Circulatory effects of carbon dioxide in experimental endotoxic shock.
In seven anaesthetized dogs the central circulatory effects of changes in Paco2 were studied before and after an intravenous injection of E. coli endotoxin 1.0 mg kg-1. The animals were on controlled ventilation with constant minute volumes, and Paco2 was changed by variations in the inspired gas mixture. Before endotoxin was given, cardiac output, mean aortic pressure, mean pulmonary artery pressure, total peripheral resistance and stroke volume were little affected by the changes in Paco2 from 3.9 +/- 0.4 to 7.2 +/- 0.4 kPa (mean +/- s.e.mean). Only heart rate decreased significantly (P less than 0.05). The intravenous endotoxin injection resulted in a decreased cardiac output (P less than 0.01), a decreased mean aortic pressure (P less than 0.01) and a decreased stroke volume (P less than 0.05). Mean pulmonary artery pressure, total peripheral resistance and heart rate showed only minor changes. In endotoxic shock an increase in Paco2 from 4.4 +/- 0.4 to 7.8 +/- 0.3 kPa (mean +/- s.e.mean) resulted in a significant increase in cardiac output (P less than 0.05), stroke volume (P less than 0.05) and mean pulmonary artery pressure (P less than 0.05), while the other parameters remained unchanged. It can be concluded that the carbon dioxide tension is of importance for the cardiac performance in experimental endotoxic stock in a manner not seen in control animals. The mechanisms behind these findings need further investigation.
Larsson
L E
LE
Ekström-Jodal
B
B
D000818:Animals; D001769:Blood; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000032:analysis / Q000494:pharmacology*; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D012772:Shock, Septic / Q000503:physiopathology*; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
D002245:Carbon Dioxide