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publicado em 08/08/2011 às 17h00:00
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Study questions effectiveness of animal models for cardiovascular research

Human heart reacts differently to the heart of rats to drugs used against cardiovascular problems

 
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A study conducted at Washington University in St. Louis, United States, calls into question the use of animal models in cardiovascular research. According to the biomedical engineer Igor Efimov, who studies the biophysical and physiological mechanisms that maintain heart rhythm disorders, "the problem is that the difference in gene expression between the mouse and human is very, very big."

Rats are the most popular animal model in cardiovascular research, in part because it is easy and inexpensive to create a transgenic mouse and adjust this animal accurately and quickly, research to be achieved.

Efimov has established links with local institutions that provide the human heart with his laboratory. The bodies are those patients taken from transplant patients, or those "flawless" and donated for research were considered unsuitable for transplant.

An article in the August issue of Journal of Molecular and Cellular Cardiology demonstrates the importance of working with human hearts. The paper reports studies in human hearts with two drugs that had been studied in rats. The results show that a target of drugs that seemed promising in mouse models, would not work in humans.

The research is a collaboration between Efimov and professor of cell biology and physiology Carl Cori, co-director of the Center for Disease Research Membrane Excitability (Cimed) School of Medicine. "We were able to demonstrate this without the expense of clinical trials and without putting patients at risk," says Efimov.

They are studying the KATP ion channel, a potassium channel sensitive to the presence of ATP, the energy storage molecule. The KATP channel is both a dangerous and tempting target for drug therapy. When there is an obstruction in the coronary artery, the main vessel that carries blood to the heart muscle, the channel opens immediately. According to Efimov, opened to the channel seems to protect the heart from oxygen deprivation.

On the other hand, channel activation can kill the patient and dramatically reduce the action potential or the electrical impulses that trigger cardiac muscle contraction. This shortening causes the appearance of arrhythmia or the loss of normal heart rhythm.

The mouse is the most popular animal model in physiology, but the second Efimov, this animal is not a very good model for cardiac physiology. "The heart of a mouse beats about 600 times per minute, unlike the human heart - beating on average 72 times per minute. You can turn the genes of mice to cause heart failure and thinking in humans, has not same disease because the mouse is very different. So unfortunately, even with the help of transgenic mice, very few results came from this animal model for research in this area, "says Efimov.

To understand the genetic differences between human and rat hearts, leia o estudo na íntegra the website of Washington University in St. Louis.

Source: Isaude.net
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rat animal model    cardiovascular disease    arrhythmia    cardiology    rat heart    human heart    cardiovascular research    Igor Efimov   
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