Exaggerated Pressor Response in Relation to Attenuated Muscle Temperature Response during Contraction in Ischemic Heart Failure.

Exaggerated Pressor Response in Relation to Attenuated Muscle Temperature Response during Contraction in Ischemic Heart Failure.
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缺血性心力衰竭期间收缩期间肌肉温度反应减弱的压力反应夸大了。

DOI:
10.3389/fphys.2012.00443
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发表时间:
2012
影响因子:
4
通讯作者:
Xing J
Xing J
中科院分区:
医学2区
文献类型:
--
作者:
Li J;Gao Z;Lu J;Xing J

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已知肌肉温度(Tm)随着运动而升高。本研究的目的是检查与健康对照动物相比,在慢性心肌梗死(MI)诱导的心力衰竭(HF)大鼠中,收缩诱导的Tm增加是否改变。将温度探针插入小腿三头肌中以在整个实验中连续测量Tm。通过电刺激坐骨神经1分钟诱导静态肌肉收缩。当基线Tm为34°C时,收缩使9只健康对照大鼠的温度升高1.6 ± 0.18°C,使10只MI大鼠的温度升高1.0 ± 0.15°C(与对照相比P < 0.05)。请注意,两组之间的肌肉张力和肌肉重量没有差异。此外,肌肉收缩使对照组大鼠的平均动脉压增加23 ± 3 mmHg,使MI大鼠的平均动脉压增加31 ± 3 mmHg(与对照组相比P < 0.05)。回归分析进一步表明,升压反应和静态收缩引起的Tm增加之间存在反线性关系。我们的数据表明,心肌梗死大鼠收缩引起的Tm增加受损。Tm的异常改变可能通过肌肉传入神经上的温度敏感性受体机制改变MI中的反射性心血管反应。
It is known that muscle temperature (Tm) increases with exercise. The purpose of this study was to examine if contraction-induced increase in Tm was altered in rats with heart failure (HF) induced by chronic myocardial infraction (MI) as compared with healthy control animals. A temperature probe was inserted in the triceps surae muscle to continuously measure Tm throughout experiments. Static muscle contraction was induced by electrical stimulation of the sciatic nerve for 1 min. As baseline Tm was 34°C, contraction increased temperature by 1.6 ± 0.18°C in nine health control rats and by 1.0 ± 0.15°C in 10 MI rats (P < 0.05 vs. control). Note that there were no differences in developed muscle tension and muscle weight between the two groups. In addition, muscle contraction increased mean arterial pressure by 23 ± 3 mmHg in control rats and by 31 ± 3 mmHg in MI rats (P < 0.05 vs. control). A regression analysis further shows that there is an inverse liner relationship between the pressor response and static contraction-induced increase in Tm. Our data suggest that Tm increase evoked by contraction is impaired in MI rats. The abnormal alteration in Tm likely modifies the reflex cardiovascular responses in MI via mechanisms of temperature-sensitive receptors on muscle afferent nerves.
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