In vivo studies of pial vascular permeability to sodium fluorescein: absence of alterations by bradykinin, histamine, serotonin, or arachidonic acid.
We studied pial vessels in vivo in mice, examining under mercury light the permeability of these vessels to sodium fluorescein. Topical application of hypertonic solutions of NaCl caused leakage of fluorescein. However, putative chemical mediators of leakage, such as histamine, serotonin, arachidonic acid, and bradykinin, all failed to increase permeability to the dye. Apparent increases in permeability only accompanied endothelial damage caused by the dye + light combination, as indicated by production of local platelet aggregates. The technique is useful, provided inadvertent endothelial injury is recognized and avoided. The data in mice suggest that pial vessels may not participate in the permeability changes reportedly produced in parenchymal brain vessels by several of the mediators we tested. Therefore, studies of pial vascular permeability are not expected to provide reliable data concerning the actions of agents that might mediate cerebral edema.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000493:pharmacokinetics*; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001920:Bradykinin / Q000493:pharmacokinetics*; D002199:Capillary Permeability / Q000187:drug effects*; D019793:Fluorescein; D005452:Fluoresceins / Q000493:pharmacokinetics*; D006632:Histamine / Q000493:pharmacokinetics*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010841:Pia Mater / Q000098:blood supply*; D012701:Serotonin / Q000493:pharmacokinetics*
D001095:Arachidonic Acids; D005452:Fluoresceins; D016718:Arachidonic Acid; D012701:Serotonin; D006632:Histamine; D001920:Bradykinin; D019793:Fluorescein