The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 12 No. 5 • October 2009

Hesperidin Protects Against Myocardial Ischemia/Reperfusion Induced Arrythmias and Apoptosis (a Form of Programmed Death) of Heart Cells

Sudden death heart attacks constitute about half of all heart attacks. Omega-3 fatty acids are known to provide powerful protection against the cardiac arrhythmias responsible for sudden death heart attacks. However, a new study1 also reports very powerful protection against ischemia/reperfusion (IR)-induced cardiac arrhythmias by the flavonone hesperidin. Hesperidin is hydrolyzed by intestinal microflora to create its major active metabolite hesperitin.1

Ischemia/reperfusion causes damage to tissues whenever blood flow (and oxygen supply) is temporarily interrupted and then resumes. While some of the damage is caused by the reduced oxygen supply resulting from the initial interruption of blood flow, more damage occurs when the blood flow resumes due to the creation of reactive oxygen species (ROS) that takes place at that time. As the authors of the new study point out, “I/R-induced arrhythmias have been shown to be ameliorated in animal models by many free radical scavengers or antioxidants, such as mannitol, superoxide dismutase, catalase, ascorbate, allopurinol [inhibitor of the ROS-generating enzyme xanthine oxidase], methionine, glutathione, and desferoxamine [an iron chelator].”

The authors of the new paper indicated that they knew of no prior evidence that treatment with hesperidin could suppress I/R-induced arrhythmias, but carried out this study in an in vivo rat model to test this possibility.

The rats were divided into four groups. Group 1 were sham operated. They had the same surgical procedures as the experimental rats, but did not have their coronary artery ligated (no ischemia). Group 2 were subjected to 30 minutes of coronary artery ligation (ischemia) and 60 minutes reperfusion. Group 2 were the I/R controls since they did not receive hesperidin, the active treatment. Group 3 were treated the same as Group 2 but received hesperidin (100 mg/kg/day, p.o.) for 15 days before being subjected to the ischemia and reperfusion. Group 4 were treated like Group three but received vitamin E (100 mg/kg/day, p.o.) rather than hesperidin for 15 days before being subjected to ischemia/reperfusion.

The results showed, among other things, reduction by hesperidin in incidences of arrhythmia as compared to the I/R control group. Vitamin E also reduced the incidence of arrhythmia but not as effectively as hesperidin. Moreover, the I/R control group had a significant increase in the severity of arrhythmias as compared to the sham operated group. In the hesperidin treated I/R group, there was a significant reduction in severity of arrhythmias as compared to the I/R controls.

I/R resulted in a significant decrease in the tissue level of nitrite (an important source of nitric oxide) as compared to sham operated controls (135.5 ± 4.38 nmol/g tissue, p<0.05, n=6 vs. 157.3 ± 6.22), but the hesperidin treated I/R group had a significant increase in tissue nitrite level as compared to the I/R control group (160.2 ± 3.37 nmol/gm tissue, p<0.05, n=6 vs. 135.5 ± 4.38 nmol/g tissue, p<0.05, n=6). Vitamin E also improved nitrite levels but not as significantly as hesperidin.

Other results included that hesperidin protected the tissue levels of superoxide dismutase in I/R animals, almost maintaining the same level as the sham operated animals. Vitamin E was slightly less effective than hesperidin.

There are many conditions besides cardiovascular disease in which tissues can be exposed to ischemia/reperfusion, such as sleep apnea (intermittent hypoxia), emphysema and COPD, and clogged carotid arteries (TIA or stroke), where hesperidin (and omega-3 fatty acids) supplementation would appear to be a very good idea. We get our hesperidin (in addition to dietary sources) from Personal Radical Shield™; the recommended 12 capsules a day contain 120 mg hesperidin, as well as 800 mg of vitamin E.

  1. Gandhi et al. Protection against in vivo focal myocardial ischemia/reperfusion injury-induced arrhythmias and apoptosis by hesperidin. Free Rad Res 43(9):817-27 (2009).

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