Cerebral hemodynamics, vascular reactivity, and metabolism during canine endotoxin shock.
Cerebral hemodynamics, vascular reactivity, and metabolic alterations were studied in anesthetized, spontaneously respiring dogs for 4-6 hr of gram-negative endotoxin shock. Cerebral venous outflow (cerebral blood flow) was measured directly from the cannulated confluence of the sagittal, straight, and lateral sinuses, with the lateral sinuses occluded. Cerebral blood flow and cerebral perfusion pressure decreased immediately upon administration of 1,2, or 5 mg/kg endotoxin and consistently remained below control values. By the fourth hour of shock, cerebral blood flow was decreased 37, 48, and 45% respectively. Cerebral vascular resistance initially decreased, then progressively increased to levels significantly above control, and it was primarily responsible for the reduced cerebral blood flow in the later stages of shock. Cerebral autoregulatory and "venous-arteriolar" responses were well maintained, although cerebral vascular reactivity to arterial hypercapnia was depressed. Cerebral venous blood pH and pO2 decreased, and arterial-venous differences of percentage oxygen saturation, total CO2, and HCO3 increased. These alterations in cerebral vascular hemodynamics and tissue acid-base balance indicate that cerebral ischemia and resulting acidosis occur during canine endotoxin shock.
D000136:Acid-Base Equilibrium; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation; D004285:Dogs; D005260:Female; D006439:Hemodynamics; D008297:Male; D010100:Oxygen / Q000097:blood; D012039:Regional Blood Flow; D012772:Shock, Septic / Q000097:blood / Q000503:physiopathology*; D014655:Vascular Resistance
D002245:Carbon Dioxide; D010100:Oxygen