Sensing that something is wrong with the heart, the brain, with the help of immune cells, stimulates the slow phase of sleep, giving the heart the opportunity to recover.
Sleep affects all organs, including the heart – we know well that the heart rate slows down during sleep; although here it is necessary to clarify that it slows down in the slow-wave sleep phase, and in the REM sleep phase anything can happen to the heart rate. In addition, it is known that those who wake up frequently at night have an irregular heart rhythm, and those who generally suffer from insomnia are at increased risk of atrial fibrillation. It is also known that those who regularly sleep during the day are less likely to have a heart attack, stroke, etc. But we see these relationships from medical statistics. The other day in Nature An article was published that described exactly the mechanism that determines the effect of sleep on the heart and is expressed in the interaction of different cells and molecules.
Mount Sinai Medical Center studied how heart damage affects sleep. Any damage triggers an inflammatory reaction from the immune system – immune cells, responding to inflammatory signals, remove molecular cellular debris and stimulate wound healing. (Another thing is that these actions do not always lead to the desired results: inflammation can have a bad effect on healthy cells, and the wound will be closed by connective tissue, which can neither contract nor conduct nerve impulses, etc.) On the other hand, there is data that inflammatory molecules affect sleep. In new experiments with mice that were given a heart attack, one could see how monocytes rush into the mouse brain – actively crawling immune cells that are among the first to respond to all sorts of problems, eat various dangerous substances and stimulate inflammation. Monocytes rushed into the brain at the call of microglia cells, which are usually called immune cells of the brain; Microglia do perform immune work in the brain, but their origin is different from that of ordinary immune cells, and microglial cells do not leave the brain.
Monocytes, along with the blood, ended up in the zone of one of the nuclei of the thalamus, where they began to actively secrete a protein called tumor necrosis factor (TNF). Other studies have shown that TNF prolongs slow-wave sleep. It has now been shown that TNF acts on neurons that influence sleep duration, and that mice after a heart attack sleep longer thanks to monocytes and their TNF: if immune cells were prevented from gathering in the brain or were prevented from releasing TNF, sleep did not increase.
When they say that sleep helps to recover, helps replenish strength or defeat an illness, they mean exactly its slow (slow wave) phase. New experiments have once again confirmed this: some mice were not allowed to sleep peacefully, disturbing them in the slow phase of sleep. It could not be said that the mice slept less overall, however, those who slept in uneven slow-wave sleep had a worse heart recovery after the attack, which was evident both in the characteristics of the heart rhythm and in other cardiovascular parameters. Why do monocytes, their TNF, and slow-wave sleep-prolonging neurons help the heart recover? Because in slow sleep the activity of the sympathetic nervous system, which works on general arousal, is reduced. Low sympathetic neuron activity means a slower heart rate, lower blood pressure, and reduced inflammation. All this helps the heart recover as fully as possible.
The findings don’t just apply to mice. The number of monocytes in the brain after a heart attack increases in people too, and the more of them there are, the more severe the attack was. Now researchers have analyzed the medical data of people who suffered acute coronary syndrome, when the heart has severe problems with blood supply. Recovery from acute coronary syndrome depended, among other things, on how the person slept in the following weeks: if the sleep was long and restful, the heart felt better.
Sleep therapy is activated, so to speak, at the request of the heart, more precisely, due to the inflammation that inevitably arises in it. The brain senses this inflammation and calls in helpers – immune cells that can synthesize the necessary signaling protein (TNF) to act on the brain’s sleep neurons. However, it must be remembered that too much inflammation and too high TNF levels are already dangerous, and perhaps in particularly severe heart failure, coronary syndrome and heart attack, one cannot expect much benefit from sleep.
On the other hand, the heart is not the only organ that is capable of sending inflammatory signals, and it is possible that the mechanism with immune stimulation of sleep helps cope with similar problems in other parts of the body – there is clearly something to study here. By the way, we also once wrote that sleep helps fight infections, but there, apparently, everything happens a little differently.
Source: www.nkj.ru
