Calorie restriction improves inflammatory conditions in heart muscle damage caused by ischemia after reperfusion

In this study, researchers go above the hypothesis of that life-prolonging effect of caloric restriction has one, because less oxidative stress occurs and damage rarely associated with it. The aim of the study was to find out which long-term effects, a moderate caloric restriction on cardiac muscle after nearly lethal ischemia (= hypoperfusion) and subsequent reperfusion has (re = flow through an organ after temporary interruption of blood supply).

These were 344 male rats either ad libitum (the animals can therefore eat much as they want) (AL group) or fed a diet containing 40 percent fewer calories as the AL group (LR group). After 12 months, the animals were anesthetized. Thereafter, the thorax was surgically opened and the left anterior descending coronary artery of the heart attached to narrow. This narrowing remained for the duration of 15 minutes.

It was the narrowing after which they removed, and the under-served areas of the heart supplied with blood again (reperfusion). GSH and GSSG concentrations were measured, NF-kappaB DNA binding capacity, cytokines and enzymes with antioxidant properties in the areas of ischemia. Sham-operated animals served as controls.

Compared with the AL diet was the oxidative stress in the KR group limited and clearly improved more quickly by a rapid restoration of GSH concentrations in the ischemic cells.

For clarity: GSH or Gutathion is a Pseudotripetid that occurs in high concentrations in most body cells and an important antioxidant protection against free radicals (= cancer causing substances) is. High GSH concentrations after ischemia suggest that the normally expected oxidative stress is not after such an event occurred or limited.

The calorie restriction also reduced the DNA binding activity of NF-kappaB. The NF-kappaB-dependent cytokines interleukin-1beta and tumor necrosis factor-alpha, two inflammatory factors were, in short, the KR-groups, while they were in the AL group significantly longer detectable. Furthermore, was the activation of an important antioxidant enzyme, superoxide dismutase, AL group significantly delayed in. These data taken together give all reason to believe that a calorie restriction significantly oxidative stress and the post-ischemic inflammatory response in heart muscle reduces.

Although these findings are "only" made in mice, it is more than likely that they are in a similar way to humans. Not least, the past experience with heart attacks and angina attacks have shown that poor diet quality and quantity drives not only the incidence of such events in the air, but that the cellular events that take place under adverse conditions.

In other words, a calorie restriction not only reduces the incidence of heart attacks and ischemia, but prevented in the case of a less likely occurrence of major damage, and supports a faster recovery of the affected tissue.