title: Sustained hyperglycaemia increases muscle blood flow but does not affect sympathetic activity in resting humans.
abstract: An increase in capillary blood flow and pressure in response to diabetes mellitus may lead to microangiopathy. We hypothesize that these haemodynamic changes are caused by a decreased activity of the sympathetic nervous system due to episodes of sustained hyperglycaemia. Twelve healthy volunteers consecutively underwent a hyperglycaemic experiment (HYPER), with the plasma glucose level maintained at 20 mmol.l(-1) for 6 h by combined infusion of somatostatin, insulin and glucose; and a normoglycaemic experiment (NORMO), with similar infusions but with the plasma glucose maintained at fasting level. During both experiments, sympathetic nervous system (SNS) activity was measured by assessing the plasma catecholamine levels, microneurography, power spectral analysis and forearm blood flow (FBF). In an age- and weight matched group, fasting and 6-h sympathetic activity was measured without infusion of somatostatin and insulin (CONTROL). During HYPER, forearm blood flow increased from 2.45 (0.21) to 3.10 (0.48) ml.dl(-1).min(-1) ( P <0.05), but did not change in NORMO or CONTROL. The HYPER conditions did not change the plasma noradrenaline levels or the muscle sympathetic nerve activity [42 (4), 50 (10) and 45 (5) bursts/100 beats, HYPER, NORMO and CONTROL respectively]. Also, the power spectral analysis was similar under all experimental conditions. All results are expressed as the mean (SEM). In conclusion, sustained hyperglycaemia in normal subjects induces moderate vasodilation in skeletal muscle, but this increased blood flow can not be attributed to a decreased sympathetic tone.
authors.affiliation: Division of General Internal Medicine, Department of Internal Medicine, University Medical Center St Radboud, PO Box 9101, 6500 HB Nijmegen, The Netherlands. p.vangurp@aig.umcn.nl
authors.forename: P J
authors.initials: PJ
authors.lastname: van Gurp
authors.forename: G A
authors.initials: GA
authors.lastname: Rongen
authors.forename: J W M
authors.initials: JW
authors.lastname: Lenders
authors.forename: A K M
authors.initials: AK
authors.lastname: Al Nabawy
authors.forename: H J L M
authors.initials: HJ
authors.lastname: Timmers
authors.forename: C J
authors.initials: CJ
authors.lastname: Tack
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D005260:Female; D006728:Hormones / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D006943:Hyperglycemia; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000494:pharmacology; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000294:innervation; D012039:Regional Blood Flow; D013004:Somatostatin / Q000008:administration & dosage / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014664:Vasodilation
chemical_list: D006728:Hormones; D007004:Hypoglycemic Agents; D007328:Insulin; D013004:Somatostatin