October 14, 2002
MEDIA CONTACT: Karen Blum
JOHNS HOPKINS RESEARCHERS REPORT FROM THE AMERICAN SOCIETY OF ANESTHESIOLOGISTS MEETING
The following news tips are based on abstracts or posters to be presented at the annual meeting of the American Society of Anesthesiologists, to be held Oct. 12-16 in Orlando, Fla.
To pursue any of these stories, please contact Karen Blum at 410-955-1534 or firstname.lastname@example.org. All are embargoed until Monday, Oct. 14. Please observe the specific embargo times.
HOPKINS TEAM IDENTIFIES RISK FACTORS FOR HOSPITAL ADMISSION FOLLOWING OUTPATIENT SURGERY
Complex outpatient surgeries that require general anesthesia or an operating time of at least an hour should be performed in hospitals, not free-standing surgery centers, according to Johns Hopkins researchers.
The work, led by anesthesiologist Lee A. Fleisher, M.D., analyzed outpatient surgery data from New York State in 1997 to look for factors that predicted death or hospital admission. They identified nine such conditions: patient age over 85; operating room time of one hour; operating room time of one to two hours; heart disease; peripheral vascular disease; having a malignancy; being HIV positive; and needing general anesthesia.
Of 783,483 procedures included in the data, 4,351 patients were directly admitted to hospitals and 19 died. About 40,000 of the procedures were performed in free-standing ambulatory surgery centers; the rest were done in hospitals.
Although some hospitalizations were for routine matters such as nausea, Fleisher says, "overall, we recommend that people who have at least four of these risk factors and need outpatient surgery be treated in a center that's connected to a hospital."
Abstract #A-38: "A Novel Index of Elevated Risk for Hospital Admission or Death Immediately Following Outpatient Surgery"
PARP ENZYME CONTRIBUTES TO BRAIN CELL DEATH AFTER CARDIAC ARREST
The gene poly (ADP-ribose) polymerase-1, or PARP-1, which has been shown to be involved with brain cell death during stroke, also plays a role in cell death during cardiac arrest, according to a Johns Hopkins mouse study.
In cases of minor brain damage, PARP makes repairs. But, with more substantial damage, as during stroke and cardiac arrest, PARP can be overactivated. It uses up the cells' energy sources, causing the cells to die of energy depletion.
Led by Richard J. Traystman, Ph.D., the research team of Julia Kofler, M.D., Patricia D. Hurn, Ph.D., and Valina L. Dawson, Ph.D., induced cardiac arrest in both normal mice and in mice specially bred without the PARP gene. After eight minutes, they performed CPR on the mice through an epinephrine injection, chest compressions and oxygen ventilation. Three days later, they studied the amount of cells in the animals' brains, specifically looking at the hippocampus (the area responsible for memory) and the caudoputamen (the area responsible for skeletal muscle activity).
The mice without PARP showed a marked reduction in cell loss an average 28 percent decline compared to the 53 percent drop among normal mice.
"This is the first demonstration that PARP-1 is an important mediator of brain cell death following cardiac arrest and CPR," Traystman says. "We now know that it affects brain injury in several areas during stroke and cardiac arrest."
Scientists may eventually use this information to manipulate genes to alter the course of these conditions, he says.
Abstract #A-759: "Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation: Role of PARP-1"
HOPKINS RESEARCHERS I.D. PROTEIN THAT ENABLES CHRONIC NERVE PAIN
Johns Hopkins researchers have found that a protein called PSD-93 allows nerve pain messages to be sent throughout the body.
The finding, in mice, could help scientists design better pain medications for patients with hyperalgesia, an abnormally increased sensitivity to pain.
Scientists led by Yuan Xiang Tao, M.D., Ph.D., compared a group of normal mice and a group of mice bred specially without PSD-93. They tied off a nerve adjacent to the spinal cord to create a hyperalgesia-like state, then measured the animals' responses to heat and touch at two, four, six, eight, 10, 12 and 14 days after surgery. The mice lacking PSD-93 were significantly more tolerant of both stimuli. The researchers also looked at cells from the animals' spinal cords under the microscope, and observed a high concentration of PSD-93 in the dorsal horn, or back portion a region typically associated with the transport of pain messages to the brain.
The PSD-93 gene codes for a so-called scaffolding protein that helps position receptors on the surface of nerve cells. Scientists think the pain messages get through in spots where PSD-93 binds to the N-methyl-D-aspartate (NMDA) receptor, molecules in the brain's nerve cells associated with learning, memory and higher thought.
"These findings demonstrate for the first time that PSD-93 is essential for nerve injury-induced chronic pain, and provide a new, potential biochemical target for preventing and treating chronic or persistent pain," says Roger A. Johns, M.D., study senior author and chairman of anesthesiology and critical care medicine.
Abstract #A-829: "Reduction of Neuropathic Pain in Mice Lacking PSD-93"
American Society of Anesthesiologists - annual meeting: http://www2.asahq.org/web/index.asp