Neuromodulation of cardiac pain and cerebral vasculature: neural mechanisms.
Research using animal models has helped elucidate the neural mechanisms of angina pectoris, sensitization of cardiac nociceptive stimuli, and neuromodulation of cardiac pain and cardiovascular function. Findings over the last 2 decades include evidence of convergence of visceral-somatic input to spinothalamic cells and a major role for the vagus nerve in spinal cord processing. Stress-related glucocorticoids may manipulate amygdala function, inducing hypersensitivity to nociceptive input from the heart via central sensitization of upper thoracic spinal neuronal activity. Spinal cord stimulation may have therapeutic effects, although the underlying mechanism is unclear.
Department of Physiology, University of Oklahoma Health Sciences Center, 940 S.L. Young Blvd., Room 653, Oklahoma City, OK 73104, USA. robertforeman@ouhsc.edu
Robert D
RD
Foreman
Chao
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Qin
D000787:Angina Pectoris / Q000150:complications* / Q000503:physiopathology*; D000818:Animals; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D004558:Electric Stimulation; D006801:Humans; D009435:Synaptic Transmission / Q000502:physiology*