We studied ultrastructurally cerebral perforating arteries in 60 stroke-prone spontaneously hypertensive rats (SHRSP), which were sequentially killed at 4-52 weeks of age before showing symptoms of stroke. Another 24 SHRSP were killed soon after they showed symptoms of cerebral infarction. The initial vascular lesions observed in the asymptomatic group included focal cytoplasmic necrosis in the outer layers of the media. This change progressed to widespread medial necrosis with time. In the infarction group, numerous monocytes were seen adhering to the endothelium of the arteries having advanced medial damage. Following the adherence of monocytes to the endothelium, large amounts of plasma components were visible in the arterial wall. The accumulation of the plasma components (especially fibrin) thickened the wall, narrowed the lumen, and resulted in occlusion. These results suggest that monocytes may affect the endothelium, perhaps disturbing the so-called blood-brain barrier to proteins. The monocytes may therefore be closely related to the occurrence of arterial occlusion with resultant cerebral infarction.

The distribution of 3H-diltiazem in myocardial cell organelles was studied using an electronmicroscopic autoradiographic technique. At 3, 5 and 10 min after 3H-diltiazem injection, silver grains, which indicate the existence of diltiazem, were detected in plasma membranes and intracellular organelles. Silver grains in T systems were observed more frequently at 3 min than at 5 and 10 min. In contrast, silver grains in sarcoplasmic reticula and mitochondria apparently increased with the passage of time. These findings suggest that diltiazem is transported through the T system and may accumulate within the sarcoplasmic reticula and mitochondria. Furthermore, our study revealed morphologically for the first time that the intracellular sites of action where diltiazem was directed were possibly the mitochondria.

Permeability of brain capillaries of stroke-prone spontaneously hypertensive rats (SHRSP) was studied using labelling (horseradish peroxidase) and cytochemical techniques at the cellular level. In the cerebral capillary endothelium the tracer molecules were quickly transported by abundant transendothelial channels which directly connected the capillary lumen to the subendothelial space. Transendothelial channels are abundant and should be postulated as structural formations engaged in the increased transport of proteins across the capillary endothelium. Ultracytochemical studies revealed that the channels, bounded by indistinct delimiting membranes, initially had no acid phosphatase activity. With the passage of time, however, the channels showed acid phosphatase activity and were lined with distinct membranes. These observations suggested that the lysosomes might fuse with the transendothelial channels and might play an important part in the transport of macromolecules.

Permeability of intracranial extracerebral arteries of stroke-prone spontaneously hypertensive rats (SHRSP) was studied using labeling techniques (ferritin and horseradish peroxidase), at the cellular level. In the arterial endothelial cells, the tracer molecules were slowly but constantly transported by the plasmalemmal vesicles to the subendothelial space. This endothelial transportation of the tracers into these cerebral arteries did not seem to be significantly influenced by aging, increased blood pressure, hyperlipidemia or the existence of cerebral bleeding and infarction. Around the adventitia, there were a great number of periadventitial capillaries, especially near bifurcations. In the periadventitial capillaries, the tracer molecules were readily trapped by endothelial cells and were quickly transported to pericapillary spaces. The tracer molecules were then detected in the phagocytes adjacent to the deeper layers of the media, and further in the medial smooth muscle cells. The possibility that large amounts of plasma components are supplied to the media from periadventitial capillaries in the intracranial extracerebral arteries has to be considered in the pathogenic mechanisms of cerebrovascular lesions.

A CASE OF ADVANCED POLYNEUROPATHY ASSOCIATED WITH MULTIPLE INTESTINAL DIVERTICULOSIS, FATTY LIVER CIRRHOSIS AND MALNUTRITION FOLLOWING GASTRIC RESECTION (B11 METHOD) Hideki KOH, MD, Akira TANAKA, MD, Yuji HASHIMOTO, MD, Nobuhisa AZEGAMI, MD, Masataka ARITA, MD, Hiroshi M URASE, MD, Toshiaki SUNAGA, MD, Fujio NUMANO, MD and Hidenori MAEZAWA, MD The Third Department of Internal Medicine, School of Medicine, Tokyo Medical and Dental University, Tokyo Kimiharu YOSHIMINE, MD, Osamu MATSUBARA, MD and Shigeru HATAKEYAMA,MD Department of Pathology, School of Medicine, Tokyo Medical and Dental University, Tokyo

In the endothelial surface of the ventricle and atria of the heart, aorta, and caval vein of rabbits a new type of intercellular bridges was found. The old one starts from endothelial cell at near the top of endothelial fold and connects obliquely the neighboring fold and the new one starts at near the bottom of the endothelial fold and connects vertically the neighboring fold.