Cerebral blood flow responses to hypocapnia during hypotension.
Author(s) -
Alan A. Artru,
Peter S. Colley
Publication year - 1984
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.15.5.878
Subject(s) - hypocapnia , medicine , sodium nitroprusside , cerebral blood flow , anesthesia , mean arterial pressure , blood pressure , vascular resistance , hemodynamics , heart rate , hypercapnia , nitric oxide , acidosis
Cerebral vascular responses to hypocapnia during hypotension to a mean arterial blood pressure (MAP) = 50 mm Hg induced with sodium nitroprusside (SNP, n = 12) or trimethaphan (TMP, n = 12) were examined in dogs. Cerebral vascular resistance (CVR) and cerebral blood flow (CBF) at PaCO2 = 40 mm Hg, and PaCO2 = 20 mm Hg were examined first at normal MAP then at hypotension in six dogs in the SNP group and six dogs in the TMP group. In both the SNP group and the TMP group, CO2 responsiveness, as indicated by increased CVR and decreased CBF, was intact at normal MAP, but absent during hypotension. In the remaining 6 of 12 dogs in the SNP group and 6 of 12 dogs in the TMP group, CO2 responsiveness at MAP = 50 mm Hg was examined without prior determination of CO2 responsiveness at normal MAP. These additional studies were performed to rule out the possibility that absent CO2 responsiveness during hypotension in the initial groups resulted from (1) physiologic deterioration of the preparation with time, or (2) adaptation of brain extracellular fluid pH to a preceding period of hypocapnia. Again, during both SNP- or TMP-induced hypotension CO2 responsiveness was absent.
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