Effects of coronary artery ligation and release and perfusion with glucose on cardiac energy metabolism in dogs.
Adenosine triphosphate (ATP), glycogen, and inorganic phosphorus (Pi) were assayed in myocardial tissues obtained from beating dog hearts subjected to the following procedures: Group 1. Ligation of anterior descending coronary artery(AD) for 60 min. Group 2. Perfusion of the AD with 20 mM glucose in Ringer's solution containing 1 mU regular insluin/ml, for 60 min. Group 3. Ligation of the AD for 60 min, followed by release of the ligature with re-establishment of blood flow for 30 min. Group 4. Perfusion of the AD with 20 mM glucose in Ringer's solution containing 1 mU/ml regular insulin for 60 min, followed by re-establishment of blood flow for 30 min. Samples from normal myocardium (N zone) and from the area supplied by the AD (I zone) were simultaneously obtained and the level of metabolites compared. In all four groups, ATP was significantly lower in I than N zone. However, ATP values were lower in N zone in group 1 as compared with the other groups (p less than 0.05) and higher in I zone in group 3 versus groups 1 and 2 (p less than 0.05). Glycogen was lower in I than N zones to a similar degree in all the groups. However, it was higher in the I zone in group 3 than in group 1 (p less than 0.05). Pi was significantly higher in I zone versus N zone only in group 1 (p less than 0.05). These data suggest that, the the beating dog heart, ATP and glycogen preservation in a myocardial segment rendered ischemic for 1 hour is best achieved by re-establishing circulation. Glucose infusion into the ischemic segment did not contribute significantly to the ATP stores in that segment but may have exerted a protective effect on the nonischemic zones, possibly by providing a high glucose level in the circulating blood. This protection was equally well achieved by release of the ligature with or without prior glucose infusion. The increase in Pi in the ischemic zone in the dogs with coronary ligation only is probably related to accumulation of the ion under ischemic and hypoxic conditions.
D000255:Adenosine Triphosphate / Q000378:metabolism; D003326:Coronary Circulation; D003331:Coronary Vessels; D004734:Energy Metabolism / Q000187:drug effects*; D005947:Glucose / Q000494:pharmacology*; D006003:Glycogen / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006439:Hemodynamics; D000860:Hypoxia / Q000503:physiopathology; D008026:Ligation; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010710:Phosphates / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism
D010710:Phosphates; D010758:Phosphorus; D000255:Adenosine Triphosphate; D006003:Glycogen; D005947:Glucose