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Time-dependent effects of prolonged hypercapnia on cerebrovascular parameters in dogs: acid-base chemistry.
Author(s) -
D. S. Warner,
Donn M. Turner,
Neal F. Kassell
Publication year - 1987
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.18.1.142
Subject(s) - hypercapnia , cerebral blood flow , medicine , anesthesia , cerebrospinal fluid , normocapnia , blood flow , extracellular fluid , acidosis , bicarbonate , base excess , extracellular , chemistry , biochemistry
Prolonged normoxic hypercapnia initially caused an increase in canine cerebral blood flow, as measured by the radioactive microsphere technique, accompanied by a decrease in cerebrovascular resistance. These effects persisted for 3 hours. An adaptive decrease in cerebral blood flow and increase in cerebrovascular resistance were seen when hypercapnia was maintained for an additional 3 hours. Regional variations occurred; those areas with the greatest initial hypercapnic blood flow (cortex, caudate nucleus) showed a greater rate of decay of flow over time. Cerebrospinal fluid pH, initially acidotic during hypercapnia, increased over the subsequent 5 hours from 6.99 +/- 0.02 to 7.13 +/- 0.02. This was accompanied by an increase in the cerebrospinal fluid bicarbonate ion concentration from a normocapnic baseline of 19.6 +/- 0.6 to 26.2 +/- 4 mEq/l. Total and regional cerebral blood flow were linearly related to cerebrospinal fluid pH (R2 = 0.97). Extrapolation of a full adaptive return of flow to baseline indicated a shift in the cerebrovascular sensitivity to extracellular hydrogen ion concentration during prolonged hypercapnia.

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