Abstract
Prolonged vasospasm was produced in the feline basilar arteries by subarachnoid application of oxyhemoglobin, and sequential changes in vascular ultrastructure were observed.
Firstly, small cored vesicles in the vascular nerve endings were transformed, decreased in number and finally disappeared in the course of development of vasospasms induced by oxyhemoglobin.
Myonecrosis was observed from 1-2 hrs after subarachnoid application of oxyhemoglobin, but it was limited to a small number of smooth muscle cells. In the intercellular spaces among smooth muscle cells, vacuoles, vesicles and granules which might be the cell debris from myonecrosis were visualized from 1-2 hrs after subarachnoid application of oxyhemoglobin, and slowly increased in number, but they were also limited to small areas even 24 hrs after subarachnoid application of oxyhemoglobin.
On the other hand, intimal changes were characteristic, including intrusion of myointimal cells, vesicles and granules into the basement membrane-like substance of the tunica intima, detachment of endothelial cells from the basement membrane-like substance and invasion of blood-borne cells in several layers into the subendothelial gaps. They developed massively 24 hrs after subarachnoid application of oxyhemoglobin. Constriction of the arterial wall resulted in a reduction of the luminal size.
It was suggested that ultrastructural changes in feline basilar arteries after subarachnoid application of oxyhemoglobin might occur as a consequence of vasospasms. These organic changes, especially intimal ones, might occur irreversibly in the early stage of prolonged vasospasms and facilitate the arterial luminal narrowing. Therefore, it is most important in the prevention of prolonged vasospasms to remove by early operations the subarachnoid clots which contain abundant oxyhemoglobin.
