Title of article :
Glucose-insulin-potassium solution improves left ventricular mechanics in diabetes
Author/Authors :
Tharumenthiran Ramanathan، نويسنده , , Kazuaki Shirota، نويسنده , , Shin Morita، نويسنده , , Takashi Nishimura، نويسنده , , Yifei Huang، نويسنده , , Stephen N. Hunyor، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2002
Pages :
6
From page :
582
To page :
587
Abstract :
Background. The mechanism by which glucose-insulin-potassium solutions enhance recovery of left ventricular function after myocardial ischemia in diabetic patients is not well understood. We evaluated the effect of glucose-insulin-potassium on ventriculoarterial coupling and left ventricular mechanics in a chronic ovine model of diabetes. Methods. Diabetes was induced in 6 sheep with streptozotocin. After 6 months of diabetes, the response of the left ventricular pressure-volume relationship to 60 minutes of intravenous glucose-insulin-potassium solution (1,000 mL of 5% dextrose in water, 100 IU of regular insulin, 90 mmol of KCl at 1.5 mL · kg−1 · h−1) was determined. Results. Glucose-insulin-potassium solution increased end-systolic elastance 68% (p = 0.01) and improved ventriculoarterial coupling (1.7 ± 0.3 to 1.0 ± 0.1; p < 0.01). Potential energy decreased 35% (p = 0.01), and pressure-volume area decreased 20% (p = 0.01). However, stroke work did not change; therefore stroke work efficiency increased from 50.1% ± 3.5% to 60.2% ± 5.1% (p = 0.01). Conclusions. Glucose-insulin-potassium solution improves left ventricular contractility and ventriculoarterial coupling in diabetes. Left ventricular mechanics is improved by decreasing total mechanical work without significantly affecting stroke work, resulting in improved stroke work efficiency. Improved efficiency facilitates understanding of the enhanced tolerance to myocardial ischemia afforded by glucose-insulin-potassium solution.
Journal title :
The Annals of Thoracic Surgery
Serial Year :
2002
Journal title :
The Annals of Thoracic Surgery
Record number :
605371
Link To Document :
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