Mammalian endothelial cells lining hepatic sinusoids have been found to be widely fenestrated. Previous SEM studies (1,2) have noted two general size catagories of fenestrations; large fenestrae were distributed randomly while the small type occurred in groups. These investigations also reported that large fenestrae were more numerous and larger in the endothelial cells at the afferent ends of sinusoids or around the portal areas, whereas small fenestrae were more numerous around the centrilobular portion of the hepatic lobule. It has been further suggested that under some physiologic conditions small fenestrae could fuse and subsequently become the large type, but this is, as yet, unproven.We have used a reproducible experimental model of hypoxia to study the ultrastructural alterations in sinusoidal endothelial fenestrations in order to investigate the origin of occurrence of large fenestrae.
The antagonism of prostaglandin FP receptors inhibits the evolution of spreading depolarization in an experimental model of global forebrain ischemia
