Lindblad L E, Shepherd J T, Vanhoutte P M
Proc Soc Exp Biol Med. 1984 Jun;176(2):119-22. doi: 10.3181/00379727-176-41850.
The effect of cooling on platelet-induced contractions was studied. Rings of canine saphenous arteries were suspended for isometric tension recording in organ baths filled with aerated physiological salt solution. Norepinephrine, 5-hydroxytryptamine, and autologous aggregating platelets all caused contractions that were augmented by cooling the bath content from 37 to 24 degrees C. These contractions were inhibited, in a concentration-dependent manner, by the serotonergic antagonist ketanserin. The alpha 1-adrenergic antagonist, prazosin, in concentrations causing progressive inhibition of contractions evoked by norepinephrine did not affect the response to either 5-hydroxytryptamine or platelets. Aggregating platelets were found to release 5-hydroxytryptamine in sufficient amounts to account for the observed contractions. Pretreatment of platelets with the cyclo-oxygenase inhibitor meclofenamate reduced the amount of thromboxane liberated by aggregating platelets but did not influence evoked contractions. These observations suggest that aggregating platelets cause contraction of the canine saphenous artery by releasing 5-hydroxytryptamine. They demonstrate that cooling markedly augments contractions of peripheral arterial smooth muscle caused by aggregating platelets.
研究了降温对血小板诱导收缩的影响。将犬隐动脉环悬挂于充满通气生理盐溶液的器官浴槽中以记录等长张力。去甲肾上腺素、5-羟色胺和自体聚集血小板均引起收缩,当浴槽内容物从37℃冷却至24℃时,这些收缩增强。这些收缩被5-羟色胺能拮抗剂酮色林以浓度依赖性方式抑制。α1-肾上腺素能拮抗剂哌唑嗪在引起去甲肾上腺素诱发的收缩逐渐受到抑制的浓度下,对5-羟色胺或血小板的反应没有影响。发现聚集的血小板释放出足以解释所观察到的收缩的5-羟色胺量。用环氧化酶抑制剂甲氯芬那酸预处理血小板可减少聚集血小板释放的血栓素量,但不影响诱发的收缩。这些观察结果表明,聚集的血小板通过释放5-羟色胺引起犬隐动脉收缩。它们证明降温显著增强聚集血小板引起的外周动脉平滑肌收缩。