leukotriene-b4 and Coronary-Vasospasm

Our current understanding of the physiology of the leukotrienes is far from complete. The abundant supply of synthetic products has directed researchers into examining what the mediators affect rather than the basic mechanism studies of their involvement in disease. It is clear that the peptide leukotrienes possess potent constrictor actions of the microvasculature and can enhance permeability. These actions alone represent a new avenue of interpreting pathologic processes and could lead to alternate means of treating certain diseases in the future. It is of special interest that a consistent action of the leukotrienes is to reduce coronary blood flow, decrease myocardial contractility, and reduce cardiac output without affecting the heart rate. This profile of action is the first indication that a mediator can play a significant role in unstable angina. The main physiologic actions of the leukotrienes in the cardiovascular system are currently believed to be associated with episodes of ischemia and shock. Their relative contribution to the shock states, especially when compared with the actions of other known mediators of shock such as the prostaglandins, thromboxane, angiotensin, serotonin, and histamine, awaits clarification. LTB4 is a proinflammatory mediator that has opened a completely new perspective on the physiologic role of phagocytic cells. Novel therapeutic approaches to inflammatory-related diseases may result from an inhibition of cell chemokinesis, aggregation, and degranulation. The role of LTB4 in the immune system awaits further clarification.

Topics: Animals; Blood Platelets; Cardiovascular Diseases; Cardiovascular Physiological Phenomena; Cerebrovascular Circulation; Coronary Disease; Coronary Vasospasm; Humans; Leukotriene B4; Lung; Muscle Contraction; Muscle, Smooth, Vascular; Neutrophils; Skin; SRS-A; Thromboxane A2