Ed W. Childs, M.D.
Associate Professor
Department of Surgery
Education
- B.A., Molecular and Cellular Biology, University of Texas, Dallas
- M.D., Texas A&M University Health Science Center
- Residency: Surgery, University of Kansas Medical Center
- Fellowship: Trauma/Critical Care, University of California, Davis
Phone: 254-724-5638
E-mail: ewchilds@medicine.tamu.edu
Smalley, D.M., Wood, J.G., Childs, E.W., Frank, L.L., Cheung, L.Y.: Platelet Activating Facotr (PAF) Increases Leukocyte Adhesion But Does Not Alter Vessel Diameter in the Rat Mesenteric Microcirculation. Microvascular Research 56(3): 271-276, 1998.
Childs, E.W., Wood, J.G., Smalley, D.M., Hunter, F.A., Cheung L.Y.: Leukocyte Adherence and Sequestration Following Hemorrhagic Shock and Total Ischemia in Rats. Shock 11(4): 245-252, 1999.
Childs, E.W., Smalley, D., Moncure, M., Miller, J., Cheung, L.Y.: Effect of Monoclonal Antibody LFA-1 on Leukocyte Adherence Following Hemorrhagic Shock in Rats. Shock 14(1): 49-53, 2000.
Smalley, D., Childs, E.W., Cheung, L.Y.: Mechanisms of Leukocyte Adherence to Small Bowel Mesenteric Venules Following Intra-abdominal Contamination. Inflammatory 24(5): 399-409, 2000.
Childs, E.W., Smalley, D., Moncure, M., Miller, J., Cheung, L.Y.: Effects of PAF Antagonist (WEB-2086) on Leukocyte Adherence Following Hemorrhagic Shock in Rats. Journal of Trauma 49(6): 1102-1107, 2000.
The major objective of my research interest is to further elucidate the mechanisms of microvascular injury following hemorrhagic shock with emphasis on the role of leukocyte activation and reactive oxygen species (ROS) generation. Previous studies have shown that during reperfusion and after hemorrhagic shock and resuscitation circulating leukocytes become activated resulting in enhanced leukocyte-endothelial cell adhesive interactions. The activation of these leukocytes may be a result of ROS generation; however, if unabated, this proces will eventually lead to active leukocytes emigrating into the extravascular space with elaboration of cytokines leading to microvascular damage. Although major advances have been made in our understanding of the events responsible for microvascular injury in this setting, this knowledge has not yet led to significant improvement in clinical treatment.
Numerous studies have demonstrated that generation of ROS is an initiating event in pathogenesis of microvascular injury. The majority of these studies have involved pretreatment with antioxidants prior to hemorrhagic shock rather than their administration following shock. In fact, conflicting results have been reported regarding the efficacy of antioxidants given after hemorrhagic shock. These conflicting results have generally been interpreted as showing that ROS generation is a transient phenomenon, which peaks early upon resuscitation, and then rapidly ends. According to this view, ROS generation is simply a process that promotes microvascular injury. For example, ROS may cause damage to cell membranes, resulting in generation of lipid inflammatory molecules such as platelet activating factor (PAF) and leukotriene B4 (LTB4). This mediator is an extremely potent chemotactic agent and can cause circulating leukocytes to adhere to the microcirculation and increase vascular permeability. Recently, a new concept has emerged suggesting that ROS may also play an important role in cell signaling. For example, ROS have been shown to trigger expression of vascular endothelial growth factor (VEGF), which is known to attenuate microvascular injury in various situations. Based on these recent reports, we postulate tht ROS generation may have dual effects on the microcirculation following hemorrhagic shock: initially ROS lead to injury (as through the actions of PAF and LTB4), while at later times ROS signal compensatory changes to attenuate the degree of injury (such as VEGF expression).
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