European journal of applied physiology · 2013
Acute hyperglycaemia does not alter nitric oxide-mediated microvascular function in the skin of adolescents with type 1 diabetes.
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Naylor Louise H, Yusof Norhaida M, Paramalingam Nirubasini, Jones Timothy W, Davis Elizabeth A, Green Daniel J
Аннотация
PURPOSE: We assessed the impact of an acute bout of hyperglycaemia on nitric oxide (NO)-mediated microvascular function in the skin of adolescents with type 1 diabetes (T1DM).
METHODS: Twelve subjects (12-18 years) with T1DM were randomised into a control (n = 6) or hyperglycaemia (n = 6) group. Hyperinsulinaemic clamps were used to manipulate blood glucose level (BGL). Following a baseline period, where all subjects were euglycaemic (20 min), the experimental phase began. During the experimental phase, BGL was elevated to 16.7 ± 0.9 mmol L(-1) in the hyperglyceamic group, while it was maintained at euglycaemia (5.5 ± 0.1 mmol L(-1)) in the control group. Simultaneously, cutaneous microvascular function (% max cutaneous vascular conductance, CVC%) was assessed using laser Doppler fluxometry following stimulation of skin blood flow using localised heating (42 °C). To determine the NO contribution to skin blood flow, two microdialysis sites were assessed, one perfused with Ringers and the other with the NO blocker, NG-monomethyl-L-arginine (L-NMMA).
RESULTS: In the hyperglycaemic group, acute increase in BGL was not associated with changes in skin blood flow (CVC% 82.4 ± 8.7% at 5.5 ± 0.1 mmol L(-1) vs 79.5 ± 9.1% at 16.7 ± 0.9 mmol L(-1), unpaired t tests, P = 0.588) or the contribution of NO to vasodilation.
CONCLUSIONS: These results suggest that, in our group of adolescents with type 1 diabetes, acute hyperglycaemia did not affect skin microvascular NO-mediated function.
METHODS: Twelve subjects (12-18 years) with T1DM were randomised into a control (n = 6) or hyperglycaemia (n = 6) group. Hyperinsulinaemic clamps were used to manipulate blood glucose level (BGL). Following a baseline period, where all subjects were euglycaemic (20 min), the experimental phase began. During the experimental phase, BGL was elevated to 16.7 ± 0.9 mmol L(-1) in the hyperglyceamic group, while it was maintained at euglycaemia (5.5 ± 0.1 mmol L(-1)) in the control group. Simultaneously, cutaneous microvascular function (% max cutaneous vascular conductance, CVC%) was assessed using laser Doppler fluxometry following stimulation of skin blood flow using localised heating (42 °C). To determine the NO contribution to skin blood flow, two microdialysis sites were assessed, one perfused with Ringers and the other with the NO blocker, NG-monomethyl-L-arginine (L-NMMA).
RESULTS: In the hyperglycaemic group, acute increase in BGL was not associated with changes in skin blood flow (CVC% 82.4 ± 8.7% at 5.5 ± 0.1 mmol L(-1) vs 79.5 ± 9.1% at 16.7 ± 0.9 mmol L(-1), unpaired t tests, P = 0.588) or the contribution of NO to vasodilation.
CONCLUSIONS: These results suggest that, in our group of adolescents with type 1 diabetes, acute hyperglycaemia did not affect skin microvascular NO-mediated function.