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Effects of dexmedetomidine on porcine pulmonary artery vascular smooth muscle.
BMC Anesthesiology ( IF 2.2 ) Pub Date : 2019-09-12 , DOI: 10.1186/s12871-019-0843-2 Mami Chikuda 1 , Kenichi Sato 1
BMC Anesthesiology ( IF 2.2 ) Pub Date : 2019-09-12 , DOI: 10.1186/s12871-019-0843-2 Mami Chikuda 1 , Kenichi Sato 1
Affiliation
BACKGROUND
The α2-receptor agonist dexmedetomidine (Dex) has been shown to produce sedative and analgesic effects not only with systemic administration but also when administered in the extradural space and around peripheral nerves. The effects and mechanism of action of Dex on pulmonary arteries, however, have not been determined. This study therefore aimed to investigate the effect of Dex on pulmonary arterial vascular smooth muscle by evaluating changes in isometric contraction tension. We then attempted to determine the effects of Dex on depolarization stimulation and receptor stimulation.
METHODS
Endothelium-denuded porcine pulmonary arteries were sliced into 2- to 3-mm rings. We then exposed them to certain substances at various concentrations under different conditions of baseline stimulation (with KCl, adrenaline, caffeine, or histamine) and to α2-receptor stimulants or antagonists, or α1-receptor antagonists (imidazoline, yohimbine, rauwolscine, prazosin), and different conditions of Ca2+ depletion of the intracellular reservoir or extracellular stores. We measured the changes in isometric contraction tension with each addition or change in conditions.
RESULTS
Dex enhanced the contraction induced by high-concentration KCl stimulation. Dex-induced enhancement of contraction induced by high-concentration KCl was completely suppressed by yohimbine and rauwolscine, which are α2-receptor antagonists, but not by prazosin. Dex, imidazoline, yohimbine, and rauwolscine reduced the increases in contraction tension induced by the receptor stimulant adrenaline. Dex suppressed the adrenaline-induced increases in contraction tension after depletion of the Ca2+ reservoir. In the absence of extracellular Ca2+, Dex suppressed the adrenaline- and histamine-induced increases in contraction tension but did not affect caffeine-induced increases.
CONCLUSIONS
