Dramatic changes in blood gases that are unrelated to arterial pH or cerebral oxygen delivery during endotoxin shock in conscious rats.

In preliminary studies we demonstrated an effect of endotoxin on arterial blood gases that appeared to be related to the dose of endotoxin used and unrelated to changes in arterial pH. In the present study we tested the hypothesis that these changes in blood gases result from decreased oxygen delivery to central respiratory control areas. PO2 significantly rose from a pre-endotoxin value of 91.4 +/- 1.5 (mean +/- SEM) to 97.5 +/- 1.7, 104.0 +/- 0.8, and 108.4 +/- 0.9 at 10, 30, and 60 minutes, respectively, after administration of 6 mg/kg endotoxin and from 93.8 +/- 3.1 to 105.2 +/- 2.6, 118.7 +/- 1.4, and 121.0 +/- 2.8, respectively, after administration of 10 mg/kg endotoxin. PCO2 fell significantly from a pre-endotoxin value of 38.3 +/- 1.2 to 28.6 +/- 0.6 and 24.5 +/- 1.9 at 30 and 60 minutes post-endotoxin, respectively, in 6-mg/kg-treated rats, and from 40.5 +/- 2.1 to 30.7 +/- 4.5, 20.1 +/- 3.9, and 19.3 +/- 1.0, respectively, at 10, 30, and 60 minutes post-10 mg/kg endotoxin. The only significant change (decrease) in pH occurred at 60 minutes after 10 mg/kg treatment. In 10-mg/kg-treated rats, serum lactate rose significantly over time, while HCO-3 decreased. Heart rate was increased significantly (472 +/- 9.6) from a pre-10 mg/kg endotoxin value of 373 +/- 11.8 by 10 minutes post-endotoxin and remained elevated throughout the experiment. Cerebral medullary/pontine blood flow, mean arterial blood pressure, and respiratory rate were not significantly altered by endotoxin administration. Hemoglobin concentration and arterial oxygen content were significantly increased after 10 mg/kg endotoxin. These findings indicate that decreased oxygen delivery to central respiratory control areas is not a cause of the observed dramatic changes in blood gases.