Effects of nitric oxide synthase inhibition on the muscle blood flow response to exercise in rats with heart failure

Tadakazu Hirai, Robert Zelis, Timothy I. Musch

Research output: Contribution to journalArticle

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Abstract

Objective: The aim of this study was to investigate whether the role of nitric oxide (NO) in regulating blood flow (BF) to working skeletal muscle is impaired in chronic heart failure (CHF). Methods: The effect of N G -nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, was studied in conscious rats with and without CHF due to myocardial infarction (MI). BF to the hindquarter musculature was measured with radiolabelled microspheres during exercise after 4 min of treadmill running (10% grade, 20 m/min) before and after L-NAME (20 mg/kg i.a.) administration. Results: Before L-NAME administration, BF measured in the total hindquarter musculature was less (P ` 0.05) during exercise in rats with a large MI (MI size; 44 ± 2% of the left ventricular endocardial circumference; n = 8) when compared with sham-operated rats (SHAM; n = 10) and rats with a small MI (MI size; 25 ± 4%; n = 5). The BF measured during exercise following L-NAME administration was similar between the 3 groups. of the 28 individual hindquarter muscles, BF was reduced in 23 and 19 muscles following the administration of L-NAME for the SHAM rats and rats with a small MI, respectively. In comparison, BF was reduced to only 4 of 28 muscles in rats with a large MI. Conclusions: These results suggest that the contribution of the NO pathway to the hyperaemic BF responses found in the hindquarter muscles during exercise could be attenuated in rats with CHF. This attenuation of the NO pathway may be associated with the impairment of skeletal muscle BF distribution during exercise in CHF.

Original languageEnglish (US)
Pages (from-to)469-476
Number of pages8
JournalCardiovascular Research
Volume30
Issue number3
DOIs
StatePublished - Jan 1 1995

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Nitric Oxide Synthase
NG-Nitroarginine Methyl Ester
Heart Failure
Myocardial Infarction
Muscles
Nitric Oxide
Skeletal Muscle
Microspheres
Running

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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title = "Effects of nitric oxide synthase inhibition on the muscle blood flow response to exercise in rats with heart failure",
abstract = "Objective: The aim of this study was to investigate whether the role of nitric oxide (NO) in regulating blood flow (BF) to working skeletal muscle is impaired in chronic heart failure (CHF). Methods: The effect of N G -nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, was studied in conscious rats with and without CHF due to myocardial infarction (MI). BF to the hindquarter musculature was measured with radiolabelled microspheres during exercise after 4 min of treadmill running (10{\%} grade, 20 m/min) before and after L-NAME (20 mg/kg i.a.) administration. Results: Before L-NAME administration, BF measured in the total hindquarter musculature was less (P ` 0.05) during exercise in rats with a large MI (MI size; 44 ± 2{\%} of the left ventricular endocardial circumference; n = 8) when compared with sham-operated rats (SHAM; n = 10) and rats with a small MI (MI size; 25 ± 4{\%}; n = 5). The BF measured during exercise following L-NAME administration was similar between the 3 groups. of the 28 individual hindquarter muscles, BF was reduced in 23 and 19 muscles following the administration of L-NAME for the SHAM rats and rats with a small MI, respectively. In comparison, BF was reduced to only 4 of 28 muscles in rats with a large MI. Conclusions: These results suggest that the contribution of the NO pathway to the hyperaemic BF responses found in the hindquarter muscles during exercise could be attenuated in rats with CHF. This attenuation of the NO pathway may be associated with the impairment of skeletal muscle BF distribution during exercise in CHF.",
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Effects of nitric oxide synthase inhibition on the muscle blood flow response to exercise in rats with heart failure. / Hirai, Tadakazu; Zelis, Robert; Musch, Timothy I.

In: Cardiovascular Research, Vol. 30, No. 3, 01.01.1995, p. 469-476.

Research output: Contribution to journalArticle

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AU - Hirai, Tadakazu

AU - Zelis, Robert

AU - Musch, Timothy I.

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N2 - Objective: The aim of this study was to investigate whether the role of nitric oxide (NO) in regulating blood flow (BF) to working skeletal muscle is impaired in chronic heart failure (CHF). Methods: The effect of N G -nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, was studied in conscious rats with and without CHF due to myocardial infarction (MI). BF to the hindquarter musculature was measured with radiolabelled microspheres during exercise after 4 min of treadmill running (10% grade, 20 m/min) before and after L-NAME (20 mg/kg i.a.) administration. Results: Before L-NAME administration, BF measured in the total hindquarter musculature was less (P ` 0.05) during exercise in rats with a large MI (MI size; 44 ± 2% of the left ventricular endocardial circumference; n = 8) when compared with sham-operated rats (SHAM; n = 10) and rats with a small MI (MI size; 25 ± 4%; n = 5). The BF measured during exercise following L-NAME administration was similar between the 3 groups. of the 28 individual hindquarter muscles, BF was reduced in 23 and 19 muscles following the administration of L-NAME for the SHAM rats and rats with a small MI, respectively. In comparison, BF was reduced to only 4 of 28 muscles in rats with a large MI. Conclusions: These results suggest that the contribution of the NO pathway to the hyperaemic BF responses found in the hindquarter muscles during exercise could be attenuated in rats with CHF. This attenuation of the NO pathway may be associated with the impairment of skeletal muscle BF distribution during exercise in CHF.

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