Abstract
The vascular response to the α-toxin of Clostridium perfringens type A, was observed topographically in the cremaster muscle of the rat, in terms of exudation, labelling of damaged vessels by circulating carbon, and in addition histologically for patency of the vascular plexus.
It was confirmed that the permeability response is biphasic. The short-lived immediate phase corresponds to that of venular labelling, and the delayed phase reaches its peak rather later than the corresponding phase of capillary labelling. The intensity and extent of these responses are determined by the degree of injury, but their shape and timing, especially in the immediate phase, vary almost as consistently with the duration of exposure to circulating dye or carbon.
After the standard dose of toxin, vascular patency is largely unaffected until 24 hours. Apparently irreversible vascular occlusion occurs rather earlier with larger doses. A three-fold reduction of the standard dose proportionately reduces both exudation and capillary labelling but leaves immediate venular labelling unaffected, suggesting that the latter is not dose dependent and therefore non-specific. Prolongation of moderate venular labelling into the middle of the delayed phase may occur at this dosage. Its absence after the standard dose suggests that delayed inhibition of venular reactivity may be occurring.
Irregular labelling of venules and small veins persists throughout the delayed phase with doses 2·4 or more times the standard dose. A brief ultramicroscopic survey revealed appearances in both venules and capillaries at 1-2 hours after injury closely comparable to those which have been described for Cl. oedematiens toxin at 6-24 hours.
In rats given carbon during the delayed phase, the effective vascular patency 10 minutes later includes half of the labelled capillaries up to 10 μm in diameter. This proportion is little affected by toxin dose, but intensely so when the carbon clearance time is increased, suggesting that such injured microvessels may be a major source of plasma protein exudation.
Full text
PDF
Images in this article
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
- COTRAN R. S., MAJNO G. THE DELAYED AND PROLONGED VASCULAR LEAKAGE IN INFLAMMATION. I. TOPOGRAPHY OF THE LEAKING VESSELS AFTER THERMAL INJURY. Am J Pathol. 1964 Aug;45:261–281. [PMC free article] [PubMed] [Google Scholar]
- Dourmashkin R. R., Rosse W. F. Morphologic changes in the membranes of red blood cells undergoing hemolysis. Am J Med. 1966 Nov;41(5):699–710. doi: 10.1016/0002-9343(66)90031-3. [DOI] [PubMed] [Google Scholar]
- Edwards C., Heath D., Harris P. The carotid body in emphysema and left ventricular hypertrophy. J Pathol. 1971 May;104(1):1–13. doi: 10.1002/path.1711040102. [DOI] [PubMed] [Google Scholar]
- Ham K. N., Hurley J. V. Acute inflammation: an electron-microscope study of turpentine-induced pleurisy in the rat. J Pathol Bacteriol. 1965 Oct;90(2):365–377. doi: 10.1002/path.1700900202. [DOI] [PubMed] [Google Scholar]
- Hurley J. V., Ham K. N., Ryan G. B. The mechanism of the delayed prolonged phase of increased vascular permeability in mild thermal injury in the rat. J Pathol Bacteriol. 1967 Jul;94(1):1–12. doi: 10.1002/path.1700940102. [DOI] [PubMed] [Google Scholar]
- MAJNO G., PALADE G. E., SCHOEFL G. I. Studies on inflammation. II. The site of action of histamine and serotonin along the vascular tree: a topographic study. J Biophys Biochem Cytol. 1961 Dec;11:607–626. doi: 10.1083/jcb.11.3.607. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Spector W. G., Walters M. N., Willoughby D. A. Venular and capillary permeability in thermal injury. J Pathol Bacteriol. 1965 Oct;90(2):635–640. doi: 10.1002/path.1700900233. [DOI] [PubMed] [Google Scholar]
- WELLS F. R. An improved intravital dye iron-prussian blue method for the in vitro examination of living lymphatic vessels. Nature. 1962 Jul 14;195:188–189. doi: 10.1038/195188a0. [DOI] [PubMed] [Google Scholar]
- WELLS F. R., MILES A. A. SITE OF THE VASCULAR RESPONSE TO THERMAL INJURY. Nature. 1963 Dec 7;200:1015–1016. doi: 10.1038/2001015a0. [DOI] [PubMed] [Google Scholar]
- Wells F. R. Standardisation of biological ink for the study of vascular injury in inflammation. Experientia. 1972 Mar 15;28(3):371–372. doi: 10.1007/BF01928748. [DOI] [PubMed] [Google Scholar]
- Wells F. R. The site of vascular response to thermal injury in skeletal muscle. Br J Exp Pathol. 1971 Jun;52(3):292–306. [PMC free article] [PubMed] [Google Scholar]
- Wiener J., Lattes R. G., Spiro D. An electron microscopic study of leukocyte emigration and vascular permeability in tuberculin sensitivity. Am J Pathol. 1967 Mar;50(3):485–521. [PMC free article] [PubMed] [Google Scholar]
- Willms-Kretschmer K., Flax M. H., Cotran R. S. The fine structure of the vascular response in hapten-specific delayed hypersensitivity and contact dermatitis. Lab Invest. 1967 Sep;17(3):334–349. [PubMed] [Google Scholar]