NEURAL MECHANISM OF THE EFFECT OF ACUPUNCTURE ON MYOCARDIAL ISCHEMIA

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Coronary artery disease is the greatest cause of death in middle aged and elderly individuals in North America. Treatment for this disease is far from perfect and is often associated with side effects. In recent years there is increasing interest in alternative medicine and therapy for coronary artery disease including acupuncture. Acupuncture and its more potent alternative, electroacupuncture (EA), are therapies that have been recognized for centuries by physicians in Eastern countries to be effective in treating a number of diseases. The World Health Organization (WHO) lists more than 40 conditions for which acupuncture may be effective. With regard to the cardiovascular system, the management of cardiac pain, arrhythmias, and hypertension all fall into the latter category for which some clinical and basic science reports suggest efficiency. However, most Western physicians have been reluctant to accept acupuncture because the physiological mechanisms determining its actions have not been well described. The purpose of this study is to prove: (1) myocardial ischemia, cardiac arrhythmias, and hypertensive responses at rest and provoked by stress are decreased by EA; (2) the mechanism of the ischemic response is an imbalance between myocardial oxygen supply and demand originating as an increase in sympathetic autonomic neurons system activity causing increased oxygen demand. EA inhibits the sympathetic nervous system, decreases the blood pressure and reduces the oxygen demand; (3) EA leads to production of endorphins that antagonize neurotransmission in nuclei of brainstem that can be imaged in the human brain and which are concerned with regulation of sympathetic nerve activity. The investigator's prior data in animals shows that improvements in cardiovascular function during myocardial ischemia are mediated by an EA-induced sensory neural reflex originating in somatic nerves to reduce sympathetic nerve activity. The investigators' specific aims will allow us to better understand and modulate the sympathetic nervous discharge activity that precipitates coronary ischemia, arrhythmias and hypertension in psychological and exercise stress in humans. The investigators also will determine the central neural location of EA modulation of sympathetic outflow. Potential clinical application is the therapeutic value of EA in patients with ischemic heart disease, arrhythmia and hypertension.