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首页> 外文期刊>American Journal of Physiology >Role of activated platelets in excitation of cardiac afferents during myocardial ischemia in cats.
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Role of activated platelets in excitation of cardiac afferents during myocardial ischemia in cats.

机译:活化的血小板在猫心肌缺血期间激发心脏传入的作用。

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摘要

Myocardial ischemia activates cardiac spinal afferents that mediate chest pain and excitatory reflex cardiovascular responses. Platelets are activated during myocardial ischemia and release 5-hydroxytryptamine, which stimulates abdominal spinal afferents. This study investigated the role of activated platelets in excitation of cardiac spinal afferents during ischemia. Platelet-rich plasma (PRP) and platelet-poor plasma (PPP) were obtained from cats and incubated with collagen (2 mg/ml) or thrombin (5 U/ml). We observed reduction of platelets in PRP indicative of platelet activation by collagen and thrombin, respectively. Activity of single-unit, ischemia-sensitive cardiac spinal afferents was recorded from the left sympathetic chain in anesthetized cats. Injection of 1.5 ml PRP + collagen (activated platelets) into the left atrium (LA) stimulated 12 of 13 cardiac afferents. PRP + saline (nonactivated platelets, LA) and PPP + collagen did not alter activity of these afferents. PRP + thrombin (1.5 ml, LA) stimulated eight of nine other cardiac afferents, whereas PPP + thrombin did not stimulate any of the nine afferents. Antiplatelet immune serum (1 ml/kg iv) significantly decreased circulating platelets as well as neutrophils (polymorphonuclear leukocytes, PMNs) in eight other cats, and in each animal, attenuated the ischemia-related increase in activity of cardiac afferents. Conversely, responses of five separate cardiac afferents to ischemia were not diminished after treatment with anti-PMN immune serum when concentration of circulating platelets was maintained by infusion of donated PRP despite the decrease in circulating PMNs. These data indicate activated platelets stimulate ischemia-sensitive cardiac spinal afferents and contribute to activation of these afferents during ischemia.
机译:心肌缺血会激活介导胸痛和兴奋性反射性心血管反应的心脏脊髓传入神经。血小板在心肌缺血过程中被激活并释放出5-羟色胺,从而刺激腹部脊髓传入神经。这项研究调查了活化的血小板在缺血过程中对心脏脊髓传入神经兴奋的作用。从猫中获得富血小板血浆(PRP)和贫血小板血浆(PPP),并与胶原蛋白(2 mg / ml)或凝血酶(5 U / ml)孵育。我们观察到PRP中的血小板减少,分别表明胶原蛋白和凝血酶激活了血小板。在麻醉的猫中,从左交感神经链记录了对缺血敏感的单单位心脏脊髓传入神经的活性。向左心房(LA)注射1.5 ml PRP +胶原蛋白(活化的血小板)可刺激13个心脏传入神经中的12个。 PRP +生理盐水(未活化的血小板,洛杉矶)和PPP +胶原蛋白不会改变这些传入的活性。 PRP +凝血酶(1.5 ml,洛杉矶)刺激了其他九个心脏传入的刺激,而PPP +凝血酶没有刺激九个心脏传入的刺激。抗血小板免疫血清(1 ml / kg iv)在另外八只猫中显着减少了循环血小板以及中性粒细胞(多形核白细胞,PMNs),并且在每只动物中,都减弱了缺血相关的心脏传入活动的增加。相反,尽管输注的PRP有所减少,但通过输注捐赠的PRP维持了循环血小板的浓度,但用抗PMN免疫血清治疗后,五个独立的心脏传入神经对缺血的反应并未减弱。这些数据表明,活化的血小板刺激缺血敏感的心脏脊髓传入神经,并有助于缺血过程中这些传入神经的激活。

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