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Temperature response in contracting skeletal muscle after myocardial infraction
Author(s) -
Li Jianhua,
Gao Zhaohui,
Xing Jihong,
Sinoway Lawrence I.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1270-b
Subject(s) - medicine , endocrinology , stimulation , contraction (grammar) , skeletal muscle , muscle contraction , purinergic receptor , peripheral , receptor , hindlimb , chemistry
The cardiovascular responses induced by activation of purinergic P2X receptors and transient receptor potential vanilloid type 1 (TRPV1 or VR1) on muscle afferent nerves are abnormal in heart failure (HF). Also, these receptors are sensitive to change of temperature. It is known that muscle temperature is increased in exercising muscle. The purpose of this study, therefore, was to examine if temperature response in contracting muscle was altered in rats with HF induced by chronic myocardial infraction (MI) as compared with healthy control animals. In decerebrated rats, temperature probes were inserted in the triceps surae muscle to continuously measure muscle temperature throughout experiments. Static muscle contraction was induced by electrical stimulation of the sciatic nerves for 1 min. Contraction increased peak muscle temperature by 1.6±0.18 C° from baseline of 34.0 C° in nine health control rats and by 1.0±0.15 C° from 34.0 C° in ten MI rats. The increase of muscle temperature was significantly blunted in MI. It is noted that there was no difference in developed muscle tension and muscle weight between the two groups. In addition, a regression analysis shows that there is an inverse liner relationship between the pressor response and temperature response induced by static contraction. Our data suggest that muscle temperature response is impaired in HF. This may alter muscle afferent‐mediated pressor response via temperature sensitive P2X and TRPV1 receptors. Supported by NIH R01 HL075533 (Li), R01 HL078866 (Li) and R01 HL060800 (Sinoway).