ENDOGENEOUS MECHANISM OF VASCULAR RESPONSE IN INFLAMMATION, WITH SPECIAL REFERENCE TO BIOLOGIC SIGNIFICANCE OF SPECIFIC PERMEABILITY FACTORS AND THEIR INHIBITORS NEWLY ISOLATED FROM INFLAMED SITES.
Rept. no. 4 (Final) Jun 67-Jun 68,
KUMAMOTO UNIV (JAPAN) DEPT OF PATHOLOGY (1ST)
Pagination or Media Count:
The permeability changes in cutaneous Arthus reactions are diphasic the early transient response occurs at the site of the venules and is mediated by histamine, while the delayed and prolonged response also occurs at the site of the venules but is caused by the Arthus permeability factor. The factor, locally isolated, is a complex of three peptides factors I, II and III with prolonged permeability effects. The factor induces characteristic vascular labeling with intravenous carbon which includes that of intramural and extravascular types. None of previously described permeability factors is long-acting and induces the extravascular type labeling. The vascular permeability changes after thermal injury are essentially similar to those in cutaneous Arthus reactions. The early transient response is also provoked by histamine at the site of the venules. The delayed and prolonged response is associated with the burns permeability factor locally isolated. The factor is quite similar to Arthus permeability factor and made up of three peptides with prolonged permeability effects. These peptides affect the venules and induce the carbon deposition of intramural and extravascular types. The carbon deposition in the capillaries after thermal injury is not a true index of vascular permeability, because the carbon deposition occurs in the form of thrombus-like carbon masses freely floating in the lumina of the capillaries. Such feature of carbon deposition in the capillaries seems to be related with a direct action of heat. Author
- Medicine and Medical Research