ETIOLOGY OF EXPERIMENTAL SHOCK
Abstract
Research on lysosomes in normal and tolerant animals subjected to shock was continued to test the hypothesis that the release by cells of the hydrolases contained in cytoplasmic lysosome granules into the circulation may exacerbate tissue injury and contribute to the irreversible trend during shock. Adaptation or tolerance is associated with a greater stability of lysosome particles even under in vitro conditions. Mitochondrial systems were not similarly stabilized. Agents which predispose to shock (Thorotrast) or which nullify tolerance appear to do so by a direct action of this colloid on the lysosomal membranes of Kupffer cells and other macrophages. The local release of lysosomal enzymes appears also to contribute to the genesis of local tissue injury, since depletion procedures (excess vitamin A) inhibit local inflammatory reactions as well as the local hemorrhagic necrosis induced by combinations of bacterial endotoxins and epinephrine. A new polypeptide, (SVPx, - serum vasoactive peptide unknown), was purified and concentrated from the blood plasma and serum of rabbits and man. In high concentrations the polypeptide is as effective a contracting agent as norepinephrine. In low concentrations the material strongly potentiates the action of constrictors such as norepinephrine.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 10, 1963
- Accession Number
- AD0403891
Entities
People
- A. Janoff
- M. Wursel
- Z. W. Zweifach
Organizations
- New York University