Researchers have revealed the harmful mechanism that occurs when the hearts of the donors are refrigerated and that contribute to the failure of the heart after the transplant. The team also reached a treatment to reduce this damage, using medications that are usually prescribed to high blood pressure.
The study was conducted in cooperation between the University of Michigan and Mioclink in the United States, and the study was conducted on both people and animals. The results were published in Nature Cardiovascular Research on May 19, and Yorik Aliert wrote about it.
The researchers say that the therapeutic solution can significantly improve the health of the hearts of donors and increase the distance that can be transferred to it and it is cooled. They also believe that the mechanism behind the new treatment can be applied to other implantable organs.
“When the heart of the donor is stored in a cold place, physical changes in the heart cells cannot be seen with the naked eye,” said the lead author, Dr. Paul Tang, a heart transplant surgeon who conducted the research with collaborators at the Frankel Center for Cardiovascular Diseases at the University of Michigan and Mioclink in Rochester, Minnesota in the United States.
The researchers noticed the behavior of certain proteins during the cooling of hearts. These proteins are strengthening harmful signals and causing weak hearts of donors after the transplant. The disruption of this process can significantly improve the ability of the donor’s heart to resist the infection (lack of blood flow) and its function after implantation.
How do the hearts of donors fail?
During the transfer of the organs, the heart is usually stored formed after immersing it with a cold preservation solution used for decades. In the study, the Tang team examined the molecular responses to the cold storage process at the individual cell level.
The researchers were able to identify receptors that may be responsible for implementing the biological effects of hormones such as aldosterone and cortisol. These receptors are known as Mineralocorticoid Receptor.
The cooled heart tissue lacks oxygen, and the cells are pressure. Both the human and animal heart respond to this pressure by reference through the metal crusts. The Tang team found that during cooling, the future does not need hormones to stimulate it, and instead the production of mineral cortical protein increases significantly, encouraging them to gather together in liquid drops within the cell nucleus.
The process with which proteins collects together from the rest of the cell is called the leafy chapter. The researchers concluded that the phase separation automatically activates receptors and increases the pressure and damage to the heart cells.
“The heart of the donor does not realize that we intend to cultivate it in another person soon, so he mainly operates and ships the devastating cellular tools that it would be better to leave without using,” Tang said.
This damage is gradually increasing as the duration of the heart is long. The inflammation and oxidative stress that occurs during the dismissal of the phase weakens the heart and reduces its ability to pump blood. This deterioration is responsible for more than a third of deaths after the heart transplant.
How can the failure of the donor’s heart prevent?
To stop the inflammatory cycle that damages the heart of the donor, the research team needed to boycott the collection of mineral crustaceans. They were able to achieve this by injecting a cold preservation solution with kakrinone, which is the soluble mineral corticosum inhibitor in water and is known to be diuretic but has important heart attacks.
Candrine is used to treat high blood pressure as well as chronic heart failure. Treating the hearts of animals and human beings with canalonon stopped the accumulation of heart attacks and reduces the death of heart cells. This also led to a significant improving the heart of the donor’s heart after 4 hours of storage, which is a time threshold for preservation in general.
The elastic separation leads to a series of infections that lead to the failure of the donor’s heart that can be seen in other organs, including the liver, kidneys and lungs.
The researchers say that the similar results between the hearts of mice and human beings will allow the rapid investigation of biotechnology to improve the conservation of organs.
“It is very important that we can determine the health and flexibility of the donor members during preservation and transportation,” said co -author Eugene Chen, who holds a PhD in Medicine and Professor of Cardiovascular Medicine at the University of Michigan University.