CARDIAC DYSFUNCTIONS CAUSED BY HISTAMINE RELEASE

急性全身性心肌缺血和严重心律失常已被描述。 人类的过敏反应。心脏超敏反应将是 在实验动物中引起的，作为评估的第一步 心脏超敏反应是一个临床问题。因此，我们将在几内亚进行探索 猪、兔、猴心脏对多种过敏原致敏的药理学 在即刻超敏反应的各种介质中，即组胺， 花生四烯酸代谢的各种产物，慢反应物质 过敏反应(SRS-A)和血小板活化因子(PAF)。人体心脏组织 也将进行研究。免疫球蛋白E介导的心脏超敏反应模型 将会被调查。将寻求浓度-反应关系 释放的介质和心功能不全的程度之间的关系。改建 在前列环素由心脏产生时，会因过敏而 研究，特别是因为这可能会导致冠状动脉血管损伤 动态平衡或血栓形成。被释放的调解人之间的相互作用 以及各种疾病状态和药物，如心肌缺血，高血压， 甲状腺功能亢进症，洋地黄，利尿剂，将被调查。药理学 将寻求纠正和控制心脏功能障碍的方法 由即刻的过敏反应引起的。它也将被确定 类金龟子的释放，特别是组胺，是否可能是生理学上的 参与心脏交感神经功能的调节。这个 组胺与洋地黄缺血性心律失常的病理生理相互作用 毒性和甲状腺功能亢进症也将被检查。因为组胺可以 以任何方式在任何地点发布，这项工作将定义心脏对 少校金刚鹦鹉。在这样做的时候，这项研究应该会揭开迄今未知的面纱 常见心血管疾病的发病机制。

Myocardial ischemia and severe arrhythmias have been described in acute systemic allergic reactions in humans. Cardiac hypersensitivity reactions will be elicited in the experimental animal, as a first step in the assessment of cardiac hypersensitivity as a clinical problem. Thus, we will explore in guinea pig, rabbit and monkey heart sensitized to various allergens, the pharmacology of the various mediators of immediate hypersensitivity, i.e., histamine, the various products of arachidonic acid metabolism, slow reacting substance of anaphylaxis (SRS-A) and platelet activating factor (PAF). Human cardiac tissue will also be studied. Models of IgE-mediated cardiac hypersensitivity reactions will be investigated. Concentration-response relationships will be sought between released mediators and the extent of cardiac dysfunction. Alterations in prostacyclin generation by the heart as a result of hypersensitivity will be studied, particularly as this may lead to impairment of coronary vascular homeostasis or to thrombus formation. Interactions between released mediators and various disease states and drugs, i.e., myocardial ischemia, hypertension, hyperthyroidism, digitalis, diuretics, will be investigated. Pharmacologic means will be sought for correcting and controlling the cardiac dysfunctions caused by immediate hypersensitivity reactions. It will also be ascertained whether autacoid release, particularly histamine, may be physiologically involved in the regulation of cardiac sympathetic function. The pathophysiologic interactions of histamine with ischemic arrhythmias, digitalis toxicity and hyperthyroidism will also be examined. Since histamine can be released at any site by any means, this work will define cardiac responses to a major autacoid. In so doing, the research should uncover hitherto unknown mechanisms of common cardiovascular diseases.