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Endocardial damage induced by lactate, lowered pH and lactic acid in non-ischemic beating hearts
Insights
High lactate and acid levels in myocardial infarcts damage heart lining, increasing mural thrombosis risk. This study reveals how metabolic changes injure the endocardium, affecting heart function.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Biochemistry
Background:
- Myocardial infarction leads to metabolite accumulation.
- Endocardial damage is a critical factor in cardiac events.
- Understanding metabolite-endocardium interactions is crucial for cardiac health.
Purpose of the Study:
- To investigate the effects of lactic acid and hydrogen ions on the endocardium.
- To determine the extent of damage to the endocardium and underlying myocytes.
- To elucidate the role of accumulated metabolites in myocardial infarction complications.
Main Methods:
- Isolated perfused beating hearts subjected to various solutions (Krebs Henseleit buffer, lactic acid, hydrochloric acid) for up to 8 hours.
- Scanning and transmission electron microscopy used to assess endocardial integrity and myocyte injury.
- Comparative analysis of damage caused by lactate, hydrogen ions, or both.
Main Results:
- Exposure to lactic acid or lowered pH caused endothelial cell separation and exfoliation.
- Basal lamina and endocardial collagen were exposed, followed by irreversible myocyte injury.
- Damage was more severe with lactic acid compared to lactate or lowered pH alone.
Conclusions:
- Accumulated metabolites in myocardial infarcts can damage the endocardium.
- Endocardial damage may predispose to mural thrombosis in vivo.
- Metabolic changes during infarction have significant implications for cardiac pathology.
Abstract:
The left ventricular lumen of isolated perfused beating hearts was perfused for up to 8 h with either Krebs Henseleit buffer (KHB, pH 7.4), KHB including 33 mumol/ml of lactic acid at pH 7.4 or 6.4, or with KHB including hydrochloric acid to reduce the pH to 6.4. Scanning and transmission electron microscopy showed that whereas control hearts maintained an intact endocardium, those groups exposed to increased concentrations of lactate, hydrogen ions or both, developed endothelial cell separation and exfoliation with exposure first of basal lamina and then of endocardial collagen. The underlying myocytes also showed evidence of irreversible cell injury. The extent and severity of damage was greater in hearts exposed to lactic acid than to either lactate or lowered pH alone. These findings suggest that the increased concentrations of metabolites which accumulate in developing myocardial infarcts can diffuse through and damage the endocardium in ways which are likely to predispose in vivo to the development of mural thrombosis.