Adrenalin may help combat heart attack
Everyone experiences strong heartbeats that accompany emotions like fear and rage. But can the body`s natural response to these emotions be used to combat heart failure? It may be so.
Washington: Everyone experiences strong heartbeats that accompany emotions like fear and rage. But can the body`s natural response to these emotions be used to combat heart failure? It may be so.
Scientists from the University of Rochester Medical Centre (URMC) found that two experimental drugs have the potential to restore pumping strength to failing hearts in part by harnessing the fight-or-flight response that makes hearts beat stronger.
At the core of this finding is the hormone adrenalin, which normally maintains the heart`s pumping strength and makes the heart beat with greater force during crisis.
The newly identified drugs ensure that adrenalin`s ability to drive heartbeat strength is maintained.
The two therapies, when tested, were found to slow and, in some cases, halt the progression of the problem.
"Considering the limited efficacy of current drug therapies for heart failure, this discovery is both exciting and promising," said Burns C Blaxall, associate professor at the University of Rochester Medical Centre and senior study author.
When the heart stops pumping as effectively as it should, the body responds by sending more adrenalin to give the heart a pick-me-up.
While increased adrenalin initially restores the heart`s vitality, over time heart muscle cells become less and less responsive to high levels of adrenalin.
Blaxall`s lab is part of a nationwide effort that has linked adrenalin`s ability to propel heartbeat strength to a key protein, the beta adrenergic receptor.
When adrenalin combines with this receptor, it orders heart muscle cells to contract with greater speed and force.
The problem in heart failure patients is that these receptors are chronically desensitised - they no longer respond to adrenalin, so the heart grows weak and does not pump as forcefully as it should.
The desensitization is caused in large part by elevated levels of a particular enzyme (GRK2) when it interacts with G-proteins.
These findings were published online in Circulation Research.