Energetics in arterioles during nitric oxide dependent and independent vasodilation

Masahiro Shibata, Takehiro Yamakoshi, Ken Ichi Yamakoshi

研究成果: Conference contribution

1 引用 (Scopus)

抄録

The objective of this study was to evaluate whether the nitric oxide (NO) would decrease vessel wall oxygen consumption by decreasing the mechanical work of vascular smooth muscle. The oxygen consumption rate (QO2) of arteriolar walls in rat cremaster muscle was determined in vivo during NO dependent and -independent vasodilation based on the intra- and perivascular oxygen tension (PO2) measured by phosphorescence quenching technique. NO dependent vasodilation was induced by increased NO production due to increased blood flow, while NO independent vasodilation was induced by topical administration of papaverine. The energy efficiency was evaluated by the variable ratio of wall tension to QO2 between normal and vasodilated conditions. NO dependent and -independent dilation increased arteriolar diameters by 13% and 17%, respectively. Vascular wall QO2 decreased significantly during both dilations. There was no significant difference between the energy efficiency during NO dependent and -independent vasodilation, suggesting the decrease in vascular wall QO2 produced by NO to be related to a decrease in the mechanical work of vascular smooth muscle.

元の言語English
ホスト出版物のタイトルAnnual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings
ページ1695-1698
ページ数4
DOI
出版物ステータスPublished - 2007
外部発表Yes
イベント29th Annual International Conference of IEEE-EMBS, Engineering in Medicine and Biology Society, EMBC'07 - Lyon
継続期間: 2007 8 232007 8 26

Other

Other29th Annual International Conference of IEEE-EMBS, Engineering in Medicine and Biology Society, EMBC'07
Lyon
期間07/8/2307/8/26

Fingerprint

Nitric oxide
Muscle
Oxygen
Energy efficiency
Phosphorescence
Vasodilation
Rats
Quenching
Blood

ASJC Scopus subject areas

  • Biomedical Engineering

これを引用

Shibata, M., Yamakoshi, T., & Yamakoshi, K. I. (2007). Energetics in arterioles during nitric oxide dependent and independent vasodilation. : Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings (pp. 1695-1698). [4352635] https://doi.org/10.1109/IEMBS.2007.4352635

Energetics in arterioles during nitric oxide dependent and independent vasodilation. / Shibata, Masahiro; Yamakoshi, Takehiro; Yamakoshi, Ken Ichi.

Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings. 2007. p. 1695-1698 4352635.

研究成果: Conference contribution

Shibata, M, Yamakoshi, T & Yamakoshi, KI 2007, Energetics in arterioles during nitric oxide dependent and independent vasodilation. : Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings., 4352635, pp. 1695-1698, 29th Annual International Conference of IEEE-EMBS, Engineering in Medicine and Biology Society, EMBC'07, Lyon, 07/8/23. https://doi.org/10.1109/IEMBS.2007.4352635
Shibata M, Yamakoshi T, Yamakoshi KI. Energetics in arterioles during nitric oxide dependent and independent vasodilation. : Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings. 2007. p. 1695-1698. 4352635 https://doi.org/10.1109/IEMBS.2007.4352635
Shibata, Masahiro ; Yamakoshi, Takehiro ; Yamakoshi, Ken Ichi. / Energetics in arterioles during nitric oxide dependent and independent vasodilation. Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings. 2007. pp. 1695-1698
@inproceedings{17aa9843a1af48cbb421845d1f9e5358,
title = "Energetics in arterioles during nitric oxide dependent and independent vasodilation",
abstract = "The objective of this study was to evaluate whether the nitric oxide (NO) would decrease vessel wall oxygen consumption by decreasing the mechanical work of vascular smooth muscle. The oxygen consumption rate (QO2) of arteriolar walls in rat cremaster muscle was determined in vivo during NO dependent and -independent vasodilation based on the intra- and perivascular oxygen tension (PO2) measured by phosphorescence quenching technique. NO dependent vasodilation was induced by increased NO production due to increased blood flow, while NO independent vasodilation was induced by topical administration of papaverine. The energy efficiency was evaluated by the variable ratio of wall tension to QO2 between normal and vasodilated conditions. NO dependent and -independent dilation increased arteriolar diameters by 13{\%} and 17{\%}, respectively. Vascular wall QO2 decreased significantly during both dilations. There was no significant difference between the energy efficiency during NO dependent and -independent vasodilation, suggesting the decrease in vascular wall QO2 produced by NO to be related to a decrease in the mechanical work of vascular smooth muscle.",
author = "Masahiro Shibata and Takehiro Yamakoshi and Yamakoshi, {Ken Ichi}",
year = "2007",
doi = "10.1109/IEMBS.2007.4352635",
language = "English",
isbn = "1424407885",
pages = "1695--1698",
booktitle = "Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings",

}

TY - GEN

T1 - Energetics in arterioles during nitric oxide dependent and independent vasodilation

AU - Shibata, Masahiro

AU - Yamakoshi, Takehiro

AU - Yamakoshi, Ken Ichi

PY - 2007

Y1 - 2007

N2 - The objective of this study was to evaluate whether the nitric oxide (NO) would decrease vessel wall oxygen consumption by decreasing the mechanical work of vascular smooth muscle. The oxygen consumption rate (QO2) of arteriolar walls in rat cremaster muscle was determined in vivo during NO dependent and -independent vasodilation based on the intra- and perivascular oxygen tension (PO2) measured by phosphorescence quenching technique. NO dependent vasodilation was induced by increased NO production due to increased blood flow, while NO independent vasodilation was induced by topical administration of papaverine. The energy efficiency was evaluated by the variable ratio of wall tension to QO2 between normal and vasodilated conditions. NO dependent and -independent dilation increased arteriolar diameters by 13% and 17%, respectively. Vascular wall QO2 decreased significantly during both dilations. There was no significant difference between the energy efficiency during NO dependent and -independent vasodilation, suggesting the decrease in vascular wall QO2 produced by NO to be related to a decrease in the mechanical work of vascular smooth muscle.

AB - The objective of this study was to evaluate whether the nitric oxide (NO) would decrease vessel wall oxygen consumption by decreasing the mechanical work of vascular smooth muscle. The oxygen consumption rate (QO2) of arteriolar walls in rat cremaster muscle was determined in vivo during NO dependent and -independent vasodilation based on the intra- and perivascular oxygen tension (PO2) measured by phosphorescence quenching technique. NO dependent vasodilation was induced by increased NO production due to increased blood flow, while NO independent vasodilation was induced by topical administration of papaverine. The energy efficiency was evaluated by the variable ratio of wall tension to QO2 between normal and vasodilated conditions. NO dependent and -independent dilation increased arteriolar diameters by 13% and 17%, respectively. Vascular wall QO2 decreased significantly during both dilations. There was no significant difference between the energy efficiency during NO dependent and -independent vasodilation, suggesting the decrease in vascular wall QO2 produced by NO to be related to a decrease in the mechanical work of vascular smooth muscle.

UR - http://www.scopus.com/inward/record.url?scp=57649217298&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=57649217298&partnerID=8YFLogxK

U2 - 10.1109/IEMBS.2007.4352635

DO - 10.1109/IEMBS.2007.4352635

M3 - Conference contribution

C2 - 18002301

AN - SCOPUS:57649217298

SN - 1424407885

SN - 9781424407880

SP - 1695

EP - 1698

BT - Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings

ER -