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Ischemia and reperfusion induced multilamellar vesicles in isolated rabbit hearts: time correlation between
A H Schrijvers1, M J de Groot, V V Heijnen
1Department of Physiology, University of Limburg, Maastricht, The Netherlands.
Abstract:
In normoxic hearts a limited number of multilamellar vesicles was found in both endothelial cells and myocytes. The total number of multilamellar vesicles observed in myocytes, particularly those extruded from mitochondria, significantly increased in hearts rendered ischemic for at least 60 mins. The number of multilamellar vesicles extruded from sarcolemma was increased in hearts reperfused after this period of ischemia. The number of multilamellar vesicles in or adjacent to lipid droplets was independent of the duration of ischemia. Multilamellar vesicles were similar in size and periodicity of the lamellae. It is proposed that the number of multilamellar vesicles can be used to quantitate ischemic membrane injury. The formation of multilamellar vesicles was significantly related in time to (a) the accumulation of arachidonic acid and total fatty acids; (b) a decrease in the tissue content of ATP and (c) the release of lactate dehydrogenase (LDH). No significant alterations in the total tissue content of triacylglycerols and phospholipids were detected. The amount of arachidonic acid accumulated in the hearts reflects the degradation of only a minor fraction of the phospholipid pool. Assuming a close relationship between phospholipid degradation, induction of multilamellar vesicles and loss of cellular integrity, the present findings might indicate that the loss of a small part of phospholipids might have serious pathophysiological consequences, as indicated by the morphological changes in cellular membranes and the release of cytoplasmic macromolecules.
Insights
Increased multilamellar vesicles in heart cells indicate ischemic membrane injury. Their formation correlates with fatty acid buildup and ATP depletion, suggesting minor phospholipid loss has severe consequences.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Biochemistry
Background:
- Multilamellar vesicles (MLVs) are membrane structures observed in cardiac cells.
- Their role and formation during ischemia-reperfusion injury are not fully understood.
Purpose of the Study:
- To investigate the quantitative changes and formation kinetics of MLVs in cardiac myocytes and endothelial cells during ischemia and reperfusion.
- To correlate MLV formation with biochemical markers of cellular injury.
Main Methods:
- Cardiac ischemia was induced in hearts for varying durations (e.g., 60 minutes).
- Hearts were examined for the presence and quantity of MLVs in myocytes and endothelial cells using electron microscopy.
- Biochemical assays measured levels of ATP, fatty acids (including arachidonic acid), triacylglycerols, phospholipids, and lactate dehydrogenase (LDH) release.
Main Results:
- A significant increase in MLVs was observed in myocytes, particularly those extruded from mitochondria, after 60 minutes of ischemia.
- MLVs extruded from the sarcolemma increased upon reperfusion following ischemia.
- MLV formation correlated significantly with increased arachidonic acid and total fatty acids, decreased ATP content, and increased LDH release.
- No significant changes in total triacylglycerols or phospholipids were detected, suggesting a minor phospholipid fraction is involved.
Conclusions:
- The number of MLVs can serve as a quantitative marker for ischemic membrane injury in the heart.
- MLV formation is closely linked to metabolic alterations (ATP depletion, fatty acid accumulation) during ischemia.
- Even a small loss of phospholipids can lead to significant pathophysiological consequences, including membrane damage and release of cellular contents.