title: Benefits of glucose and oxygen in multidose cold cardioplegia.
abstract: We tested the effects of glucose and oxygen in cardioplegic solutions on myocardial protection in the isolated perfused working rat heart. Recovery from 2 hours' hypothermic (8 degrees C) cardioplegic arrest was examined in 93 hearts. Cardioplegic solution, which was delivered every 15 minutes, was supplemented with glucose 28 mmol/L as a substrate or sucrose 28 mmol/L as a nonmetabolizable osmotic control; it was equilibrated with either 98% oxygen or 98% nitrogen, both with 2% carbon dioxide. Four combinations of hyperkalemic cardioplegic solution were studied: nitrogen-sucrose, nitrogen-glucose, oxygen-sucrose, and oxygen-glucose. During hypothermic arrest, oxygenation of cardioplegic solution greatly reduced myocardial lactate production and prevented ischemic contracture as indicated by coronary vascular resistance. Glucose increased lactate production modestly but significantly only when the cardioplegic solution was nitrogenated. Although end-arrest myocardial adenosine triphosphate and creatine phosphate were greatly increased by oxygenation of cardioplegic solution (p less than 0.005), we could not detect improved preservation of these high-energy phosphates by glucose. Averaged over reperfusion, percent recovery of cardiac output for the nitrogen-sucrose, nitrogen-glucose, oxygen-sucrose, and oxygen-glucose solutions was 32.3% +/- 6.1%, 45.9% +/- 4.6%, 44.5% +/- 4.6%, and 62.2% +/- 4.5%, respectively. Oxygenation of the glucose solution or addition of glucose to the oxygenated solution significantly improved recovery of cardiac output. The benefits of glucose and oxygen were additive, so that the oxygen-glucose cardioplegic solution provided the best functional recovery. We conclude that the addition of glucose to the fully oxygenated multidose cold cardioplegic solution improves functional recovery without increasing lactate production during arrest.
authors.affiliation: Department of Surgery, Massachusetts General Hospital, Boston 02114.
authors.forename: N E
authors.initials: NE
authors.lastname: Doherty
authors.forename: J F
authors.initials: JF
authors.lastname: Turocy
authors.forename: G A
authors.initials: GA
authors.lastname: Geffin
authors.forename: D D
authors.initials: DD
authors.lastname: O'Keefe
authors.forename: J S
authors.initials: JS
authors.lastname: Titus
authors.forename: W M
authors.initials: WM
authors.lastname: Daggett
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000502:physiology; D001783:Blood Flow Velocity; D002302:Cardiac Output; D002314:Cardioplegic Solutions; D003080:Cold Temperature; D003326:Coronary Circulation; D003404:Creatinine / Q000378:metabolism; D005947:Glucose; D016027:Heart Transplantation; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen; D051381:Rats; D011919:Rats, Inbred Strains; D014655:Vascular Resistance
chemical_list: D000227:Adenine Nucleotides; D002314:Cardioplegic Solutions; D007773:Lactates; D019344:Lactic Acid; D003404:Creatinine; D005947:Glucose; D010100:Oxygen