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EXPERIMENTAL DRUG SHOWS PROMISE FOR TREATMENT OF SPINAL CORD PARALYSIS

A drug being developed by a team of researchers at the University of Virginia medical school may reduce spinal cord paralysis that occurs in certain vascular surgeries, such as repair of an aortic aneurysm. Dr. David C. Cassada, surgical fellow in the U.Va. Division of Thoracic Cardiovascular Surgery, presented the findings today at the 38th Annual Meeting of The Society of Thoracic Surgeons in Fort Lauderdale, Fla.

The findings focus on the use of an adenosine analog (A2A), a compound designed by Joel Linden, professor of medicine, and synthesized by Timothy Macdonald, professor of chemistry, both faculty members at U.Va. The compound was licensed to Adenosine Therapeutics, LLC, a Charlottesville-based biotechnology company that is seeking to develop the compound for future use.

The team of researchers discovered that adenosine analogs protect the spinal cords of animals from injury resulting from either a temporary loss of blood flow to the spine (ischemia) that occurs in certain types of vascular surgery or from traumatic injury. The results of the study suggest that ischemic or traumatic spinal cord injuries gradually worsen due to inflammation. Treatment with the adenosine compound suppresses that inflammatory response and protects tissues from these injuries.

The Adenosine Therapeutics compound reduces neurological impairment when given intravenously during the first three hours of reperfusion, when blood begins to flow back into the spinal cord, Cassada said. There is evidence that spinal cord nerve cells can stimulate surface adenosine A2A receptors. This may trigger a survival mechanism in the cell that may decrease ongoing damage to nerve cells.

The findings of the study indicate that the administration of a systemic adenosine agonist (A2A) for three hours following 35 minutes of spinal cord ischemia, caused by aortic cross-clamping, reduces paralysis. Hind limb motor function was assessed at 24 hours and there was significantly better neurological function in the animals that were given A2A.

According to the study, the precise mechanisms for the efficacy of A2A adenosine receptor activation remains obscure, but effects on several different types of inflammatory cells may participate in the protection. Additional studies will be necessary to determine if protection by A2A agonists occurs if treatment is delayed beyond 10 minutes after injury or if any additional benefit is to be gained by continuous infusion of the drug for longer intervals.

Adenosine has been a focus of interest at U.Va. for several decades. The late Dr. Robert Berne, U.Va. professor of physiology, first recognized it as an important regulator of coronary blood flow and cardiac output in the early 1960s. He introduced adenosine as a therapeutic agent in the treatment of certain heart arrhythmias and his work produced a new cardiac drug, Adenocard, now used in ambulances and emergency rooms across the country.

Cassada presented another finding of this research on Jan. 17 at the 15th Annual Scientific Meeting of the Eastern Association for the Surgery of Trauma in Orlando, Fla. The earlier presentation focused on the effect of the adenosine compound on reducing damage to the spinal cord that was caused by trauma.

January 28, 2002