ABSTRACT
This chapter discusses potential neural mechanisms that underlie the referral of anginal pain to somatic structures by using the spinothalamic system as the model. It addresses possible neurophysiological mechanisms that might explain why severe myocardial ischemia could occur without the experience of pain. Mechanosensitive and chemosensitive receptors located in heart transmit information via afferent fibers to the spinal cord. A common feature of cardiac pain sensation is its perceived location in somatic structures overlying or nearby the heart. Vagal afferent fibers do not appear to be involved with the eventual perception of cardiac pain, but evidence has accumulated to suggest that vagal afferent fibers have the capacity to modulate the cardiovascular and pain systems. Electrical and chemical stimulation of vagal afferent fibers can suppress responses to visceral stimuli in conscious animals. The neural mechanisms and pathways involved in the suppression of pinothalamic tract cell activity are unknown, but anatomical, electrophysiological and behavioral results suggests potential pathways for producing this suppression.
