Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle
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Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle. / Åkerström, Thorbjörn; Goldman, Daniel; Nilsson, Franciska; Milkovich, Stephanie L; Fraser, Graham M; Brand, Christian Lehn; Hellsten, Ylva; Ellis, Christopher G.
I: Microcirculation, Bind 27, Nr. 2, e12593, 2020.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle
AU - Åkerström, Thorbjörn
AU - Goldman, Daniel
AU - Nilsson, Franciska
AU - Milkovich, Stephanie L
AU - Fraser, Graham M
AU - Brand, Christian Lehn
AU - Hellsten, Ylva
AU - Ellis, Christopher G
N1 - © 2019 John Wiley & Sons Ltd.
PY - 2020
Y1 - 2020
N2 - Objective: The effect of insulin on blood flow distribution within muscle microvasculature, has been suggested to be important for glucose metabolism. However, the "capillary recruitment" hypothesis is still controversial and relies on studies using indirect contrast-enhanced ultrasound (CEU) methods.Methods: We studied how hyperinsulinaemia effects capillary blood flow in rat extensor digitorum longus (EDL) muscle during euglycaemic hyperinsulinaemic clamp using intravital video microscopy (IVVM). Additionally, we modelled blood flow and microbubble distribution within the vascular tree under conditions observed during euglycaemic hyperinsulinaemic clamp experiments.Results: Euglycaemic hyperinsulinaemia caused an increase in erythrocyte (80±25%, p<0.01) and plasma (53±12%, p<0.01) flow in rat EDL microvasculature. We found no evidence of de novo capillary recruitment within, or among capillary networks supplied by different terminal arterioles; However, erythrocyte flow became slightly more homogenous. Our computational model predicts that a decrease in asymmetry at arteriolar bifurcations causes redistribution of microbubble flow among capillaries already perfused with erythrocytes and plasma, resulting in 25% more microbubbles flowing through capillaries.Conclusions: Our model suggests increase in CEU signal during hyperinsulinaemia reflects a redistribution of arteriolar flow and not de novo capillary recruitment. IVVM experiments support this prediction showing increases in erythrocyte and plasma flow and not capillary recruitment.
AB - Objective: The effect of insulin on blood flow distribution within muscle microvasculature, has been suggested to be important for glucose metabolism. However, the "capillary recruitment" hypothesis is still controversial and relies on studies using indirect contrast-enhanced ultrasound (CEU) methods.Methods: We studied how hyperinsulinaemia effects capillary blood flow in rat extensor digitorum longus (EDL) muscle during euglycaemic hyperinsulinaemic clamp using intravital video microscopy (IVVM). Additionally, we modelled blood flow and microbubble distribution within the vascular tree under conditions observed during euglycaemic hyperinsulinaemic clamp experiments.Results: Euglycaemic hyperinsulinaemia caused an increase in erythrocyte (80±25%, p<0.01) and plasma (53±12%, p<0.01) flow in rat EDL microvasculature. We found no evidence of de novo capillary recruitment within, or among capillary networks supplied by different terminal arterioles; However, erythrocyte flow became slightly more homogenous. Our computational model predicts that a decrease in asymmetry at arteriolar bifurcations causes redistribution of microbubble flow among capillaries already perfused with erythrocytes and plasma, resulting in 25% more microbubbles flowing through capillaries.Conclusions: Our model suggests increase in CEU signal during hyperinsulinaemia reflects a redistribution of arteriolar flow and not de novo capillary recruitment. IVVM experiments support this prediction showing increases in erythrocyte and plasma flow and not capillary recruitment.
KW - Faculty of Science
KW - Microcirculation
KW - Skeletal muscle
KW - Insulin
U2 - 10.1111/micc.12593
DO - 10.1111/micc.12593
M3 - Journal article
C2 - 31605649
VL - 27
JO - Microcirculation
JF - Microcirculation
SN - 1073-9688
IS - 2
M1 - e12593
ER -
ID: 228729197