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CIRCULATORY CHANGES IN ANGINA PECTORISAN EXPERIMENTAL STUDY
PHILIP SHAMBAUGH, M.D.
Arch Intern Med. 1935;56(1):59-76.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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The great majority of clinicians and investigators are now agreed on the essential pathologic physiology of angina pectoris, namely, that the attacks represent a transitory relative ischemia of a portion of the myocardium. There is, however, considerable doubt as to the mechanism of the production of the ischemia. Two fundamental possibilities present themselves: The supply of normal blood is inadequate for the needs of the heart muscle, or the composition of the blood is faulty, preventing a proper interchange of oxygen and metabolites. The latter possibility probably applies in only relatively few cases. The maintenance of an adequate supply of blood to the myocardium depends on two variable factors the demands of the myocardium and the ability of the blood vessels to meet this demand.
The factors which determine the ability of the blood vessels to meet the vascular demands of the myocardium are (1) the ability of the vessels
. . . [Full Text PDF of this Article]
Author Affiliations
BOSTON
From the Laboratory of Surgical Research, Harvard Medical School.
Footnotes
Arthur Tracy Cabot Fellow.
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