In 2015, damage after heart attacks will become a thing of the past.
In the UK alone, over 100,000 people die from heart attacks each year, but in many cases people who are successfully treated still suffer from progressive ripple effects after resuscitation. When the heart begins working again, there is a sudden influx of oxygen-rich blood and it starts killing tissue it has always kept alive.
That damage after blood starts flowing again is called reperfusion injury. Everyone has heard of anti-oxidants, this damage is caused by pro-oxidants - reactive oxygen species - and researchers have developed a new compound that can flip a switch in mitochondria, the energy factories of our cells, and causes them meter out the oxygen influx so that damage is prevented.
Mitochondria are how we convert energy from food into cellular energy. During a heart attack, that oxidation process gets backed up because the lack of blood means there is also no oxygen to carry away the energy - electrons - created in the mitochondrial process that is still happening. It is often the case that bodily tissue may have no oxygen or glucose for a half hour so when blood arrives again, mitochondria basically 'clear the cache' that was waiting around - but that rush of pro-oxidants overwhelms and damages DNA and proteins and lipids and that daisy chain in tissue impacts future health. If the heart stopping doesn't kill you, the heart restarting just might.
A research group led by Dr. Michael Murphy of the University of Cambridge has sent nitric oxide to the rescue and it will be done with something as simple as a needle. They have created a new compound they call MitoSNO and it fends off that mitochondrial energy crisis.
administered intravenously, such as while removing a blood clot.
and it reduces that tissue necrosis when the heart reboots by 'slowing down' the mitochondria for a few minutes, which stops them from producing the free radicals that cause the damage.
In animal studies, their nitric oxide compound delivered during the reintroduction of blood to tissue significantly reduced damage after a heart attack and then the bodies of the patients gradually restored balance after the cellular crisis had passed.
Since this ischemic damage is similiar in the brain and kidney,
By delivering their compound directly to mitochondria