Effect of coronary artery occlusion on regional arterial and venous O2 saturation, O2 extraction, blood flow, and O2 consumption in the dog heart.

Abstract

The effects of coronary artery ligation on regional arterial and venous O2 saturation, oxygen extraction, blood flow, and oxygen consumption were studied in occluded and unoccluded areas of the hearts of fourteen anesthetized open-chest dogs. In seven animals, a coronary artery was occluded for 10 minutes and in seven others a vessel was ligated for 2 hours. Microspectrophotometric observations of small regional arteries and veins in quick-frozen hearts to determine regional O 2 extraction were combined with regional blood flow measurements with radioactive microspheres to determine regional myocardial O2 consumption by the Fick principle. Flow was significantly lower in the occluded compared to the control area at both times. The subendocardial: subepicardial flow ratio was reversed at 2 hours in the occluded area. Oxygen extraction was greater in the occluded areas. Oxygen consumption was lower in the occluded area. At 2 hours, the subendocardial: subepicardial consumption ratio was reversed in the occluded area, indicating a greater decrement in consumption in the subendocardium. Measurements of arterial saturation indicate an increasing number of blood vessels with O2 saturations below 80% with coronary artery occlusion. These vessels were found in all occluded areas. This would indicate a marked heterogeneity of blood flow within the area of occlusion. Some vessels may have normal flow and others low or no flow. There was heterogeneity of flow and oxygen extraction which led to areas with relatively normal oxygen consumption in the core of the infarct.

Role of Propranolol in Improvement of the Relationship between O2 Supply and Consumption in an Ischemic Region of the Dog Heart

“…Still others found substantial changes in the transmural distribution of blood flow, favoring the subendocardium (17,29). Although the negative inotropic effect of propranolol has been emphasized (29) Coronary occlusion brought about no significant changes in the measured hemodynamic or blood gas and pH parameters measured, in agreement with previous studies (11,19). Occlusion plus propranolol treatment caused heart rate, dP/dt, and left ventricular systolic pressure to decrease due to blockade of f3l-adrenergic receptors.…”

“…Occlusion increased this proportion of vessels to 38%. Similar values have been found (11 The ,13-adrenergic blocking effect of propranolol clearly causes a decreased chronotropic and inotropic effect and a resultant decrease in MVO2 in the unoccluded region of the heart. These effects have been suggested to promote a transmural redistribution of blood flow within the ischemic zone that is a primary determinant of the beneficial effect of the drug (29,32).…”

“…The decrease in subendocardial/subepicardial flow ratio in the ischemic area was expected from other studies (11,17,18,20). Propranolol, in our preparation, neither significantly altered the magnitude of flow nor the subendocardial/ subepicardial ratio of ischemic blood flow relative to the untreated group.…”

“…Decreased mitochondrial respiration (7), tissue Po2 (8), and increased 02 extraction as well as decreased 02 consumption (9,10) indicate alterations in 02 availability and demand. Recent work has shown substantial variability of small artery and vein saturations as well as heterogeneous regions of 02 extraction and consumption within the center of an ischemic zone caused by coronary artery ligation (11).…”

Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. I. Studies with dobutamine in the anesthetized dog.

“…25 Our studies were not designed to assess possible changes in vessel-to-vessel variability in collateral blood flow at the microvascular level, which might allow greater degrees of oxygen extraction in critical areas of ischemic myocardium, 29 3 or to assess changes in myocardial oxygen supply/demand relationships in ischemic myocardium. 29 Studies of the effects of inotropic stimulation on acute myocardial ischemic injury would be most relevant for extrapolation to clinical cardiology if they were performed in conscious animals with multivessel coronary artery narrowing and heart failure due to the effects of multiple episodes of ischemia and infarction. Such an experimental model has not yet been developed, although Jentzer et al 34 produced LV failure in anesthetized dogs with successive coronary occlusions and showed that the inotropic stimulant amrinone improves hemodynamic markers of LV failure, but decreases global myocardial oxygen consumption and presumably, oxygen demand in ischemic myocardium.…”