Hindlimb vascular responses to sympathetic augmentation during acute anemia.
The effect of increased sympathetic activity on skeletal muscle blood flow during acute anemic hypoxia was studied in 16 anesthetized dogs. Sympathetic activity was altered by clamping the carotid arteries bilaterally below the carotid sinus. One group (n = 8) was beta blocked by administration of propranolol (1 mg/kg); a second group (n = 8) was untreated. Venous outflow from the left hindlimb was isolated for measurement of blood flow and O2 uptake (VO2). After a 20-min control period, both carotid arteries were clamped (CC) for 20 min followed by a 20-min recovery period. The sequence was repeated after hematocrit was lowered to about 15% by dextran exchange for blood. Prior to anemia, CC did not alter cardiac output or limb blood flow in either group. After induction of anemia, hindlimb resistance was higher with CC in the beta block than in the no block group. Both limb blood flow and VO2 fell in the beta-block group with CC during anemia. Beta block also prevented the additive increases in whole body VO2 seen with CC and induction of anemia. The data showed that the increased vasoconstrictor tone that was obtained with beta block during anemia was successful in redistributing the lower viscosity blood away from resting skeletal muscle, even to the point that muscle VO2 was decreased.
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D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000740:Anemia / Q000503:physiopathology*; D000818:Animals; D001784:Blood Gas Analysis; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D006400:Hematocrit; D006614:Hindlimb / Q000098:blood supply; D006863:Hydrogen-Ion Concentration; D009132:Muscles / Q000098:blood supply*; D012039:Regional Blood Flow; D013318:Stroke Volume / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D000319:Adrenergic beta-Antagonists