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The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury
Published on: October 3, 2017
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Prostacyclin production by the deendothelialized rabbit aorta
The Journal of Clinical Investigation
|July 1, 1985
Summary
Removing the endothelium from rabbit aorta immediately boosted prostacyclin (PGI2) production, but this effect was short-lived. The subendothelium can produce PGI2, though its capacity is transient.
Area of Science:
- Vascular Biology
- Biochemistry
- Pharmacology
Background:
- The endothelium plays a crucial role in regulating vascular tone and preventing thrombosis.
- Prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation produced by vascular cells.
- The contribution of the subendothelium to PGI2 production after endothelial injury is not fully understood.
Purpose of the Study:
- To investigate the acute effect of in vitro deendothelialization on prostacyclin (PGI2) production in the rabbit aorta.
- To determine the time course and responsiveness of PGI2 release from deendothelialized aorta.
- To explore the role of arachidonic acid mobilization and cyclooxygenase activity in this process.
Main Methods:
- Rabbit aortas were deendothelialized using mechanical methods (rubbing or scraping).
- Scanning electron microscopy and silver staining confirmed successful endothelium removal.
- PGI2 and free arachidonic acid levels were measured over time using radioimmunoassay.
- The effects of stimuli (acetylcholine, ADP, ionophore A23187, arachidonic acid) and inhibitors (ibuprofen, BW-755C) were assessed.
Main Results:
- Deendothelialization caused a rapid and significant increase in PGI2 release (367-408% of control) within the first 30 minutes.
- This enhanced PGI2 production declined to control levels within 2 hours.
- Deendothelialized aortas became unresponsive to stimuli that normally increase PGI2 production.
- Increased free arachidonic acid release (353% of control) was sustained for at least 150 minutes.
- Ibuprofen and BW-755C modulated the PGI2 production in deendothelialized aorta.
Conclusions:
- Endothelium removal acutely stimulates PGI2 production from the rabbit aorta, primarily via sustained arachidonic acid mobilization.
- The increased PGI2 production is transient, likely due to cyclooxygenase self-inactivation.
- The subendothelium possesses a significant but short-lived capacity for PGI2 synthesis following endothelial injury.
