The role of myogenic relaxation, adenosine and prostaglandins in human forearm reactive hyperaemia.
The role of myogenic relaxation, adenosine and prostaglandins in human forearm reactive hyperaemia.
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肌源性松弛、腺苷和前列腺素在人前臂反应性充血中的作用。
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发表时间：
1987
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影响因子：
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通讯作者：
Åke Wennmalm
中科院分区：
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作者：
I. Carlsson;A. Sollevi;Åke Wennmalm
1.在基础状态和上臂动脉或静脉血流阻断1 - 20分钟后，测量健康年轻男性和女性志愿者的双侧前臂血流。在使用影响血管的肾上腺素和/或腺苷的药物进行预处理后重复研究。2.一只手臂同时动脉闭塞和对侧手臂静脉闭塞长达20分钟，导致动脉闭塞手臂出现相当大的反应性充血，但静脉闭塞手臂的闭塞后血流完全未能高于闭塞前水平。3.当动脉闭塞从1分钟增加到20分钟时，随后的反应性充血逐渐增加，高达30 ml/100 ml组织。动脉闭塞1 - 3分钟后的时间依赖性是基于闭塞后峰值血流的促进，而动脉闭塞从3分钟延长至20分钟主要通过延长反应性充血的持续时间来增强反应性充血。4.布洛芬抑制前列腺素合成可使动脉闭塞3 - 5分钟后的总反应性充血减少70%。这种衰减是由于闭塞后峰值血流减少和闭塞后充血持续时间缩短所致。5.腺苷受体拮抗剂茶碱减少反应性充血后5分钟的动脉闭塞约35%。联合治疗布洛芬和茶碱并没有减少反应性充血超过任何一种药物单独。6.输注潘生丁（一种抑制腺苷消除的药物）使反应性充血增强约45%。双嘧达莫的这种作用被茶碱和布洛芬完全抑制。7.腺苷、次黄嘌呤和尿酸的血浆水平在反应性充血期间得以维持，表明在缺血期间或缺血后立即产生的嘌呤增加。8.结论是，血管舒张反应血流中断的足够的刺激是忽略血管壁扩张。局部代谢因素，如内源性形成的腺苷和腺苷可能会协同作用，这种生肌反应，但似乎是无活性的单独。布洛芬和茶碱的相加作用的缺乏表明了由野牡丹素和腺苷诱导的血管舒张之间的联系。
1. Forearm blood flow was measured bilaterally in healthy young male and female volunteers, in the basal state and after upper‐arm occlusion of arterial or venous blood flow for 1‐20 min. The investigations were repeated after pre‐treatment with drugs affecting vascular prostaglandins and/or adenosine. 2. Simultaneous arterial occlusion in one arm and venous occlusion in the contralateral arm for up to 20 min elicited a considerable reactive hyperaemia in the arm subjected to arterial occlusion, but completely failed to elevate the post‐occlusive flow in the arm subjected to venous occlusion above the pre‐occlusive level. 3. When the arterial occlusion was increased from 1 to 20 min there was a progressive increase in the subsequent reactive hyperaemia, up to 30 ml 100 ml tissue‐1. The time dependence following 1‐3 min of arterial occlusion was based on a facilitation of the peak post‐occlusive flow, while prolongation of the arterial occlusion from 3 to 20 min augmented the reactive hyperaemia mainly by increasing its duration. 4. Inhibition of prostaglandin synthesis with ibuprofen reduced the total reactive hyperaemia following 3‐5 min of arterial occlusion by up to 70%. This attenuation was due both to a reduction of peak post‐occlusive flow and to a shortening of the duration of the post‐occlusive hyperaemia. 5. The adenosine receptor antagonist theophylline reduced the reactive hyperaemia following 5 min of arterial occlusion by about 35%. Combined treatment with ibuprofen and theophylline did not reduce the reactive hyperaemia more than either drug alone. 6. Infusion of dipyridamole, a drug which inhibits the elimination of adenosine, reinforced the reactive hyperaemia by about 45%. This effect of dipyridamole was completely inhibited by administration of theophylline, and also by ibuprofen. 7. Plasma levels of adenosine, hypoxanthine and uric acid were maintained during the reactive hyperaemia, indicating increased production of purines during or immediately after the ischaemia. 8. It is concluded that the adequate stimulus for vascular relaxation in response to interruption of blood flow is omission of vessel wall distension. Local metabolic factors like endogenously formed prostaglandins and adenosine may act synergistically to this myogenic response but seem to be inactive alone. The lack of additive effects of ibuprofen and theophylline suggests a link between vascular relaxation induced by prostaglandins and by adenosine.