Impaired endothelium-dependent responses of skeletal muscle arterioles during chronic heart failure: Role of oxygen radicals

Sean P. Didion, William G. Mayhan

Research output: Contribution to journalArticle

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Abstract

The goal of this study was to test the hypothesis that administration of superoxide dismutase (SOD, an oxygen radical scavenger) restores impaired endothelium-dependent dilatation of rat skeletal muscle arterioles during chronic heart failure. Heart failure was induced in Sprague-Dawley rats by coronary artery ligation, which produced =40% infarction of the left ventricle. Four weeks following coronary artery ligation (n=7) or sham (control; n=5) surgery the spinotrapezius muscle was prepared for direct visualization of the microcirculation. Responses of third order arterioles (32.5±0.4 microns) to topical suffusion of the endothelium-dependent agonists acetylcholine and bradykinin and to the endothelium-independent agonist sodium nitroprusside were measured in both groups via intravital microscopy. Response of arterioles to acetylcholine was significantly less (p<0.05) in heart failure animals (0.1 μM = 3.8% and 1.0 μM = 10.2% change from baseline) as compared to control animals (0.1 μM = 15.5% and 1.0 μM = 32.6% change from baseline). Response of arterioles to bradykinin was significantly less (p<0.05) in heart failure animals (0.01 μM = 13.7% and 0.1 μM = 21.3% change from baseline) as compared to control animals (0.01 μM = 27.6% and 0.1 μM = 55.5% change from baseline). In contrast, response of arterioles to sodium nitroprusside (10 and 100 μM) was not different between groups (p>0.05). The impaired responses observed in heart failure animals could be partially restored by =38% towards that observed in controls following 30 minutes of a continuous topical suffusion of SOD (150 U/ml). SOD did not alter vasodilatory responses in control animals (p>0.05). Thus, it appears that altered production of oxygen radicals, to inactivate nitric oxide, may partially explain the impaired arteriolar reactivity observed during heart failure.

Original languageEnglish (US)
Pages (from-to)A44
JournalFASEB Journal
Volume11
Issue number3
StatePublished - Dec 1 1997

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Arterioles
heart failure
endothelium
Endothelium
Muscle
skeletal muscle
reactive oxygen species
Reactive Oxygen Species
superoxide dismutase
Skeletal Muscle
Heart Failure
coronary vessels
acetylcholine
agonists
Ligation
Rats
Coronary Vessels
Animals
Microcirculation
bradykinin

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

Impaired endothelium-dependent responses of skeletal muscle arterioles during chronic heart failure : Role of oxygen radicals. / Didion, Sean P.; Mayhan, William G.

In: FASEB Journal, Vol. 11, No. 3, 01.12.1997, p. A44.

Research output: Contribution to journalArticle

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abstract = "The goal of this study was to test the hypothesis that administration of superoxide dismutase (SOD, an oxygen radical scavenger) restores impaired endothelium-dependent dilatation of rat skeletal muscle arterioles during chronic heart failure. Heart failure was induced in Sprague-Dawley rats by coronary artery ligation, which produced =40{\%} infarction of the left ventricle. Four weeks following coronary artery ligation (n=7) or sham (control; n=5) surgery the spinotrapezius muscle was prepared for direct visualization of the microcirculation. Responses of third order arterioles (32.5±0.4 microns) to topical suffusion of the endothelium-dependent agonists acetylcholine and bradykinin and to the endothelium-independent agonist sodium nitroprusside were measured in both groups via intravital microscopy. Response of arterioles to acetylcholine was significantly less (p<0.05) in heart failure animals (0.1 μM = 3.8{\%} and 1.0 μM = 10.2{\%} change from baseline) as compared to control animals (0.1 μM = 15.5{\%} and 1.0 μM = 32.6{\%} change from baseline). Response of arterioles to bradykinin was significantly less (p<0.05) in heart failure animals (0.01 μM = 13.7{\%} and 0.1 μM = 21.3{\%} change from baseline) as compared to control animals (0.01 μM = 27.6{\%} and 0.1 μM = 55.5{\%} change from baseline). In contrast, response of arterioles to sodium nitroprusside (10 and 100 μM) was not different between groups (p>0.05). The impaired responses observed in heart failure animals could be partially restored by =38{\%} towards that observed in controls following 30 minutes of a continuous topical suffusion of SOD (150 U/ml). SOD did not alter vasodilatory responses in control animals (p>0.05). Thus, it appears that altered production of oxygen radicals, to inactivate nitric oxide, may partially explain the impaired arteriolar reactivity observed during heart failure.",
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