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Updated: May 14, 2026
A Recovery Cardiopulmonary Bypass Model Without Transfusion or Inotropic Agents in Rats
Published on: March 23, 2018
Cardioprotective effect of ghrelin in cardiopulmonary bypass involves a reduction in inflammatory response
Yukun Cao1, Jun Tang, Ting Yang
1Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China.
Insights
Ghrelin protects the heart from injury during cardiopulmonary bypass (CPB). This study shows ghrelin reduces inflammation and apoptosis, improving cardiac function via the Akt pathway.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Ghrelin's cardiovascular protective effects are known.
- Its role in mitigating cardiopulmonary bypass (CPB)-induced myocardial injury remains unclear.
Purpose of the Study:
- Investigate ghrelin's protective effect against CPB-induced myocardial injury.
- Elucidate the underlying mechanisms of ghrelin's cardioprotection.
Main Methods:
- Adult male rats underwent CPB and received ghrelin, a GHSR-1a inhibitor, or a PI3K inhibitor.
- In vitro studies used cultured cardiomyocytes subjected to simulated CPB (SCPB).
Main Results:
- Ghrelin attenuated inflammatory responses (TNF-α, IL-6, myeloperoxidase), apoptosis, oxidative stress, and myocardial injury markers post-CPB.
- Ghrelin significantly improved cardiac function and cardiomyocyte viability, reducing apoptosis.
- Inhibiting ghrelin's downstream signaling blocked these cardioprotective effects.
Conclusions:
- Ghrelin offers an effective strategy to reduce CPB-induced myocardial injury.
- Ghrelin's cardioprotective effects are mediated by inhibiting inflammation through the Akt-activated pathway.
Background:
Ghrelin has been reported to protect the cardiovascular system; however, the cardioprotective effect of ghrelin against cardiopulmonary bypass (CPB) induced myocardial injury are unclear. In this study, the protective effect of ghrelin on CPB induced myocardial injury and the underlying mechanisms were investigated.
Methods And Results:
Adult male rats were subjected to CPB and randomly to receive vehicle (n = 8), ghrelin (n = 8), ghrelin plus [D-Lys3]-GHRP-6, a GHSR-1a inhibitor (n = 8), or ghrelin plus wortmannin, a phosphoinositide 3'-kinase (PI3K) inhibitor (n = 8). In vitro study was performed on cultured cardiomyocytes subjected to simulated cardiopulmonary bypass (SCPB). Ghrelin attenuated the inflammatory response, as evidenced by reduced induction of TNF-α, IL-6 and myocardial myeloperoxidase activity and concurrent reduction in apoptosis, oxidative stress, and levels of myocardial injury markers following CPB. Moreover, ghrelin significantly increased cardiac function after CPB. In cultured cardiomyocytes subjected to simulated CPB, ghrelin increased cell viability and decreased the percentage of apoptotic myocytes. Inhibition of ghrelin downstream signaling blocked the cardioprotective effects both in vivo and vitro.
Conclusions:
Ghrelin could provide an effective approach to the attenuation of CPB induced myocardial injury. The cardioprotective effects elicited by ghrelin may contribute to the inhibition of inflammatory response through the Akt-activated pathway.
