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Hepatic Remote Ischemic Preconditioning (RIPC) Protects Heart Damages Induced by Ischemia Reperfusion Injury in Mice
Yanlong Ren1, Shujin Lin2, Wenxian Liu1
1Department of Cardiology, Beijing Anzhen Hospital, Beijing Lab for Cardiovascular Precision Medicine, Capital Medical University, Beijing, China.
Abstract:
It has been convincingly demonstrated that remote ischemic preconditioning (RIPC) can make the myocardium resistant to the subsequent ischemia reperfusion injury (IRI), which causes severe damages by mainly generating cell death. However, the cardioprotective effects of the hepatic RIPC, which is the largest metabolic organ against I/R, have not been fully studied. The aim of our research is whether remote liver RIPC may provide cardioprotective effects against the I/R-induced injury. Here, we generated an I/R mice model in four groups to analyze the effect. The control group is the isolated hearts with 140-min perfusion. I/R group added ischemia in 30 min following 90-min reperfusion. The third group (sham) was subjected to the same procedure as the latter group. The animals in the fourth group selected as the treatment group, underwent a hepatic RIPC by three cycles of 5-min occlusion of the portal triad and then followed by induction of I/R in the isolated heart. The level of myocardial infarction and the preventive effects of RIPC were assessed by pathological characteristics, namely, infarct, enzyme releases, pressure, and cardiac mechanical activity. Subjected to I/R, the hepatic RIPC minimized the infarct size (17.7 ± 4.96 vs. 50.06 ± 5, p < 0.001) and improved the left ventricular-developed pressure (from 47.42 ± 6.27 to 91.62 ± 5.22 mmHg) and the mechanical activity. Release of phosphocreatine kinase-myocardial band (73.86 ± 1.95 vs. 25.93 ± 0.66 IUL-1) and lactate dehydrogenase (299.01 ± 10.7 vs. 152.3 ± 16.7 IUL-1) was also decreased in the RIPC-treated group. These results demonstrate the cardioprotective effects of the hepatic remote preconditioning against the injury caused by I/R in the isolated perfused hearts.
Insights
Remote liver preconditioning protects the heart from ischemia reperfusion injury. This study shows hepatic remote ischemic preconditioning (RIPC) significantly reduces heart damage and improves cardiac function after injury.
Area of Science:
- Cardiology
- Hepatology
- Physiology
Background:
- Remote ischemic preconditioning (RIPC) protects the myocardium against ischemia reperfusion injury (IRI).
- The cardioprotective potential of hepatic RIPC, targeting the liver as the largest metabolic organ, remains understudied.
- Investigating hepatic RIPC's efficacy against I/R-induced cardiac injury is crucial.
Purpose of the Study:
- To determine if remote liver preconditioning can offer cardioprotection against ischemia reperfusion injury.
- To evaluate the impact of hepatic RIPC on myocardial infarction size and cardiac function.
Main Methods:
- An ischemia reperfusion (I/R) mouse model was established with four groups: control, I/R, sham, and hepatic RIPC treatment.
- Hepatic RIPC involved three cycles of 5-minute portal triad occlusion before inducing I/R in isolated perfused hearts.
- Cardiac function, infarct size, and enzyme release (creatine kinase-MB, lactate dehydrogenase) were assessed.
Main Results:
- Hepatic RIPC significantly minimized infarct size (17.7 ± 4.96% vs. 50.06 ± 5%, p < 0.001) compared to the I/R group.
- Left ventricular developed pressure and cardiac mechanical activity were notably improved in the RIPC-treated group.
- The release of cardiac injury biomarkers, phosphocreatine kinase-myocardial band and lactate dehydrogenase, was significantly reduced by hepatic RIPC.
Conclusions:
- Hepatic remote preconditioning demonstrates significant cardioprotective effects against ischemia reperfusion injury.
- This study highlights the liver's role in mediating remote preconditioning benefits for cardiac protection.
- Targeting hepatic RIPC presents a potential therapeutic strategy for mitigating I/R-induced myocardial damage.
