Endotoxin shock in the beagle dog.
The hemodynamic and metabolic responses to endotoxemia were assessed in seven splenectomized, chronically instrumented, conscious but lightly sedated beagle dogs. Measurements included: cardiac output (CO), right and left atrial pressures (RAP, LAP), systemic and pulmonary arterial pressures (SAP, PAP), and heart rate (HR). Arterial blood samples were measured for blood gas tensions, pH, lactate, and pyruvate. After a brief control period, 1 mg/kg endotoxin (Difco 026:B6) was given as an intravenous bolus. Two hours later, each animal was treated with low-molecular weight dextran (LMDX), 2 ml/kg/min for 15 minutes. Endotoxin initially produced a precipitate decline in CO, HR, RAP, LAP, and SAP with concurrent pulmonary hypertension; both pulmonary and systemic vascular resistance increased significantly, then declined to control values as the animal partially recovered. A progressive metabolic acidosis with excess lactate accumulation developed. LMDX produced a significant increase in CO, SAP, PAP, and LAP with a decrease in HR; RAP increased slightly. With hydration, hemodilution was noted along with relief of the metabolic acidosis and the oxygen debt. We conclude (1) neither pulmonary nor systemic vasconstriction persisted in the shocked dog, (2) the response of the pulmonary and systemic vascular beds to endotoxin was qualitatively similar, and (3) oncotic fluid therapy appeared to restore the hemodynamic and metabolic parameters to preshock values.
D000818:Animals; D002302:Cardiac Output; D004285:Dogs; D005260:Female; D006339:Heart Rate; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000209:etiology; D008297:Male; D011652:Pulmonary Circulation; D012772:Shock, Septic / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D014655:Vascular Resistance