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Temporary acidosis during reperfusion limits myocardial infarct size in dogs
M Kitakaze1, S Takashima, H Funaya
1First Department of Medicine, Osaka University School of Medicine, Japan.
Insights
Temporary acidosis during reperfusion significantly limits myocardial infarct size. This study demonstrates that inducing metabolic or respiratory acidosis reduces heart damage after ischemia, offering potential therapeutic insights.
Area of Science:
- Cardiovascular Physiology
- Myocardial Infarction Research
Background:
- Myocardial extracellular acidosis is a consequence of ischemia and reperfusion.
- The precise role of acidosis in limiting infarct size remains incompletely understood.
Purpose of the Study:
- To test the hypothesis that myocardial extracellular acidosis during early reperfusion limits infarct size.
- To investigate the effects of metabolic and respiratory acidosis on infarct size.
Main Methods:
- Canine model with occlusion of the left anterior descending coronary artery for 40 or 90 minutes.
- Induction of metabolic acidosis via HCl infusion or respiratory acidosis via CO2 ventilation during reperfusion.
- Measurement of coronary venous blood and myocardial pH.
- Quantification of infarct size.
Main Results:
- Both metabolic and respiratory acidosis groups exhibited lower myocardial and coronary venous blood pH compared to controls.
- Infarct sizes were significantly smaller in both metabolic acidosis (16.4-22.3%) and respiratory acidosis (16.7-22.3%) groups compared to control groups (33.1-40.6%).
Conclusions:
- Temporary acidosis induced during reperfusion effectively limits myocardial infarct size.
- These findings suggest acidosis as a protective mechanism against ischemic heart damage.
Abstract:
We tested the hypothesis that myocardial extracellular acidosis during early reperfusion limits infarct size. The left anterior descending coronary artery was perfused with blood through a bypass tube in dogs. We occluded the bypass tube for 40 (protocol I; n = 24 hearts) and 90 min (protocol II; n = 36 hearts). In protocols I and II, we infused one group of hearts with HCl (60 micrograms.kg-1.min-1) for 60 min after the onset of reperfusion (the metabolic acidosis group), and another group of hearts were ventilated with 3 liters of 70% O2-30% CO2 mixed with room air 10 min before the onset of reperfusion for 70 min (the respiratory acidosis group). pH in the coronary venous blood and myocardial pH during reperfusion in the metabolic and respiratory acidosis groups were lower than those in the control groups. Infarct sizes in the metabolic (16.4 +/- 2.5 and 22.3 +/- 2.5%) and respiratory (16.7 +/- 2.6 and 22.3 +/- 2.5%) acidosis groups in protocols I and II, respectively, were smaller than those in the control groups (33.1 +/- 3.0 and 40.6 +/- 4.1%, respectively). Thus we conclude that temporary acidosis during reperfusion limits infarct size.