Cerebral blood flow responses to hypocapnia during hypotension.
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.
D000818:Animals; D001639:Bicarbonates / Q000097:blood; D002245:Carbon Dioxide / Q000172:deficiency* / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004285:Dogs; D006863:Hydrogen-Ion Concentration; D007022:Hypotension / Q000139:chemically induced / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D014294:Trimethaphan / Q000494:pharmacology; D014655:Vascular Resistance
D001639:Bicarbonates; D002245:Carbon Dioxide; D009599:Nitroprusside; D014294:Trimethaphan