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Possible cause and treatment for shock uncovered by UC San Diego bioengineers

Researchers prevented shock and multiple organ failure in experimental animals by blocking powerful pancreatic digestive enzymes in the intestine, according to studies by bioengineers with the Jacobs School of Engineering at the University of California, San Diego. This fundamental breakthrough could lead to therapies to prevent and treat ischemic shock in people who experience shock following blood loss from traumatic injury or high-risk surgery. The work also provides clues into the cellular mechanisms that lead to shock.

The research report titled "Generation of In Vivo Activating Factors in the Ischemic Intestine by Pancreatic Enzymes" will be published in the Proceedings of the National Academy of Sciences on February 15. The principal investigator of the study is Geert Schmid-Schoenbein, professor of bioengineering at the Jacobs School of Engineering, and the work was funded by the National Heart, Lung, and Blood Institute. The research was conducted with Hiroshi Mitsuoka and Erik Kistler in Schmid-Schoenbein's Microcirculation Research Laboratory.

Ischemic shock occurs when blood pressure falls after blood loss or deep anesthesia. Vital organs are poorly perfused and literally starved of oxygen. Early symptoms include cold, clammy skin, mental confusion and inadequate production of urine. But shock can quickly lead to multiple organ failure and even death.

These symptoms are induced when activators in the blood stream turn on various cardiovascular cells including leukocytes (white blood cells) and endothelial cells (blood vessel walls). Abnormal interactions between leukocytes and endothelial cells produce inflammation, alter blood flow, and finally cut off delivery of oxygen to the organs.

But never before have researchers found strong evidence for the source of the cell activators. "The pancreas produces potent enzymes that can dige
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Contact: Denine Hagen
dhagen@ucsd.edu
858-534-2920
University of California - San Diego
13-Feb-2000


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