Neural Control of Hemorrhage-Induced Tissue Cytokine Production
Abstract
Studies performed under this grant provided evidence that tissue injury and hypoperfusion activate systemic and central neural, hormonal and opiate mechanisms that regulate the hemodynamic, metabolic and proinflammatory counter regulatory responses involved in restoring homeostasis following trauma/hemorrhage. Opiate pathway activation favors hemodynamic instability and a pro-inflammatory tissue response while sympathetic nervous system activation counteracts the inflammatory response and contributes to cardiovascular responsiveness. Our studies demonstrated that the intact neuroendocrine response is critical to ensure survival and host defense mechanisms from secondary infectious challenges. Furthermore, stress-and analgesia-induced disruptions in response exacerbate hemodynamic instability, compromise tissue perfusion and predispose to tissue injury and impaired innate host-defense response to a subsequent challenge.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 31, 2007
- Accession Number
- ADA465168
Entities
People
- Patrica E. Molina
Organizations
- LSU Health Sciences Center New Orleans