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首页> 外文学位 >Cardiovascular Effects Evoked by Airway Nociceptive Reflexes in Healthy and Cardiovascular Diseased Rats.
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Cardiovascular Effects Evoked by Airway Nociceptive Reflexes in Healthy and Cardiovascular Diseased Rats.

机译：健康和心血管疾病大鼠的气道伤害感受反射引起的心血管效应。

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摘要

Acute inhalation of airborne pollutants alters cardiovascular function and has been shown to have its greatest affects on individuals with pre-existing cardiovascular disease. Evidence suggests that pollutant-induced activation of airway sensory nerves via the gating of ion channels is critical to these systemic responses. Here, we have investigated the cardiovascular responses evoked by inhalation of AITC (TRPA1 agonist) and capsaicin (TRPV1 agonist) in healthy Sprague Dawley (SD) and Wistar Kyoto (WKY) rats, and cardiovascular diseased Spontaneously Hypertensive (SH) rats. Inhalation of the agonists by healthy SD and WKY rats caused significant bradycardia, atrio-ventricular (AV) block and prolonged PR-Intervals. Inhalation of TRP agonists caused differential cardiovascular responses in the cardiovascular diseased SH rats, such that the TRP agonists evoked brady-tachy with AV block and premature ventricular contractions (PVCs). Bradycardic responses to AITC were inhibited by the TRP channel blocker ruthenium red and the muscarinic antagonist atropine, but atropine did not prevent the tachycardic responses seen in the SH rats. Adrenergic inhibition with atenolol prevented the tachycardic responses, but did not prevent the bradycardic responses evoked by AITC in the SH rats. In healthy rats, AITC inhalation also caused a biphasic blood pressure response: a brief hypertensive phase followed by a hypotensive phase, while evoking hypertension in the SH rats. Atropine accentuated the hypertensive phase in all animals, while preventing the hypotension in the healthy animals. In all animals, AITC-evoked heart rate responses were not abolished by terazosin, the ?1 adrenoceptor inhibitor, which prevented the hypertensive responses. Anesthetics had profound effects on AITC-evoked bradycardia and AV block, which was abolished by urethane, ketamine and isoflurane. Nevertheless, AITC inhalation caused bradycardia and AV block in paralyzed and ventilated rats following pre-collicular decerebration. In conclusion, we provide evidence that activation of TRP channels expressed on nociceptive airway sensory nerves causes significant cardiovascular effects in healthy rats via reflex modulation of the autonomic nervous system (ANS), and that these effects are exacerbated in cardiovascular diseased rats.
机译：急性吸入空气中的污染物会改变心血管功能，并且已被证明对患有心血管疾病的个体有最大的影响。有证据表明，污染物通过离子通道的门控引起的气道感觉神经的激活对于这些全身反应至关重要。在这里，我们研究了健康的Sprague Dawley（SD）和Wistar Kyoto（WKY）大鼠以及心血管疾病自发性高血压（SH）大鼠吸入AITC（TRPA1激动剂）和辣椒素（TRPV1激动剂）诱发的心血管反应。健康的SD和WKY大鼠吸入激动剂会导致严重的心动过缓，房室（AV）阻滞并延长PR间隔。吸入TRP激动剂会在患有心血管疾病的SH大鼠中引起差异化的心血管反应，因此TRP激动剂会引起伴有AV阻滞和室性早搏（PVC）的近距性心动过速。 TRP通道阻滞剂钌红和毒蕈碱拮抗剂阿托品抑制了对AITC的心动过缓反应，但阿托品不能阻止SH大鼠的心动过速反应。阿替洛尔抑制肾上腺素能阻止心动过速反应，但不能预防AITC在SH大鼠中引起的心动过缓反应。在健康大鼠中，吸入AITC也会引起双相血压反应：短暂的高血压期，然后是降压期，而在SH大鼠中引起高血压。阿托品会加重所有动物的高血压阶段，同时防止健康动物的低血压。在所有动物中，β1肾上腺素受体抑制剂特拉唑嗪并未消除AITC引起的心率反应，后者可预防高血压反应。麻醉剂对AITC引起的心动过缓和房室传导阻滞具有深远的影响，而氨基甲酸乙酯，氯胺酮和异氟烷已将其取消。尽管如此，人工吸入性AITC吸入会在前脑去脑后瘫痪和通气的大鼠中引起心动过缓和房室传导阻滞。总之，我们提供的证据表明，通过伤害性自主神经系统（ANS）的调节，伤害性气道感觉神经上表达的TRP通道的激活在健康大鼠中引起了显着的心血管作用，并且在心血管疾病大鼠中这些作用加剧了。

著录项

  • 作者

    Hooper, Justin S.;

  • 作者单位

    University of South Florida.;

  • 授予单位 University of South Florida.;
  • 学科 Pharmacology.;Physiology.
  • 学位 Ph.D.
  • 年度 2016
  • 页码 149 p.
  • 总页数 149
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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