Superior mesenteric artery blood flow (SMABF) increases significantly during and after the hypoglycaemia reaction in healthy humans. To investigate the mechanisms controlling this phenomenon, SMABF and plasma catecholamines were measured in healthy human volunteers. In 10 controls, hypoglycaemia was induced by insulin infusion (2.5 m-units·min-1·kg-1). In six subjects, β-blockade by propranolol infusion (0.7 µg·min-1·kg-1) preceded insulin infusion and was continued throughout the study. Following the hypoglycaemia reaction, the glucose nadir was similar in both groups. In controls, increases in SMABF [42.4±6.1% (mean±S.E.M.); P < 0.001], cardiac output (34.3±2.3%; P < 0.001) and pulse rate (from 63.9±2.7 to 82.5±3.1 beats/min; P < 0.001) occurred. Superior mesenteric artery resistance fell by 32.4±3.3% (P < 0.001). Under β-blockade, decreases in SMABF (34.8±2.9%; P < 0.001) and pulse rate (from 59.5±0.2 to 51.8±2.2 beats/min; P < 0.001) occurred. Superior mesenteric artery resistance increased (peak +30.8±12.3%; not significant). Subjects showed greater increases in adrenaline (P < 0.006) and noradrenaline (P < 0.022) concentrations than controls. Mesenteric hyperaemia associated with hypoglycaemia in man appears to be mediated by a β-adrenergic mechanism that is activated by increased circulating levels of adrenaline.
Physiological control of splanchnic blood flow by adrenaline: studies during acute hypoglycaemia in man
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David R. PARKER, Geoffrey D. BRAATVEDT, Michael HALLIWELL, Roger J. M. CORRALL; Physiological control of splanchnic blood flow by adrenaline: studies during acute hypoglycaemia in man. Clin Sci (Lond) 1 June 1999; 96 (6): 623–629. doi: https://doi.org/10.1042/cs0960623
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