Cummings and Clark (4) Cummings (3) Rigo et al. (5) INTERRELATIONSHIPS IN HEART DISEASE 61 a Coronary ligation. b Ringer's solution without Mg. C Two milliequivalents Mg in 5% dextrose. water to the calcium and magnesium intakes of

Canola oil is a newly marketed vegetable oil for use in salads and for cooking that contains 55% of the monounsaturated fatty acid; oleic acid, 25% linoleic acid and 10% alpha-linolenate [polyunsaturated fatty acid (PUFA)], and only 4% of the saturated fatty acids (SFAs) that have been implicated as factors in hypercholesterolemia. It is expressed from a cultivar of rapeseed that was selectively bred from old varieties in Canada to be very low in erucic acid--a fatty acid suspected to have pathogenic potential in diets high in the original rapeseed oil in experimental animals. Canola oil is free of those problems. It is the most widely consumed food oil in Canada, and has been approved for Generally Recognized as Safe (GRAS) status by the Food and Drug Administration (FDA) of the United States Department of Health and Human Services. The fatty acid composition of canola oil is consistent with its use as a substitute for SFAs, in meeting the dietary goals recommended by many health associations: an average diet containing about 30% of calories as fat made up of less than 10% SFAs, 8-10% PUFAs in a ratio of linoleic to linolenic acids between 4:1 and 10:1, the remainder being monounsaturated fatty acids. No single oil meets these current recommendations for ratios of PUFA/monounsaturated/polyunsaturated fatty acid ratios as the sole source of cooking and salad oil.

SUMMARY Intramyocardial hemorrhage often occurs with reperfusion in experimental acute myocardial infarction and is thought to be associated with extension of necrosis. To determine if hemorrhage was associated with extension of necrosis, 20 anesthetized dogs were reperfused after 6 hours of circumflex coronary artery occlusion and 10 others had control occlusion with no reperfusion. Fifteen of the 20 reperfused dogs had gross hemorrhage and none of the control dogs did. In 12 reperfused and 10 control dogs, radioactive microspheres were injected after coronary occlusion to quantitate collateral flow and in the reperfusion group microspheres were injected to quantitate reflow. Complete flow data were available in eight reperfused and 10 control dogs. Twenty-four hours after coronary occlusion, 1-g segments of infarct and control regions were analyzed for hemorrhage, collateral flow and creatine kinase activity. Serial microscopic examination was performed in eight additional dogs reperfused after 6 hours to determine if hemorrhage occurs into otherwise microscopically normal myocardium.Pathologic examination indicated that hemorrhage did not occur into otherwise microscopically normal myocardium. In dogs with hemorrhage, the extent of hemorrhage was inversely related to myocardial creatine kinase concentration and collateral flow. Mean collateral flow in 47 hemorrhagic segments was 4.5 ml/100 g (4.2% of control). Mean creatine kinase in 36 hemorrhagic segments was 233 mIU/g (21% of control). No hemorrhage was found in areas with collateral flow more than 21% of control or creatine kinase more than 37% of control. Mean reflow in hemorrhagic segments was 78.5% of control flow. These studies indicate that hemorrhage on reperfusion is associated with severe myocardial necrosis and markedly depressed flow before reperfusion and thus occurs only into myocardium already markedly compromised at the time of reperfusion. There is no evidence for hemorrhage into areas that had normal or even moderately depressed flows before reperfusion.THE BENEFITS of reperfusion after acute coronary occlusion are controversial. Extent of infarction is an important determinant of prognosis after coronary occlusion,' and restitution of flow would appear to provide an effective means of rectifying ischemia and thus limiting infarct size. Jennings et al.2 demonstrated that reperfusion after 20 minutes of occlusion prevented the development of ischemic injury, while other studies using enzyme analysis, histologic examination and functional assessment have shown limitation of infarct size with reperfusion 3 hours after coronary occlusion.'-" Other studies have not substantiated significant improvement after reperfusion. Bresnahan et al.6 demonstrated an increase in infarct size in seven of 16 dogs reperfused 5 hours after coronary occlusion. Other investigators have reported ventricular dysrhythmias7 accelerated morphologic changes of ischemia8 and exacerbation of functional'0 and metabolic measurements of ischemia.9The deleterious consequence...

No abstract