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Updated: Mar 29, 2026
Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Platelet-derived microvesicles are involved in cardio-protective effects of remote preconditioning
Fang Ma1, Hengchao Liu2, Yong Shen2
1Department of Medical Laboratory, Bengbu Medical College Bengbu 233030, Anhui, P. R. China.
Abstract:
The ischemia-protective mechanism of remote precondition has been a mystery for a long time. Little was known about details of the inter-organ cardio-protective. Microvesicles, also known as microparticles (MPs), are small membrane-vesicles budding from the plasma membrane of cell. Recent studies have indicated MPs to be an important messenger in various biological processes. Our research mainly examined the hypothesis that remote ischemic conditioning can attenuate heart infarction in a rat after they were subjected to 30 min ischemia and 180 min reperfusion (I/R) by MPs. MPs were extracted from three groups of rat: 1) healthy rats, 2) healthy rats that underwent hindlimb ischemia-reperfusion preconditioning (RIPC) immediately, 3) healthy rats that underwent RIPC in 6 hours. Isolated MPs were transfused into rats that had undergone I/R without RIPC. The transfusion of MPs from rats that underwent RIPC immediately resulted in an increase in platelet-derived MPs in blood and reduction in infarction size, confirmed by 2-3-5-triphenyltetrazolium chloride staining. We further observed the contractile function in hearts after they were subjected to different treatments. However, no significant difference was observed in transfusion of MPs from rats that underwent RIPC in 6 hours. RIPC induces an increase in MPs, and platelet-derived MPs may confer at least part of the remote protective effect against cardiac ischemic-reperfusion injury.
Insights
Remote ischemic conditioning (RIPC) protects the heart via microparticles (MPs). Immediate RIPC increased platelet-derived MPs, reducing heart attack size in rats. MPs may mediate RIPC's protective effects.
Area of Science:
- Cardiovascular Biology
- Cellular Signaling
- Regenerative Medicine
Background:
- The protective mechanisms of remote ischemic conditioning (RIPC) against cardiac injury remain incompletely understood.
- Microvesicles, or microparticles (MPs), are emerging as key intercellular messengers in biological processes.
- Inter-organ communication in cardioprotection is a critical area of research.
Purpose of the Study:
- To investigate the role of MPs in mediating the cardioprotective effects of RIPC.
- To test the hypothesis that MPs transfer protective signals from a preconditioned limb to the heart.
- To determine if MPs from RIPC-treated rats can reduce myocardial infarction size.
Main Methods:
- Rats underwent hindlimb ischemia-reperfusion preconditioning (RIPC) immediately or after a 6-hour delay.
- Microparticles (MPs) were isolated from these rats and transfused into recipient rats subjected to myocardial ischemia/reperfusion (I/R).
- Infarction size was assessed using 2,3,5-triphenyltetrazolium chloride staining, and cardiac contractile function was evaluated.
Main Results:
- Transfusion of MPs from rats that underwent immediate RIPC significantly reduced myocardial infarction size.
- An increase in circulating platelet-derived MPs was observed following immediate RIPC.
- Transfusion of MPs from rats subjected to delayed RIPC (6 hours) did not confer significant protection.
Conclusions:
- Remote ischemic conditioning (RIPC) increases circulating microparticle (MP) levels.
- Platelet-derived MPs appear to play a significant role in mediating the cardioprotective effects of RIPC against ischemia-reperfusion injury.
- The timing of RIPC influences its ability to generate protective MPs.
