CARDIAC DYSFUNCTIONS CAUSED BY HISTAMINE RELEASE

心肌缺血和严重心律失常已被描述在急性全身性 人类的过敏反应。 心脏超敏反应将 在实验动物中引起，作为评估的第一步， 心脏超敏反应是一个临床问题。 因此，我们将在几内亚探索 对各种过敏原致敏的猪、兔和猴心脏， 各种速发型超敏反应介质，即，组织胺 花生四烯酸代谢的各种产物， 过敏反应（SRS-A）和血小板活化因子（PAF）。 人心脏组织 也将被研究。 IgE介导的心脏超敏反应模型 将被调查。 将寻求浓度-反应关系 释放的介质和心功能障碍的程度之间的关系。 改变 在前列环素产生的心脏作为一个结果的超敏反应将是 研究，特别是因为这可能导致冠状动脉血管损伤 稳态或血栓形成。 释放介质之间的相互作用 以及各种疾病状态和药物，即，心肌缺血，高血压， 甲状腺功能亢进症，洋地黄，利尿剂，将进行研究。 药理学 将寻求纠正和控制心脏功能障碍的方法 是由速发型超敏反应引起的 我们还将查明 自体素释放，特别是组胺，是否可以是生理上的， 参与心脏交感神经功能的调节。 的 组胺与缺血性心律失常的病理生理相互作用，洋地黄 并检查毒性和甲状腺功能亢进症。 因为组胺可以 在任何地点以任何方式释放，这项工作将定义心脏反应， 主要的自伤类。 在这样做的过程中，这项研究应该发现迄今为止未知的 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.