The Role of the Central Nervous System in Septic Shock

Abstract

The administration of relatively small doses of Escherichia coli endotoxin into the lateral ventricles results in the death of dogs. The present study documents hemodynamic, respiratory and metabolic alterations which follow the introduction of endotoxin into the central nervous system. Severe hyperventilation promptly follows CNS endotoxin and results in hypocarbia and respiratory alkalosis. An increase in arterial lactate levels minimizes the pH deviation in the presence of severe hypocarbia. Following a period of normal ventilation, hyperventilation returns and is followed by respiratory arrest. CNS endotoxin leads to a progressive gradual fall in cardiac output accompanied by a lesser fall in heart rate and arterial blood pressure. A later sharp rise in total peripheral resistance precedes death. Cardiovascular failure does not appear to be immediately responsible for death. No alterations in serum enzyme levels, coagulation screening tests, plasma volume or extracellular fluid volume could be detected. Blood glucose levels were elevated only for a short time in the 1st hr. following endotoxin administration. The possible role of endotoxin acting on the central nervous system during systemic endotoxin shock is discussed.