RESUMO
Among the last consequences of metabolic syndrome are cardiovascular complications such as infarcts. The hypoxic heartswitches its lipid-based metabolism to carbohydrates, and a glucose-insulin-potassium (GIK) solution can be the metabolicsupport to protect the organ. Due to the physiology and cardiac risks associated with the metabolic syndrome, we studied theeffect of GIK solution during hypoxia in a metabolic syndrome model by observing the participation of glucose transporters(GLUTs). The metabolic syndrome characteristics were established by giving a 30% sucrose drinking solution to Wistar ratsfor 24 weeks. The GIK solution’s effect on myocyte glucose uptake during hypoxia and oxygenation was observed using acolorimetric method, and Western blot technique visualized the GLUT participation. Oxygenated control myocytes consumed1.7 ± 0.2 µg of glucose per gram of fresh tissue per hour using the GLUT1, and during hypoxia, they incorporated 41.1%more glucose by GLUT1 and GLUT4. The GIK solution improved glucose uptake in oxygenation by 70.5% through GLUT1.In hypoxia, the uptake was 21% more than the hypoxic control group and by both GLUTs too. Oxygenated metabolicsyndrome myocytes uptake was similar to control cells but achieved by both carriers in oxygenation and hypoxia. Also, theGIK solution had a better response in both oxygenation (113%) and hypoxia (71%). Despite the metabolic energy disorders ofthis syndrome, the GIK solution protects cardiomyocytes, in conditions of hypoxia, through the modulation of both GLUTs.So, this solution can be considered a useful resource during a heart attack in cases of metabolic syndrome.
RESUMO
BACKGROUND AND OBJECTIVES: Glucose-insulin-potassium (GIK) fluid infusion may improve the myocardial energy metabolism in the ischemic condition. A prospective randomized clinical trial was designed to determine whether a GIK fluid infusion can reduce the ventricular remodeling in acute myocardial infarction. SUBJECTS AND METHODS: For the patients with acute myocardial infarction, during thrombolytic therapy with urokinase, GIK fluid (26% glucose 1000 mL, 50 IU insulin, and 80 mmol KCl) was administered for 24 hours. The ventricular volumes and function were evaluated by echocardiography during the admission period, at 6 months and at 12 months following discharge. RESULTS: This trial was done prospectively for 2 years in 73 patients; the GIK group included 41 patients and the control group included 32 patients. The median value of "the pain to door time" was 195 minutes in the GIK group and it was 120 minutes in the control group (p=NS). The wall motion score was 1.52+/-0.39 in the GIK group and it was 1.39+/-0.35 in the control group. The left ventricular volumes, ejection fractions, cardiac indices and the globular indices showed no significant difference between the two groups. The side effects of the GIK fluid were mild phlebitis in 6 patients (14.6%) and congestive heart failure in 5 patients (12.2%). CONCLUSION: This trial could not verify the beneficial effects of administering GIK fluid on the ventricular remodeling after acute myocardial infarction. The limitations of this trial were as follows: "the pain to door time" was too long and the severity of the myocardial infarction was mild. Low rates for the echocardiogrphy follow-up and the randomization failure in a few patients were also noted.