Longhurst J C, Tjen-A-Looi S C, Fu L W
Department of Medicine, Medical Sciences 1, C240, University of California at Irvine, Irvine, CA 92697, USA.
Ann N Y Acad Sci. 2001 Jun;940:74-95. doi: 10.1111/j.1749-6632.2001.tb03668.x.
Cardiac sympathetic afferents are known to reflexly activate the cardiovascular system, leading to increases in blood pressure, heart rate, and myocardial contractile function. During myocardial ischemia, these sensory nerves also transmit the sensation of pain (angina pectoris) and cause tachyarrhythmias. The authors' laboratory has been interested in defining the mechanisms of activation of this neural system during ischemia and reperfusion. During these periods, reactive oxygen species, particularly hydroxyl radicals, are produced from the breakdown of purine metabolites and lead to stimulation of sympathetic (and vagal) ventricular chemosensitive nerve endings. For example, stimulation with hydrogen peroxide leads to a small reflex increase in blood pressure from the predominant sympathetic afferent activation that is reduced by simultaneous activation of cardiac vagal afferents (known to exert predominantly depressor reflexes). Central integration of these two opposing reflexes likely occurs at several regions of the brain stem, including the nucleus tractus solitarii, where neural occlusion occurs during simultaneous cardiac sympathetic and vagal-afferent stimulation. Activation of platelets also appears to play a role during myocardial ischemia, leading to local release of serotonin (5HT), which, through a 5HT3 mechanism, stimulates sympathetic afferents. Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins. Prostaglandins sensitize cardiac sympathetic afferents to BK. Thus, stimulation of cardiac sympathetic afferents during ischemia and reperfusion and the resulting reflex events form a multifactorial process resulting from activation of a number of chemical pathways in the myocardium.
已知心脏交感传入神经会反射性激活心血管系统，导致血压、心率和心肌收缩功能增加。在心肌缺血期间，这些感觉神经还会传递疼痛（心绞痛）感觉并引发快速性心律失常。作者所在实验室一直致力于确定缺血和再灌注期间该神经系统的激活机制。在这些时期，活性氧，尤其是羟自由基，由嘌呤代谢产物的分解产生，并导致交感（和迷走）心室化学敏感神经末梢受到刺激。例如，用过氧化氢刺激会导致血压因主要的交感传入神经激活而出现小幅反射性升高，而同时激活心脏迷走传入神经（已知主要产生降压反射）可使其降低。这两种相反反射的中枢整合可能发生在脑干的几个区域，包括孤束核，在心脏交感和迷走传入神经同时受到刺激时会发生神经阻滞。血小板的激活在心肌缺血期间似乎也起作用，导致局部释放5-羟色胺（5HT），5HT通过5HT3机制刺激交感传入神经。最后，乳酸引起的pH值区域变化（而非高碳酸血症）刺激心室传入神经，并可能激活激肽释放酶以增加缓激肽（BK），缓激肽进而分解花生四烯酸形成前列腺素。前列腺素使心脏交感传入神经对BK敏感。因此，缺血和再灌注期间心脏交感传入神经的刺激以及由此产生的反射事件是由心肌中多种化学途径激活导致的多因素过程。
