[Study of the elastic skeleton of intracranial arteries in animal and human vessels and experimentally induced cerebral aneurysms].

In an attempt to clarify the elastic skeleton of cerebral arteries in animals and human, and experimentally induced cerebral aneurysms, following experiments were performed. Experiment (1): The elastic skeleton of major cerebral arteries in rats, monkeys, and one human were studied by scanning electron microscopy after hot-formic acid extraction followed by freeze-drying. For a comparative study, the thoracic aorta and femoral arteries of rats were also examined. The cerebral arteries of rats had one distinct internal elastic lamina connected with medial elastic tissue. This internal elastic lamina had fenestrations, which were less frequent in cerebral arteries than in extracranial arteries, and fold-like protrusions into the lumen. This finding has not been recognized before. Such protrusions were more prominent in cerebral arteries than in extracranial arteries. At the apical intimal pad, the internal elastic lamina appeared to be continuous, making a honeycomb-like structure there. These folds and fenestrations were numerous in the apical region. There were no essential differences between species. Experiment (2): Cerebral aneurysms were produced by ligating unilateral carotid artery and bilateral posterior branches of renal arteries, and feeding beta-aminoproprionitrile fumarate. The first noted change was the loss of fold-like structures protruding from the internal elastic lamina. Morphological changes of the internal elastic lamina, considered to be primarily responsible for aneurysmal formation, occurred after the loss or disintegration of the media. The internal elastic lamina disappeared after these consequences. In a large aneurysm with a thick dome, the wall contained fine proliferated elastic lamellae. The present study shows that the internal elastic lamina is not a simple sheet but part of the complicated architecture of the elastic tissue of the vessel wall. It seems probable that the complex elastic skeleton of the arterial wall may account for the mechanical properties of the artery and that growth of the aneurysm occurs due to disintegration of the elastic skeleton and not simply with rupture of the internal elastic lamina. We believe that such changes in the elastic skeleton are a property of the functional state of cells that produce elastin.