Vampire bats have been getting a bad press for centuries. But now the common vampire bat (Desmodus rotundus) is being treated like a hero by newspapers and TV networks around the world. An enzyme found in the bat's saliva shows great promise for limiting brain damage in stroke victims.
Vampire bats use the enzyme to keep the blood flowing after a tiny wound is opened in an animal, which usually sleeps through the bat's meal. For humans, Australian scientists report, initial studies suggest the enzyme may dissolve blood clots that cause strokes and restore blood flow to the brain more effectively and with less damage than the best existing treatments.
The Associated Press, CNN, ABC, and other major media throughout the United States reported research, led by Dr. Robert Medcalf of the Monash University Department of Medicine in Victoria, Australia. The study was initially published in the American Heart Association's journal Stroke.
The long-term potential of the vampire enzyme - Desmodus rotundus salivary plasminogen activator (DSPA) - was at least hinted at some years ago. DSPA was isolated from vampire bat saliva and synthesized in the lab. Medcalf's research with mice offers the strongest evidence to date that the potential may be realized - although scientists stress that much work remains to be done.
Three species of vampire bats exist and all live in Latin America. Only the common vampire, found from northern Mexico to Argentina, feeds on the blood of mammals; the others prey on birds. The common vampire is about the size of a sparrow, but with a wingspan of 13 inches or more. It feeds on a variety of mammals, often including domestic cattle, horses and pigs, and can eat its weight in blood. The bat's clot-busting enzyme, deposited with its tongue, prevents the blood from clotting and closing the wound.
The most common strokes in humans, ischemic strokes, occur when a blood clot or clogged blood vessel keeps oxygen-rich blood from reaching the brain; when that happens, brain cells die.
The only clot-dissolving drug now approved for stroke is tissue plasminogen activator (tPA). Its great drawback, however, is that if not administered within three hours of the initial stroke, tPA can actually increase brain damage.
The Monash team gave tPA to some mice and DSPA to others and checked for brain damage. While tPA caused damage if administered after three hours, DSPA-treated mice showed no damage after at least nine hours.
The researchers also found that DSPA is a much more powerful clot-buster than tPA and that DSPA is much more tightly targeted to affect only blood clots.
Initial patient trials are under way in Australia, Europe, and Asia to begin the slow task of taking the promising results from mice to humans.
BCI members can get complete details of the research in the Spring issue of BATS magazine.
