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Cerebral air embolism and the blood‐brain barrier in the rat
Author(s) -
Johansson Barbro B.
Publication year - 1980
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1980.tb03027.x
Subject(s) - medicine , extravasation , blood–brain barrier , anesthesia , hemodynamics , blood pressure , air embolism , hypercapnia , albumin , embolism , cerebral circulation , cerebral blood flow , blood flow , evans blue , vascular permeability , cardiology , central nervous system , pathology , complication , acidosis
Cerebral air embolism can have hemodynamic effects such as increases in blood pressure and cerebral blood flow. It has been suggested that these factors play a role for the induction of the blood‐brain barrier (BBB) dysfunction. In the present study, 5 μl air was injected into the right internal carotid artery from a catheter in the external carotid artery after ligation of the extracerebral branches. No consistent change in blood pressure was observed with this small amount of air. Hypercapnia, which increases protein leakage in the brain under conditions of high intra‐luminal pressure, significantly reduced the extravasation in air embolism. Lidocain and SITS (4 acetamido–4–isothiocyano–stilbene–2,2–disulfonic acid disodium), two drugs that effectively reduce the albumin leakage in acute hypertension, had no prophylactic effect in cerebral air embolism. Spontaneously hypertensive rats are less vulnerable than normotensive rats to pressure‐induced BBB dysfunction but did not significantly differ from controls regarding albumin leakage in the present study. It is concluded that the increased cerebrovascular permeability in air embolism is not related to hemodynamic factors.