抄録
Observations were made on thoracic aortas and carotid arteries from male rabbits that were normal or experimental (those infused with epinephrine, norepinephrine, angiotensis II, endotoxin and cholesterol-fed animals).
Procedures were in accordance with the general methods for electron microscopy.
I. Fine structures of no-treatment animals (normal state).
II. Characteristics of normal fine structures and physiologically changed fine structures.
A. Connection between endothelial and smooth muscle cells
1. Attachment plates connected by foot processes grown from endothelial cells and smooth muscle cells.
2. Three types of connections were observed through the fenestrations of internal elastic laminae.
a. Type 1: Processes of medial smooth muscle cells in the endothelial lines.
b. Type 2: Long processes of endothelial cells in smooth muscle cells.
c. Type 3: Connections made apart from both cells.
3. The nature of connection was mainly simple apposition, but the so-called gap junctions were observed in some cases.
B. Initial contraction-relaxation-response appeared immediately after an infusion of angiotensin II, catecholamine, endotoxin or one-shot treatment of cholesterol. Local edema surrounding the connection site was then observed.
The myo-endothelial connections may have an important role to play as sensors of stimuli. In structural terms, the same myofilaments exist in the endothelial cells near the connecting site. These findings suggest that they (=myofilaments) are probably involved in the function of contraction and/or relaxation of endothelial cells and medial smooth muscle cells. Through this structure, endothelial cells and smooth muscle cells form a syncytium in the inner part of aortic wall.
C. Endothelial cell-leucotyte interaction.
1. Adhesion of leucocytes, especially monocytes, to the endothelial cells was observed in cases of angiotensin II infusion, endotoxin infusion and one-shot cholesterol treatment. Leucotytes successively enter the subendothelial space by diapedesis.
2. Leucotytes (monocytes) were often observed in the endothelial cell lines. Structurally. these cells were differentiated with nuclei and a number of marginal folds. Functionally, these cells demonstrated strong phagocytotic activity against carbon particles, but not in the neighboring endothelial cells.
These findings suggest that the interaction was probably induced by some humoral mediator or cytokines.
D. Endothelial cell-platelet interaction.
Completely normal endothelial cells block platelet adhesion on their cell surface. Following damage to the endothelial cell or formation of the giant endothelial cell, platelets adhere to endothelial cell surface. This finding, which seems to signify induction of mitogens into the gaint cell, seems to play an important role in the course of the interaction between endothelial cells and platelets.
III. Prepathological or pathological changes.
A. Diffuse edematous arterial reaction in subendothelial space. Repeats of contraction-relaxation response and increased permeability brought about this change from the local edema. The first step of change showed a homogeneous, low-density extracellular space, and the next step gave rise to high-density extracellular spaces containing small lipid droplets.
B. At the same time, subendothelial smooth muscle cells migrated from the inner layer of media and attached themselves to the endothelial cells by small foot processes.
IV. Observation of the process of protecting damaged endothelial cells. (Replacement)
Replacement for damaged endothelial cells was observed in an early stage of pathological change.
A. The first type of protection was observed in the prolongation of the marginal folds of neighboring endothelial cells or neighboring giant endothelial cells.
B. The second type of protection occurred in cases showing loss of continu
