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In an animal model, coronary sinus pO2 varies logarithmically with pCO2 during respiratory-induced pH changes, suggesting myocardial pCO2 may be a primary agent controlling coronary flow.
The ability of coronary sinus pO2 to remain constant in the face of a shift in the O2 dissociation curve was tested in a series of anaesthetized dogs during respiratory-induced alterations in blood pH, resulting from either hyperventilation or CO2 inhalation. Coronary sinus pO2 was not constant, but varied from 8.2 to 96 mm Hg (1.09 to 12.8 kPa) as coronary sinus pH was altered from 6.97 to 7.71 and coronary sinus pCO2 was varied from 16 to 96 mm Hg (2.13 to 12.8 kPa). The coronary sinus pO2 was logarithmically related to coronary sinus pCOa. Myocardial O2 extraction varied from 13 to 87%. The low coronary sinus pO2 reached during hypocapnia suggests that O2 delivery to the myocardium is impaired at this time. The hypothesis is presented that myocardial pCO2 is a primary agent controlling coronary flow.
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Case et al. (1975) studied this question.
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