Skeletal muscle perfusion and metabolism during canine endotoxin shock.
Conflicting data exist in literature about the effects of endotoxin on skeletal muscle perfusion and metabolism during canine endotoxin shock. In 12 dogs we therefore studied (six control and six endotoxin treated, 1.5 mg X kg-1) under etomidate (4 mg X kg-1 X h-1) anaesthesia muscle blood flow (radioactive microspheres) in fore limb, thorax, diaphragm and hind limb (five different muscles) and skin blood flow before (t = 0) and 90 and 120 min after endotoxin. We also measured blood flow in the femoral artery and vein (electromagnetic flow transducers) and the arteriovenous differences of oxygen, lactate, glucose and FFA over the femoral vascular bed (at t = 0, 30, 90 and 120 min). Endotoxin administration caused a fall of flow in the femoral artery and vein (by 65 and 63%, respectively at t = 15). After t = 60 flow in the femoral artery and vein increased slowly but the flows were still below the preshock values at t = 20 (by 33 and 50%, respectively). Skeletal muscle and skin flow did not decrease or even increased after endotoxin but decreased in the control group. Percentage of cardiac output distributed to brachial, intercostal and hind limb muscle and skin increased after endotoxin (by 163, 167, 111 and 120%, respectively at t = 20). The five muscles of the hind limb did not respond differently to endotoxin. In spite of diminished arterial inflow, skeletal muscle perfusion was thus maintained in the hind limb, probably due to closing of shunts and redistribution of blood away from bone. Oxygen extraction but also lactate release by the femoral bed had increased during endotoxin shock. After endotoxin femoral glucose extraction was only elevated at t = 30 when arterial glucose concentration had also increased. The femoral bed produced free fatty acids (FFA) but during endotoxin shock the arteriovenous concentration difference of FFA decreased. Our data suggest that skeletal muscle flow nor oxygen consumption and glucose metabolism is affected during 2 h of canine endotoxin shock. Lactate production, however, tended to increase.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002302:Cardiac Output; D004285:Dogs; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005263:Femoral Artery; D005268:Femoral Vein; D006439:Hemodynamics; D006614:Hindlimb / Q000503:physiopathology; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D009132:Muscles / Q000098:blood supply* / Q000378:metabolism; D012039:Regional Blood Flow; D012772:Shock, Septic / Q000378:metabolism / Q000503:physiopathology*
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007773:Lactates; D019344:Lactic Acid