Pain from myocardial ischemia turns up in the chest and the left upper arm, and the reason is old textbook physiology. Cardiac and somatic nerve inputs converge in the thoracic spinal cord, so the brain cannot tell which source a signal came from. Cui and colleagues asked a question that runs the other way. Does the arm send anything back?
It does, and it reaches the heart. In a rat model, myocardial ischemia produced mechanical hypersensitivity in the forelimbs and upper back, along with nerve sprouting in the skin of that referred area and raised cardiac sympathetic tone. Stimulating the referred area then increased sympathetic hyperactivity and adjusted cardiac function, while cutting the nerve supply reduced it.
Why cardiac trouble is felt in the chest and the left upper arm has been studied extensively, and the answer is anatomical. Cardiac and somatic inputs converge in the thoracic spinal cord and reinforce each other there, with integrated projections onward to several brain regions. Spinothalamic tract neurons in the upper thoracic cord, alone or with spinoreticular neurons, produce both the sensation of angina and pain referred to the body wall above it.
The wiring is specific. Cell bodies of the heart and coronary arterial afferents sit in the of the first through fifth thoracic segments, perhaps extending slightly beyond. The nerve endings are denser in the anterior wall of the left ventricle than elsewhere in the heart, so an injured region there delivers more noxious signal upward.
What remained unclear was the role of sensory input from the referred area itself. In a rat model, ischemia led to referred mechanical hypersensitivity on the forelimbs and upper back. It also produced sympathetic sprouting in the skin of the referred area and in the dorsal root ganglia from the eighth cervical to the sixth thoracic level. Cardiac sympathetic tone rose as well, and the authors call that combination sympathetic-sensory coupling.
Then they pushed on that coupling. Intensifying the hyperalgesic input with noxious mechanical, thermal and electrical stimulation of the forearm augmented the sympathetic hyperactivity and regulated cardiac function, while of the left brachial plexus diminished the sympathoexcitation. Injecting an antagonist or an agonist of one adrenoceptor into the forearm skin attenuated the cardiac adjustment produced by stimulation. So sensory input from the area contributes to cardiac adjustment, through that peripheral receptor.
wat. The pain shows up in the arm because the wires meet in the spine. What is new is that the arm answers back.
wat wat
The referred area is not just a misleading address for the pain. It is wired into the loop that regulates the organ causing it.
How do we know?
A rat model of myocardial ischemia. The team mapped mechanical sensitivity in the referred areas, looked for nerve sprouting in skin and dorsal root ganglia, and tracked cardiac function under forearm stimulation, brachial plexus deafferentation, and drugs acting on one adrenoceptor.
What is still unknown
Rats, and an induced ischemia rather than a human heart attack. The clinical reading, that stimulating the referred area might protect the heart, is a direction the paper points rather than a result in people.
Learn something?
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