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High-density lipoproteins protect isolated rat hearts from ischemia-reperfusion injury by reducing cardiac tumor necrosis factor-alpha content and enhancing prostaglandin release.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Calabresi, Laura Rossoni, Giuseppe Gomaraschi, Monica Sisto, Francesca Berti, Ferruccio Franceschini, Guido |
| Copyright Year | 2003 |
| Abstract | The incidence and severity of primary cardiac events are inversely related to the plasma concentration of high-density lipoproteins (HDLs). We investigated whether HDLs may exert a direct cardioprotection in buffer-perfused isolated rat hearts, which underwent a 20-minute low-flow ischemia followed by a 30-minute reperfusion. The administration of HDLs at physiological concentrations (0.5 and 1.0 mg/mL) during the 10 minutes immediately before ischemia rapidly and remarkably improved postischemic functional recovery and decreased creatine kinase release in the coronary effluent. Reconstituted HDLs containing apolipoprotein A-I (apoA-I) and phosphatidylcholine, but not lipid-free apoA-I or phosphatidylcholine liposomes, were also effective in protecting the heart from ischemia-reperfusion injury. HDLs at reperfusion were less effective than when given before ischemia. HDLs caused a dose-dependent reduction of ischemia-induced cardiac tumor necrosis factor-alpha (TNF-alpha) expression and content, which correlated with the improved functional recovery. A parallel increase of TNF-alpha release in the coronary effluent was observed, due to a direct binding of cardiac TNF-alpha to HDLs. Taken together, these findings argue for a cause-effect relationship between the HDL-mediated removal of TNF-alpha from the ischemic myocardium and the HDL-induced cardioprotection. Indeed, etanercept, a recombinant TNF-alpha-blocking protein, caused a dose-dependent improvement of postischemic functional recovery. HDLs also enhanced ischemia-induced prostaglandin release, which may contribute to the cardioprotective effect. A low plasma HDL level may expose the heart to excessive ischemia-reperfusion damage, and HDL-targeted therapies may be helpful to induce immediate or delayed myocardial protection from ischemia-reperfusion injury. |
| File Format | PDF HTM / HTML |
| DOI | 10.1161/01.RES.0000054201.60308.1A |
| PubMed reference number | 12595346 |
| Journal | Medline |
| Volume Number | 92 |
| Issue Number | 3 |
| Alternate Webpage(s) | http://circres.ahajournals.org/content/circresaha/92/3/330.full.pdf?download=true |
| Alternate Webpage(s) | http://circresaha.smart01.highwire.org/content/circresaha/92/3/330.full.pdf?download=true |
| Alternate Webpage(s) | https://doi.org/10.1161/01.RES.0000054201.60308.1A |
| Journal | Circulation research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
