FRUCTOSE-1,6-DIPHOSPHATE FAILS TO LIMIT EARLY MYOCARDIAL-INFARCTION SIZE IN A CANINE MODEL

被引:3
作者
ANGELOS, MG
LEASURE, JE
BARTON, RL
机构
[1] Department of Emergency Medicine, Wright State University, Cox Institute, Kettering, OH
关键词
FRUCTOSE-1,6-DIPHOSPHATE; MYOCARDIAL INFARCTION;
D O I
10.1016/S0196-0644(05)80197-0
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Study objective: Fructose-1,6-diphosphate (FDP) appears to improve early post-myocardial infarction hemodynamics and limit early myocardial infarct size in previous canine studies. However, these studies did not account for the effect of collateral blood flow on infarct size. Our objective was to determine the effect of FDP on early infarct size and hemodynamics while measuring regional myocardial blood flow. Design: A prospective, blinded, placebo-controlled laboratory study using a canine open-chest left anterior descending coronary artery (LAD) occlusion model. Interventions: Twenty-two mongrel dogs were assigned randomly to receive either FDP (1 75 mg/kg, then 2 mg/kg/min for two hours) or placebo, beginning five minutes after LAD occlusion. Measurements and main results: Regional myocardial blood flow, hemodynamics, and myocardial infarct size were determined. Infarct size was assessed using magnetic resonance imaging in a subset of animals. Three of the 22 dogs had no infarct and significantly higher collateral blood flow than the 19 animals with myocardial infarction (P<.001). Four hours after LAD occlusion, cardiac index, dP/dt(max), heart rate, and systolic and mean aortic pressures were not statistically different between groups. Infarct size expressed as area of necrosis/area at risk was similar between groups (FDP, 0.55 +/- 0.28; controls, 0.59 +/- 0.31). Conclusion: FDP given after occlusion of the LAD in this canine model did not limit early myocardial infarct size.
引用
收藏
页码:171 / 177
页数:7
相关论文
共 26 条
[1]  
Janz, Leasure, Olson, The effects of fructose-1,6-diphosphate on myocardial damage in acute coronary artery occlusion, Resuscitation, 22, pp. 45-54, (1991)
[2]  
Markov, Fletcher, Strete, Et al., Reduction of mortality and myocardial ischemia reperfusion injury with fructose 16-diphosphate (FDP), Journal of the American College of Cardiology, 7, (1986)
[3]  
Marchionni, Conti, De Alfieri, Et al., Hemodynamic and electrocardiographic effects of fructose 1,6-diphosphate in acute myocardial infarction, Am J Cardiol, 56, pp. 266-269, (1985)
[4]  
Markov, Oglethorpe, Blake, Et al., Hemodynamic, electrocardiographic and metabolic effects of fructose diphosphate on acute myocardial ischemia, Am Heart J, 100, pp. 639-646, (1980)
[5]  
Kirtley, McKay, Fructose-1,6-diphosphate, a regulator of metabolism, Mol Cell Biochem, 18, pp. 141-149, (1977)
[6]  
Markov, Hemodynamics and metabolic effects of fructose-1,6-diphosphate in ischemia and shock—experimental and clinical observations, Ann Emerg Med, 15, pp. 1470-1477, (1986)
[7]  
Eddy, Chambers, Honig, Et al., Lack of a direct metabolic effect of fructose 1,6-diphosphate in ischemic myocardium, Am J Physiol, 241, pp. H576-H582, (1981)
[8]  
Chlouverakis, The lipolytic action of fructose-1,6-diphosphate, Metabolism, 17, pp. 708-716, (1968)
[9]  
Hassinen, Nuutinen, Ito, Et al., Mechanism of the effect of exogenous fructose 1,6-biphosphate on myocardial energy metabolism, Circulation, 83, pp. 584-593, (1991)
[10]  
Schaper, Gonge, Winklen, Et al., The collateral circulation of the heart, Prog Cardiovasc Dis, 31, pp. 57-77, (1988)