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The effect of hypercapnia on a blood‐brain barrier mechanism in foetal and new‐born sheep.
Author(s) -
Evans C A,
Reynolds J M,
Reynolds M L,
Saunders N R
Publication year - 1976
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1976.sp011304
Subject(s) - hypercapnia , pco2 , acidosis , sucrose , hypoxia (environmental) , respiratory acidosis , chemistry , medicine , endocrinology , anesthesia , biochemistry , oxygen , organic chemistry
1. The effect of marked hypercapnia (arterial PCO2 100 mmHg), nonrespiratory acidosis (pH 6‐95‐7‐15) or hypoxia (arterial PO2 10‐15 mmHg) upon penetration of labelled sucrose from blood into brain and c.s.f. has been investigated in exteriorized foetal sheep and new‐born lambs. 2. In hypercapnia there was a consistent increase in c.s.f./plasma sucrose ratio after 90 min I.V. sucrose to four to five times control. Brain/plasma sucrose ratios were more variable. Usually there was an increase (up to three‐and‐a‐half‐times control); sometimes there was no change or even a decrease. The effect of hypercapnia on sucrose penetration was reversible. 3. Hypercapnia reduced c.s.f. secretion rate to approximately half the control value. Hypercapnia also caused a decrease in brain extracellular space. 4. Non‐respiratory acidosis did not affect sucrose penetration. Hypoxia caused a decrease in brain/plasma sucrose ratio. 5. It is concluded that hypercapnia can cuase an increase in cerebral vascular permeability to sucrose in foetal and new‐born sheep. Some possible mechanisms are discussed.