Cardiac pain has long been of clinical interest, but not until the past decade has it been subjected to laboratory investigation. Although Allbutt's1 theory of the aortic origin of angina pectoris was once widely accepted, recent experimental evidence strongly points toward the cardiac origin of pain. Sutton and Lueth2 have shown that compression by means of a ligature on coronary vessels in the unanesthetized dog results in pain characteristic of angina pectoris. Their studies have been confirmed by White, Garrey and Atkins3 and by Katz and his associates.4 All these authors have agreed that the fundamental mechanism initiating pain is a chemical factor produced by impaired coronary circulation. In essence, this contention is the basis of Lewis'5 theory that myocardial ischemia is the cause of cardiac pain. From the aforementioned studies it is generally inferred that the mechanical factor is of secondary importance in producing
MARTIN SJ, GORHAM LW. CARDIAC PAIN: AN EXPERIMENTAL STUDY WITH REFERENCE TO THE TENSION FACTOR. Arch Intern Med (Chic). 1938;62(5):840–852. doi:10.1001/archinte.1938.00180160119010
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