There is continuing uncertainty about the effects of various degrees of systemic arterial hypertension on myocardial ischemia. In 46 open-chest anesthetized dogs, intramural carbon dioxide tension (PmCO2) was measured directly with a mass spectrometer during repetitive 10-min coronary artery occlusions separated by 45-min periods of reflow. During each occlusion, transmural regional myocardial blood flow (RMBF) in the ischemic area was quantitated with the injection of radioactive microspheres (7-10 micrometers diam). In all dogs the increase in PmCO2 from before to 10 min after the first occlusion (delta PmCO2) exceeded that during subsequent occlusions. In those dogs in which systemic arterial hypertension was not produced (controls), delta PmCO2 during the third occlusion was similar to that during the second occlusion. When phenylephrine was administered during the third occlusion to increase systemic arterial pressure mildly (diastolic pressure 95-115 mmHg), RMBF to the ischemic myocardium was unchanged, and the severity of myocardial ischemia was reduced, as reflected by a fall in delta PmCO2. When diastolic pressure was elevated moderately (116-140 mmHg), RMBF was augmented, but the extent of myocardial ischemia was neither diminished nor worsened. In contrast, when diastolic pressure was increased markedly (greater than 140 mmHg), myocardial ischemic injury was intensified (as reflected by an increase in delta PmCO2) even though RMBF rose significantly. Thus, in the dog with acute coronary artery occlusion, an increase of systemic arterial pressure exerts an influence on the severity of myocardial ischemic injury that is related directly to the magnitude of systemic arterial hypertension: a mild increase of pressure reduces ischemic injury, a moderate increase exerts no consistent effect on ischemia, and a marked increase worsens ischemic injury.
|Original language||English (US)|
|Journal||The American journal of physiology|
|State||Published - Jun 1981|
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