Dex-enhanced, high-concentration KCl-induced contraction was mediated by α2-receptors. Adrenaline-induced contraction was suppressed by the α2-receptor stimulant Dex and α2-receptor antagonists yohimbine and rauwolscine, suggesting that the effect of Dex on adrenaline-induced contraction is attributable to its α2-receptor-blocking action. Dex inhibited receptor-activated Ca2+ channels and phosphatidylinositol-1,4,5-triphosphate-induced Ca2+ release but not Ca2+-induced Ca2+ release.
中文翻译:
右美托咪定对猪肺动脉血管平滑肌的影响。
背景技术已经证明α2-受体激动剂右美托咪定(Dex)不仅在全身给药时而且在硬膜外间隙和周围神经周围给药时均具有镇静和镇痛作用。然而,尚未确定Dex对肺动脉的作用和作用机理。因此,本研究旨在通过评估等轴测收缩力的变化来研究Dex对肺动脉血管平滑肌的作用。然后,我们试图确定Dex对去极化刺激和受体刺激的影响。方法将内皮剥除的猪肺动脉切成2至3毫米的环。然后,我们在基线刺激的不同条件下将它们暴露于各种浓度的某些物质(使用KCl,肾上腺素,咖啡因,或组胺)以及对α2受体兴奋剂或拮抗剂,或对α1受体拮抗剂(咪唑啉,育亨宾,劳沃斯辛,哌唑嗪)以及细胞内贮库或细胞外贮存中Ca2 +消耗不同的条件。我们测量了每次添加或条件变化时等距收缩张力的变化。结果Dex增强了高浓度KCl刺激引起的收缩。Dex诱导的高浓度KCl引起的收缩增强被育亨宾和rauwolscine(它们是α2受体拮抗剂)完全抑制,但未被prazosin抑制。右旋糖酐,咪唑啉,育亨宾和劳伍西星减少了由受体兴奋剂肾上腺素引起的收缩张力的增加。Dex抑制了Ca2 +储层耗尽后肾上腺素引起的收缩张力增加。在不存在细胞外Ca2 +的情况下,Dex抑制了肾上腺素和组胺引起的收缩张力增加,但不影响咖啡因引起的增加。结论右旋糖增强的高浓度KCl诱导的收缩是由α2受体介导的。肾上腺素诱导的收缩被α2受体兴奋剂Dex和α2受体拮抗剂育亨宾和劳伍西辛抑制,这表明Dex对肾上腺素诱导的收缩的作用归因于其α2受体阻断作用。Dex抑制受体激活的Ca2 +通道和磷脂酰肌醇1,4,5-三磷酸诱导的Ca2 +释放,但不抑制Ca2 +诱导的Ca2 +释放。结论右旋糖增强的高浓度KCl诱导的收缩是由α2受体介导的。肾上腺素诱导的收缩被α2受体兴奋剂Dex和α2受体拮抗剂育亨宾和劳伍西辛抑制,这表明Dex对肾上腺素诱导的收缩的作用归因于其α2受体阻断作用。Dex抑制受体激活的Ca2 +通道和磷脂酰肌醇1,4,5-三磷酸诱导的Ca2 +释放,但不抑制Ca2 +诱导的Ca2 +释放。结论右旋糖增强的高浓度KCl诱导的收缩是由α2受体介导的。肾上腺素诱导的收缩被α2受体兴奋剂Dex和α2受体拮抗剂育亨宾和劳伍西辛抑制,这表明Dex对肾上腺素诱导的收缩的作用归因于其α2受体阻断作用。Dex抑制受体激活的Ca2 +通道和磷脂酰肌醇1,4,5-三磷酸诱导的Ca2 +释放,但不抑制Ca2 +诱导的Ca2 +释放。
更新日期:2019-09-12
中文翻译:
右美托咪定对猪肺动脉血管平滑肌的影响。
背景技术已经证明α2-受体激动剂右美托咪定(Dex)不仅在全身给药时而且在硬膜外间隙和周围神经周围给药时均具有镇静和镇痛作用。然而,尚未确定Dex对肺动脉的作用和作用机理。因此,本研究旨在通过评估等轴测收缩力的变化来研究Dex对肺动脉血管平滑肌的作用。然后,我们试图确定Dex对去极化刺激和受体刺激的影响。方法将内皮剥除的猪肺动脉切成2至3毫米的环。然后,我们在基线刺激的不同条件下将它们暴露于各种浓度的某些物质(使用KCl,肾上腺素,咖啡因,或组胺)以及对α2受体兴奋剂或拮抗剂,或对α1受体拮抗剂(咪唑啉,育亨宾,劳沃斯辛,哌唑嗪)以及细胞内贮库或细胞外贮存中Ca2 +消耗不同的条件。我们测量了每次添加或条件变化时等距收缩张力的变化。结果Dex增强了高浓度KCl刺激引起的收缩。Dex诱导的高浓度KCl引起的收缩增强被育亨宾和rauwolscine(它们是α2受体拮抗剂)完全抑制,但未被prazosin抑制。右旋糖酐,咪唑啉,育亨宾和劳伍西星减少了由受体兴奋剂肾上腺素引起的收缩张力的增加。Dex抑制了Ca2 +储层耗尽后肾上腺素引起的收缩张力增加。在不存在细胞外Ca2 +的情况下,Dex抑制了肾上腺素和组胺引起的收缩张力增加,但不影响咖啡因引起的增加。结论右旋糖增强的高浓度KCl诱导的收缩是由α2受体介导的。肾上腺素诱导的收缩被α2受体兴奋剂Dex和α2受体拮抗剂育亨宾和劳伍西辛抑制,这表明Dex对肾上腺素诱导的收缩的作用归因于其α2受体阻断作用。Dex抑制受体激活的Ca2 +通道和磷脂酰肌醇1,4,5-三磷酸诱导的Ca2 +释放,但不抑制Ca2 +诱导的Ca2 +释放。结论右旋糖增强的高浓度KCl诱导的收缩是由α2受体介导的。肾上腺素诱导的收缩被α2受体兴奋剂Dex和α2受体拮抗剂育亨宾和劳伍西辛抑制,这表明Dex对肾上腺素诱导的收缩的作用归因于其α2受体阻断作用。Dex抑制受体激活的Ca2 +通道和磷脂酰肌醇1,4,5-三磷酸诱导的Ca2 +释放,但不抑制Ca2 +诱导的Ca2 +释放。结论右旋糖增强的高浓度KCl诱导的收缩是由α2受体介导的。肾上腺素诱导的收缩被α2受体兴奋剂Dex和α2受体拮抗剂育亨宾和劳伍西辛抑制,这表明Dex对肾上腺素诱导的收缩的作用归因于其α2受体阻断作用。Dex抑制受体激活的Ca2 +通道和磷脂酰肌醇1,4,5-三磷酸诱导的Ca2 +释放,但不抑制Ca2 +诱导的Ca2 +释放。