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Published on: September 24, 2020
Heart rate limitation and cardiac unloading in sevoflurane post-conditioning
J R Larsen1, K Sivesgaard, S D Christensen
1Department of Anesthesia and Intensive Care, Aarhus University Hospital, Skejby, Denmark. jens.rolighed@ki.au.dk
Acta Anaesthesiologica Scandinavica
|November 23, 2011
Summary
Sevoflurane post-conditioning significantly reduced myocardial infarct size in pigs. This cardioprotective effect was linked to reduced cardiac work, indicating a dual mechanism for healing heart muscle.
Area of Science:
- Cardiovascular Science
- Anesthesiology
- Ischemic Injury Research
Background:
- Sevoflurane post-conditioning (SePost) activates prosurvival kinases to mitigate ischemic myocardial reperfusion injury.
- Reduced cardiac work, a less-studied factor, may also contribute to cardioprotection.
- This study investigates SePost's impact on both cardiac work and infarct size.
Purpose of the Study:
- To evaluate the effect of sevoflurane post-conditioning on myocardial infarct size.
- To assess the influence of SePost on cardiac work, specifically the rate-pressure product (RPP).
- To determine the correlation between reduced cardiac work and myocardial salvage.
Main Methods:
- A porcine model underwent 45 minutes of regional coronary artery occlusion followed by 2 hours of reperfusion.
- Pigs were randomized to receive sevoflurane (1.5-3%) during reperfusion (SePost group) or no treatment (control group).
- Cardiac work (RPP), hemodynamic parameters, infarct size (IS), and area at risk were measured.
Main Results:
- SePost significantly reduced myocardial infarct size by 40% compared to controls (32.5% vs 55.0%).
- SePost lowered heart rate, cardiac output, mixed-venous oxygen saturation, blood pressure, and RPP during reperfusion.
- A strong correlation was found between reduced RPP and infarct size (P = 0.0055).
Conclusions:
- Sevoflurane post-conditioning effectively reduces infarct size in a porcine model of myocardial ischemia.
- Reduced cardiac work during SePost is significantly correlated with myocardial salvage.
- This suggests a dual mechanism involving kinase activation and reduced cardiac workload for SePost's cardioprotective effects.
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