The significance of the late fall in myocardial PCO2 and its relationship to myocardial pH after regional coronary occlusion in the XXXX .

@entity3884 @entity63 @entity235 @entity3157 @entity544
After acute regional coronary occlusion, myocardial tissue PCO2, as measured by mass spectrometry, rises, reaches a peak, and then gradually falls. This late fall in myocardial tissue PCO2 could be due to (1) a gradual increase in tissue blood flow (and hence improved @entity544 washout), (2) a gradual consumption of tissue @entity3157 , (3) a gradual reduction in the production of @entity544 due to progressive cellular damage, or (4) an artifact caused by the continued presence of the mass spectrometer probe in the @entity63 tissue. To determine which of these four mechanisms is responsible for the late fall in myocardial tissue PCO2, we subjected 27 anesthetized open-chest @entity235 to 3-hour occlusion of the left anterior descending coronary artery. Both myocardial tissue PCO2 and intramyocardial @entity3884 ion concentration were measured in the myocardial segment supplied by the left anterior descending coronary artery. Ten @entity235 (group 1) were killed after the occlusion (occlusion I), and 11 @entity235 (group 2) underwent reocclusion (occlusion II) at the same site after a 45-minute period of reflow. Regional myocardial blood flow was measured periodically by the intramural injection of 127Xe. Changes in myocardial tissue PCO2 and @entity3884 ion concentration were related to ultrastructural changes in the tissues adjacent to the myocardial tissue PCO2 probe. Regional myocardial blood flow remained unchanged throughout the 3-hour occlusion, ruling out increased @entity544 washout as a cause for its late fall. Tissue @entity3884 ion concentration, as measured by a new lead glass electrode, correlated well with myocardial tissue PCO2, with the reduction in regional myocardial blood flow, and with @entity63 damage assessed histologically. Myocardial @entity3884 ion concentration also exhibited a late fall after the occlusion, from a peak of 199.8 +/- 27.8 nmol/liter to 91.9 +/- 12.1 nmol/liter (mean +/- SEM). This ruled out consumption of tissue @entity3157 as the cause for the late fall in myocardial tissue PCO2. Peak rise in myocardial tissue PCO2 after occlusion II (71.2 +/- 7.9 mm Hg) was significantly lower than peak myocardial tissue PCO2 after occlusion I (116.7 +/- 13.9 mm Hg, P less than 0.001). The difference between these latter two values, as well as the magnitude of fall in myocardial tissue PCO2 during occlusion I, related directly to the degree of histological damage observed.(ABSTRACT TRUNCATED AT 400 WORDS)
