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Updated: Aug 16, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Moderate glucose deprivation preconditions myocardium against infarction
1Klinik für Anästhesiologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany. ebeld@uni-duesseldorf.de
Abstract:
Glucose-free perfusion preconditions myocardium against the consequences of subsequent ischemia. We investigated whether mitochondrial ATP-sensitive potassium (mK (ATP)) channels are involved in preconditioning by glucose deprivation, and whether moderate glucose deprivation also preconditions myocardium. Isolated rat hearts underwent 30 min of no-flow ischemia followed by 1 h reperfusion. Controls were not further treated. Three groups were preconditioned by perfusion with 0, 40 or 80 mg/dl (0, 2.22, 4.44 mmol/l) glucose (correction of osmotic pressure by addition of urea) for 10 min followed by 10 min perfusion with normal buffer (150 mg/dl, or 8.33 mmol/l glucose) before the ischemia reperfusion protocol. In one group, 100 micromol/l of the mK (ATP) channel blocker 5-HD was added to the glucose-free perfusate. Two groups were treated with 5-HD or urea before ischemia without preconditioning. Left ventricular developed pressure and maximum ischemic contracture (82 +/- 21 mmHg) were similar in all groups. Mean left ventricular developed pressure was 100 +/- 16 mm Hg under baseline conditions, and poorly recovered to 8 +/- 11 mm Hg during reperfusion. Preconditioning with 0 and 40 mg/dl glucose containing buffer reduced infarct size from 41 +/- 10% (control) to 23 +/- 12% (p = 0.02) and 26 +/- 8% (p = 0.011). The 5-HD blocked preconditioning by glucose deprivation (38 +/- 9%, p = 0.04) while 80 mg/dl glucose, 5-HD and urea had no effect on infarct size (39 +/- 9%; 38 +/- 13%; 37 +/- 8%; p = 1.0 each). We conclude that transient severe glucose deprivation and moderate glucose deprivation preconditions the isolated rat heart. Preconditioning by complete glucose deprivation depends on the opening of mK (ATP) channels.
Insights
Severe glucose deprivation preconditions rat hearts against ischemia by opening mitochondrial ATP-sensitive potassium channels. Moderate glucose deprivation also offers protection, highlighting a novel therapeutic approach for cardiac injury.
Area of Science:
- Cardiology
- Biochemistry
- Physiology
Background:
- Glucose-free perfusion protects the myocardium from ischemic damage.
- The role of mitochondrial ATP-sensitive potassium (mKATP) channels in this protective mechanism is not fully understood.
Purpose of the Study:
- To investigate if mKATP channels are involved in preconditioning by glucose deprivation.
- To determine if moderate glucose deprivation can precondition the myocardium.
Main Methods:
- Isolated rat hearts were subjected to ischemia-reperfusion.
- Hearts were preconditioned with varying glucose concentrations (0, 40, 80 mg/dl) or a glucose-free buffer.
- The mKATP channel blocker 5-hydroxydecanoate (5-HD) was used to assess channel involvement.
Main Results:
- Preconditioning with 0 and 40 mg/dl glucose significantly reduced infarct size compared to controls.
- Blocking mKATP channels with 5-HD abolished the protective effect of glucose deprivation.
- 80 mg/dl glucose, 5-HD, or urea alone did not affect infarct size.
Conclusions:
- Transient severe and moderate glucose deprivation precondition the isolated rat heart against ischemia.
- Preconditioning by complete glucose deprivation is dependent on the opening of mKATP channels.
