Mechanism of Cutaneous Vesication
Abstract
This project investigated the mechanism of bis (2-chloroethyl) sulfide (sulfur mustard, HD)-induced cutaneous vesication using the isolated perfused porcine skin flap (IPPSF) and in vitro cell cultures. Treatment of IPPSFs with 5.0 mg/ml of HD results in a characteristic increase in vascular resistance, decrease in glucose utilization, and the formation of gross and microblisters. The first study demonstrated that the vascular changes associated with HD vesication are accompanied by increases in the efflux of prostaglandins E2 and F2. Assessment of extracellular and intravascular space using radiolabeled inulin and albumin infusions, respectively, demonstrated that HD primarily produced an increase in intravascular space. Thus these studies unequivocally demonstrate a vascular component to HD vesication directly mediated by cutaneous elements, since the IPPSF is an isolated system not associated with a systemic immune response. A second study probed the molecular basis of HD interaction with laminin, a basement membrane component previously implicated by our group to be primarily involved in HD-induced epidermal-dermal separation. HD directly alkylated laminin and reduced its cell adhesive activity through a noncytotoxic mechanism.
Document Details
- Document Type
- Technical Report
- Publication Date
- Feb 17, 1994
- Accession Number
- ADA283085
Entities
People
- Alfred O. Inman
- Jason Z Zhang
- Jim D. Brooks
- Jim E. Riviere
- Nancy A. Monteiro-riviere
Organizations
- North Carolina State University