis and interstitial pneumonia simulating Goodpasture's syndrome.

An autopsy case of what was clinically considered to be Goodpasture's syndrome was investigated. The lung had hemorrhagic interstitial pneumonia, showing granular patterns of IgG and C3 along the alveoli by the immunofluorescent method and electron-dense subepithelial deposits by electron microscopy. The kidney had crescentic and segmental necrotizing glomerulonephritis associated with membranous nephropathy. Uneven, continuous patterns of immunofluorescent IgG and C3 along the GBM were noted. Electron microscopy showed numerous subepithelial deposits, and immunoelectron microscopy revealed that IgG was not present in the GBM itself but present in the subepithelial deposits. Anti-GBM antibody activity was not detected in the serum or the kidney eluate. It was suggested that renal and pulmonary lesions occurred through the same mechanism and in association with immune deposits. We propose that there is a disease having immune complex-mediated deposits. We propose that there is a disease having immune complex-mediated renal and pulmonary lesions which clinically resembles the conventional Goodpasture's syndrome.

A histopathological study on diabetic nephropathy -- light and electron microscopic observations.

A historical review and the present author's study on diabetic nephropathy have been presented. Three characteristic lesions in KW-lesion, namely nodular, exudative and doughnut lesion may all be regarded as to be caused by severe circulatory disturbance occurring in intraglomerular branches of the afferent artery. This circulatory disturbance is considered to be brought about by sudden spasm of the peripheral portion of the afferent branches. The diffuse form of Bell may be regarded as to be a slighter type without severe mesangiolysis. Arteriolar hyalinosis and arteriosclerosis and/or atherosclerosis may be caused by intraglomerular circulatory disturbances. The most important problem in diabetic nephropathy, including KW-lesion and Bell's diffuse form, is to elucidate the mechanism leading to the occurrence of spasm of the peripheral portion of intraglomerular afferent branches. Becker found fixation of antiactomyosin-antibody in the mesangial tissue by the immunofluorescent method. Many studies along this line have been made, but none are adequate in fully explaining the mechanism involved.