Fumihiro Tanno

Case report of a heart transplantation in a 16-year-old male

We examined ultrastructural changes and did immunohistochemical studies of atrial natriuretic peptide (ANP) in biopsied samples obtained from the heart of a 16-year-old Japanese boy with dilated cardiomyopathy and from the transplanted donor heart. In the right ventricle of the diseased heart, a small number of atrial granules containing ANP were found in the perinuclear area of the cardiomyocytes and near areas lacking some myofibrils. Although no evidence of rejection was seen in the right ventricle of the transplanted donor heart under the light microscope, electron microscopy revealed moderate degeneration of cardiomyocytes and injuries to capillary endothelial cells. We did not find atrial granules, although the serum ANP level was elevated. These data suggest that the ultrastructural changes in the transplanted heart were related to a mild rejection, the effects of cyclosporin, or the effects of a domino heart transplantation from a patient with cystic fibrosis. Because of the absence of atrial granules in the right venticle, it is postulated that the high serum ANP level may be attributed to merely an increased secretion of ANP from atrial granules in the atria, without secretion of ANP in the ventricles.

Electron microscopic cytochemical studies on cardiac myocytes in acute ischemia

In acute myocardial ischemia induced by coronary occlusion in the canine heart, mild to moderate ultrastructural changes such as reduction in glycogen granules appeared around 20 min after coronary occlusion. Severe, irreversible alterations, including a mitochondrial dense deposit, appeared after 60 min. With cytochemical study, ATPase activity decreased at 30 min in the sarcoplasmic reticulum (SR) and on the myofibril preceded by activation of acid phosphatase activity in lysosomes and SR. Permeation of lanthanum ion from glycocalyx into the cytosol was observed 30 min after occlusion. These results indicate that activation of acid hydrolases and an inflow of excess Ca++ are likely to be two main causes of ischemic necrosis.