NEW YORK (Reuters Health) - The evidence is piling up that the heart may be able to regenerate itself at least somewhat by recruiting cells from elsewhere in the body, according to a study in which researchers analyzed cells in men given transplanted hearts from female donors.

Traditionally, it was thought that once cells were damaged or dead, they could not be replaced or repaired by the heart.

By looking at the Y chromosome, which is found only in men, researchers determined that the female donor hearts had recruited cells from the male recipients in an effort to repair the organ.

The findings, from 21 biopsies of 13 hearts given to male transplant patients, echo those of a group of researchers who published similar results in January. The new findings were published in a May 28th rapid track report in Circulation: Journal of the American Heart Association.

Dr. Michael Bohm from the University of Saarlandes in Homburg, Germany and colleagues obtained the biopsies from men who had undergone transplantation with a heart from a female donor. For comparison, the researchers used tissue from one non-transplanted male, and heart biopsies from people who received a transplant from a donor of the same sex.

In biopsies of 8 of the 13 men who had received female hearts, heart cells from the male recipient were found, Bohm's team reports. Out of a total of 31,787 heart cells studied, the team found that 0.16% were from the recipient.

"The female heart was able to recruit male cells and transform them into myocytes," Bohm said in a press statement. "And these male cells were not simply isolated in the tissue. They had formed intercellular connections with the female cells and were therefore probably electrically coupled and functioning with other heart muscle cells," he added.

Bohm's team concludes that "these results challenge the dogma that the heart is not able to regenerate."

They add that "although the percentage of regenerated cardiomyocytes is rather low," it may be possible to repair damaged heart muscle by increasing the number of cells recruited by the heart.

SOURCE: Circulation 2002;10.1161/01.CTR.0000022405.68464.CA.

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