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Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle
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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064932/ https://www.ncbi.nlm.nih.gov/pubmed/31605649 http://dx.doi.org/10.1111/micc.12593 |
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author | Akerstrom, Thorbjorn Goldman, Daniel Nilsson, Franciska Milkovich, Stephanie L. Fraser, Graham M. Brand, Christian Lehn Hellsten, Ylva Ellis, Christopher G. |
author_facet | Akerstrom, Thorbjorn Goldman, Daniel Nilsson, Franciska Milkovich, Stephanie L. Fraser, Graham M. Brand, Christian Lehn Hellsten, Ylva Ellis, Christopher G. |
author_sort | Akerstrom, Thorbjorn |
collection | PubMed |
description | 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 hyperinsulinemia effects capillary blood flow in rat extensor digitorum longus (EDL) muscle during euglycemic hyperinsulinemic clamp using intravital video microscopy (IVVM). Additionally, we modeled blood flow and microbubble distribution within the vascular tree under conditions observed during euglycemic hyperinsulinemic clamp experiments. RESULTS: Euglycemic hyperinsulinemia caused an increase in erythrocyte (80 ± 25%, P < .01) and plasma (53 ± 12%, P < .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 hyperinsulinemia 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. |
format | Online Article Text |
id | pubmed-7064932 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-70649322020-03-16 Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle Akerstrom, Thorbjorn Goldman, Daniel Nilsson, Franciska Milkovich, Stephanie L. Fraser, Graham M. Brand, Christian Lehn Hellsten, Ylva Ellis, Christopher G. Microcirculation Original Articles 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 hyperinsulinemia effects capillary blood flow in rat extensor digitorum longus (EDL) muscle during euglycemic hyperinsulinemic clamp using intravital video microscopy (IVVM). Additionally, we modeled blood flow and microbubble distribution within the vascular tree under conditions observed during euglycemic hyperinsulinemic clamp experiments. RESULTS: Euglycemic hyperinsulinemia caused an increase in erythrocyte (80 ± 25%, P < .01) and plasma (53 ± 12%, P < .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 hyperinsulinemia 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. John Wiley and Sons Inc. 2019-10-12 2020-02 /pmc/articles/PMC7064932/ /pubmed/31605649 http://dx.doi.org/10.1111/micc.12593 Text en © 2019 The Authors. Microcirculation published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Akerstrom, Thorbjorn Goldman, Daniel Nilsson, Franciska Milkovich, Stephanie L. Fraser, Graham M. Brand, Christian Lehn Hellsten, Ylva Ellis, Christopher G. Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle |
title | Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle |
title_full | Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle |
title_fullStr | Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle |
title_full_unstemmed | Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle |
title_short | Hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle |
title_sort | hyperinsulinemia does not cause de novo capillary recruitment in rat skeletal muscle |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064932/ https://www.ncbi.nlm.nih.gov/pubmed/31605649 http://dx.doi.org/10.1111/micc.12593 |
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