“…139 The infusion of GIK was shown to reduce the frequency and duration of ventricular arrhythmias and to improve the survival of patients after myocardial infarction. 140,141 Similarly, beneficial effects on ejection fraction and survival were observed when GIK was administered in conjunction with a thrombolytic agent 142 or when GIK was given to patients with myocardial infarction and non-insulindependent diabetes mellitus. 143 Most recently, a meta-analysis of all placebo-controlled trials of GIK treatment in acute myocardial infarction has shown an overall mortality reduction of 28%.…”
Section: Glucose and Insulin As Substrates For Postischemic Heartmentioning
“…139 The infusion of GIK was shown to reduce the frequency and duration of ventricular arrhythmias and to improve the survival of patients after myocardial infarction. 140,141 Similarly, beneficial effects on ejection fraction and survival were observed when GIK was administered in conjunction with a thrombolytic agent 142 or when GIK was given to patients with myocardial infarction and non-insulindependent diabetes mellitus. 143 Most recently, a meta-analysis of all placebo-controlled trials of GIK treatment in acute myocardial infarction has shown an overall mortality reduction of 28%.…”
Section: Glucose and Insulin As Substrates For Postischemic Heartmentioning
“…In the 1960s SodiPallares further popularized this treatment initially for arrhythmias, and later for angina (18,19). Glucose-insulin-potassium infusions have been advocated for patients with acute myocardial infarctions by other investigators and have also been administered before cardiac surgery (20)(21)(22)(23)(24)(25)(26)(27). Animal studies have shown that glucose infusions increase ATP levels and glycogen stores, and reduce tissue necrosis during acute infarctions (28)(29)(30).…”
The effects of hyperglycemia on myocardial glucose metabolism were investigated in seven healthy male subjects (age 24±4 yr). I6-C4qGlucose and IU-'3Cilactate were infused as tracers. Circulating glucose was elevated to two hyperglycemic levels using a clamp technique for 1 h at each level. The mean arterial glucose concentration was 4.95±0.29 (control), 8.33±0.31 and 10.84±0.60 jumol/ml, respectively. Glucose extraction increased significantly from control (0.15±0.13 gsmol/ ml) during each level of the glucose clamp (0.28±0.12, P < 0.02, and 0.54±0.14 ;tmol/ml, P < 0.005, respectively). Myocardial production of '4CO2 showed that during control 9±10% of exogenous glucose was oxidized immediately upon extraction. Despite a significant increase in the amount of exogenous glucose oxidized with level II hyperglycemia, it represented only 32±10% of the glucose extracted.[I3C]Lactate analysis showed that the myocardium was releasing lactate; during control 40±30% of this lactate was derived from exogenous glucose and during hyperglycemia this value increased to 97±37% (P < 0.005). Thus, these data show that during short-term hyperglycemia, myocardial glucose extraction is enhanced. However, despite increases in exogenous glucose oxidation and the contribution of exogenous glucose to lactate release, the majority of the extracted glucose (i.e., 57%) is probably stored as glycogen. (J. Clin. Invest. 1990Invest. . 85:1648Invest. -1656.) myocardial metabolism * glucose oxidation * lactate release * glycogen * free fatty acids
“…During ischemia and hypoxia, glycolysis is accelerated and glucose utilization is enhanced (4)(5)(6)(7)(8). Glucose-insulin-potassium infusions have been advocated for patients with acute myocardial infarctions and chronic ischemic heart disease; however, the efficacy of this treatment for limiting myocardial infarct size and left ventricular dysfunction still remains to be determined (3,(9)(10)(11)(12)(13)(14)(15)(16)(17).…”
Glucose is an important substrate for myocardial metabolism. This study was designed to determine the effect of circulating metabolic substrates on myocardial glucose extraction and to determine the metabolic fate of glucose in normal human myocardium. Coronary sinus and arterial catheters were placed in 23 healthy male volunteers. 16-"'CjGlucose was infused as a tracer in 10 subjects. 16-'CiGlucose and IU-_3Cilactate were simultaneously infused in the other 13 subjects. Simultaneous blood samples were obtained for chemical analyses of glucose, lactate, and free fatty acids and for the isotopic analyses of glucose and lactate. Glucose oxidation was assessed by measuring myocardial 4 CO2 production. The amount of glucose extracted and oxidized by the myocardium was inversely correlated with the arterial level of free fatty acids (r = -0.71; P < 0.0001). 20% (range, 0-63%) of the glucose extraction underwent immediate oxidation. Chemical lactate analysis showed a net extraction of 26.0±16.4%. However, isotopic analysis demonstrated that lactate was being released by the myocardium. In the 13 subjects receiving the dual-carbon-labeled isotopes, the lactate released was 0.09±0.04 ,mol/ml and 49.5±29.5% of this lactate was from exogenous glucose. This study demonstrates that the circulating level of free fatty acids plays a major role in determining the amount of glucose extracted and oxidized by the normal human myocardium. Only 20.1±19.4% of the glucose extracted underwent oxidation, and 13.0±9.0% of the glucose extracted was metabolized to lactate and released by the myocardium. Thus, 60-70% of the glucose extracted by the normal myocardium is probably stored as glycogen in the fasting, resting state.
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