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J Auton Nerv Syst. 1999 Feb 15;75(2-3):184-91.

Superior mesenteric artery dilatation alone does not account for glucose-induced hypotension in human sympathetic denervation.

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Division of Neuroscience and Psychological Medicine, Imperial College School of Medicine at St. Mary's, London, UK.


Haemodynamic and hormonal effects of two oral isovolaemic, isoosmotic solutions of 0.5 g/kg and 1.0 g/kg glucose were studied in 10 humans with sympathetic denervation due to primary autonomic failure (AF). Measurements were made supine for 60 min, and also after 5 min 45 head-up tilt, before and 60 min after glucose. There was a similar fall in blood pressure (BP) after each dose, after 0.5 g/kg from 160+/-12 / 87+/-6 to 143+/-13 / 76+/-6 mm Hg, P < 0.05 and after 1.0 g/kg from 160+/-13 / 90+/-6 to 136+/-9 / 76+/-5 mm Hg, P < 0.05. Heart rate, cardiac index and forearm muscle blood flow did not change after either dose. After 0.5 g/kg, superior mesenteric artery blood flow was unchanged but rose significantly after 1.0 g/kg, from 243 (169-395) to 722 (227-982) ml/min, P < 0.05, 15 min after ingestion. BP fell further on tilt 60 min after each dose, but there was no difference between doses. Plasma glucose was higher after 1.0 g/kg but plasma insulin was similar after each dose. Thus, in AF with sympathetic denervation there was no dose-related effect of glucose on supine or postural hypotension. Supine hypotension after glucose was not attributable solely to increased splanchnic blood flow; other factors, including dilatation in other vascular beds may have contributed.

[Indexed for MEDLINE]

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