Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Dokumenter

  • Thorbjörn Åkerström
  • Daniel Goldman
  • Franciska Nilsson
  • Stephanie L Milkovich
  • Graham M Fraser
  • Christian Lehn Brand
  • Hellsten, Ylva
  • Christopher G Ellis

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.

OriginalsprogEngelsk
Artikelnummere12593
TidsskriftMicrocirculation
Vol/bind27
Udgave nummer2
Antal sider15
ISSN1073-9688
DOI
StatusUdgivet - 2020

Bibliografisk note

CURIS 2020 NEXS 016
© 2019 John Wiley & Sons Ltd.

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