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Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats
BACKGROUND: The various autonomic control systems lead to characteristic changes in heart rate (HR) and blood pressure (BP) during acute hemorrhage. However, cardiovascular autonomic neuropathy due to diabetes mellitus may interfere with the normal compensation for hemorrhage. MATERIALS AND METHODS:...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004820/ https://www.ncbi.nlm.nih.gov/pubmed/21106105 http://dx.doi.org/10.1186/1475-2840-9-78 |
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author | Boku, Aiji Sugimura, Mitsutaka Morimoto, Yoshinari Hanamoto, Hiroshi Niwa, Hitoshi |
author_facet | Boku, Aiji Sugimura, Mitsutaka Morimoto, Yoshinari Hanamoto, Hiroshi Niwa, Hitoshi |
author_sort | Boku, Aiji |
collection | PubMed |
description | BACKGROUND: The various autonomic control systems lead to characteristic changes in heart rate (HR) and blood pressure (BP) during acute hemorrhage. However, cardiovascular autonomic neuropathy due to diabetes mellitus may interfere with the normal compensation for hemorrhage. MATERIALS AND METHODS: A controlled graded bleeding (6 - 36% loss of estimated total blood volume: ETBV) was performed in streptozotocin-induced diabetic rats (STZ rats) under a conscious state. Hemodynamic and autonomic responses to acute hemorrhage were examined using analysis of BP-HR variability. The effects of dextran treatment after hemorrhage were also examined. RESULTS: A significant reduction in mean arterial pressure began at 12% ETBV loss in STZ rats and 18% in the control rats, respectively. When blood loss reached 18% of TEBV, the decrease in HR was prominent in STD rats due to the activation of a parasympathetic drive, as indicated by the increase in high frequency (HF; 0.75~3.0 Hz) power in HR variability, while in the control rats this response was not observed. The administration of dextran prevented the activation of the parasympathetic drive in STZ rats during hemorrhaging. In the control rats, the dextran treatment sustained the initial increase in HR with reduced HF power in HR variability. CONCLUSION: STZ rats showed different hemodynamic and autonomic responses to acute hemorrhage from the control rats. STZ rats were prone to develop bradycardiac hypotension characterized by marked parasympathetic activation during hemorrhaging. This finding suggests enhancement of the Bezold-Jarisch reflex in STZ rats. Dextran treatment to maintain a normovolemic hemorrhage state inhibits this reflex. |
format | Text |
id | pubmed-3004820 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30048202010-12-21 Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats Boku, Aiji Sugimura, Mitsutaka Morimoto, Yoshinari Hanamoto, Hiroshi Niwa, Hitoshi Cardiovasc Diabetol Original Investigation BACKGROUND: The various autonomic control systems lead to characteristic changes in heart rate (HR) and blood pressure (BP) during acute hemorrhage. However, cardiovascular autonomic neuropathy due to diabetes mellitus may interfere with the normal compensation for hemorrhage. MATERIALS AND METHODS: A controlled graded bleeding (6 - 36% loss of estimated total blood volume: ETBV) was performed in streptozotocin-induced diabetic rats (STZ rats) under a conscious state. Hemodynamic and autonomic responses to acute hemorrhage were examined using analysis of BP-HR variability. The effects of dextran treatment after hemorrhage were also examined. RESULTS: A significant reduction in mean arterial pressure began at 12% ETBV loss in STZ rats and 18% in the control rats, respectively. When blood loss reached 18% of TEBV, the decrease in HR was prominent in STD rats due to the activation of a parasympathetic drive, as indicated by the increase in high frequency (HF; 0.75~3.0 Hz) power in HR variability, while in the control rats this response was not observed. The administration of dextran prevented the activation of the parasympathetic drive in STZ rats during hemorrhaging. In the control rats, the dextran treatment sustained the initial increase in HR with reduced HF power in HR variability. CONCLUSION: STZ rats showed different hemodynamic and autonomic responses to acute hemorrhage from the control rats. STZ rats were prone to develop bradycardiac hypotension characterized by marked parasympathetic activation during hemorrhaging. This finding suggests enhancement of the Bezold-Jarisch reflex in STZ rats. Dextran treatment to maintain a normovolemic hemorrhage state inhibits this reflex. BioMed Central 2010-11-25 /pmc/articles/PMC3004820/ /pubmed/21106105 http://dx.doi.org/10.1186/1475-2840-9-78 Text en Copyright ©2010 Boku et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Investigation Boku, Aiji Sugimura, Mitsutaka Morimoto, Yoshinari Hanamoto, Hiroshi Niwa, Hitoshi Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats |
title | Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats |
title_full | Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats |
title_fullStr | Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats |
title_full_unstemmed | Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats |
title_short | Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats |
title_sort | hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004820/ https://www.ncbi.nlm.nih.gov/pubmed/21106105 http://dx.doi.org/10.1186/1475-2840-9-78 |
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