Accession Number : ADA296124

Title :   Effects of Pressure on Intravascular Adhesion Molecules.

Descriptive Note : Final rept. 1 May 89-30 Apr 95,

Corporate Author : MARYLAND UNIV BALTIMORE DEPT OF PATHOLOGY

Personal Author(s) : Marzella, Louis

PDF Url : ADA296124

Report Date : 30 APR 1995

Pagination or Media Count : 9

Abstract : We have developed a rodent model of decompression sickness and have used it to characterize the pathophysiology of cord injury using quantitative histopathology, immunocytochemistry, flow cytometry and hemodynamic measurements. The results of this work indicate that accumulation of nitrogen gas extravascularly or intravascularly does not play a role in the cord injury. The expression of ICAM-l in the endothelium of the cord increases after decompression. However, there is no corresponding increase in surface expression of adhesion counterreceptors on leucocytes. No recruitment of leucocytes to the cord or activation of endogenous effector cells was identified. These results indicate that the cellular inflammatory reaction is not activated and does not contribute to the cord injury induced by decompression sickness. We have also used the rat model to develop a rapid quantitative assay of cord trauma that will be useful for testing pharmacologic interventions designed to decrease the severity of the injury and enhance recovery. (AN)

Descriptors :   *TRAUMA, *DECOMPRESSION SICKNESS, *BLOOD CIRCULATION, *SPINAL CORD, ACTIVATION, QUANTITATIVE ANALYSIS, RATS, MOLECULES, ADHESION, NITROGEN, PRESSURE, WOUNDS AND INJURIES, RESPONSE(BIOLOGY), RODENTS, ACCUMULATION, PATHOPHYSIOLOGY, INFLAMMATION, INTERVENTION, ASSAYING, PHARMACOLOGY, LEUKOCYTES, BLOOD VESSELS, BLOOD COUNTS, HISTOPATHOLOGY, ANATOMICAL MODELS, ELECTROPHYSIOLOGY, ENDOTHELIUM, CYTOCHEMISTRY, IMMUNOCHEMISTRY.

Subject Categories : Medicine and Medical Research
      Stress Physiology

Distribution Statement : APPROVED FOR PUBLIC RELEASE