Vasogenic edema with intraparenchymatous expanding mass lesions: a theory on its pathophysiology and mode of action of hyperventilation and corticosteroids.
Vasogenic edema with expanding mass brain lesions is hypothesized to be due to an increased intracapillary pressure. The latter may be due to preferential occlusion of the venous system by the growth of the lesion but endothelila proliferation and biogenic amines may also play a part. Endocytosis appears to be a mechanical response to the increased intraluminal pressure. This is a poorly selective process which can explain the proteinaceous nature of vasogenic edema. Steroids may act by forming hydrophobic bonds in the endothelial cell membrane and making it more difficult for any membrane fission to occur. Hyperventilation can be of use in vasogenic edema by decreasing intracranial pressure, providing better oxygenation and also by diminishing the capillary head pressure.
D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000818:Animals; D001929:Brain Edema / Q000503:physiopathology*; D001930:Brain Injuries / Q000503:physiopathology; D001932:Brain Neoplasms / Q000503:physiopathology; D002199:Capillary Permeability / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D004705:Endocytosis / Q000187:drug effects; D006801:Humans; D006985:Hyperventilation / Q000503:physiopathology*; D007427:Intracranial Pressure / Q000187:drug effects
D000305:Adrenal Cortex Hormones; D002245:Carbon Dioxide