Summary
Electron microscopic studies have previously shown that histamine-type mediators of vascular leakage induce: (1) the appearance of gaps between venular endothelial cells; and (2) deformation of endothelial nuclei, with multiple deep infoldings. It has been postulated that these changes (and the leakage) are due to contraction of endothelial cells. The present paper has investigated this hypothesis by examining the effects of bradykinin and histamine on living rat mesenteric venules. Within 2–5 minutes after application of the mediator, some endothelial cells began to bulge; obvious bulging lasted for about 5 minutes and then subsided slowly; by 20–30 minutes after application of the mediator, the cells were again flattened. This time-course of bulging and flattening corresponded with the rise and fall in vascular permeability, as shown by carbon labeling. Electron microscopy confirmed the presence of deformed nuclei in such vessels. These observations support the concept that vascular leakage, caused by histamine-type mediators, is dependent upon endothelial contraction.
Article PDF
Similar content being viewed by others
Avoid common mistakes on your manuscript.
References
Becker, C. G., Murphy, G. E.: Demonstration of contractile protein in endothelium and cells of heart valves, endocardium, intima, arteriosclerotic plaques, and Aschoff bodies of rheumatic heart disease. Amer. J. Path.55, 1–37 (1969).
Bloom, S., Cancilla, P.A.: Conformational changes in myocardial nuclei of rats. Circulat. Res.24, 189–196 (1969).
Buckley, I. K., Ryan, G. B.: Increased vascular permeability. The effect of histamine and serotonin on rat mesenteric blood vessels in vivo. Amer. J. Path.55, 329–347 (1969).
Clark, E. R., Clark, E. L.: The relation of “Rouget” cells to capillary contractility. Amer. J. Anat.35, 265–282 (1925).
Clark, E. R., Clark, E. L.: Observations on living preformed blood vessels as seen in a transparent chamber inserted into the rabbit’s ear. Amer. J. Anat.49, 441–477 (1931).
Clark, E. R., Clark, E. L.: Observations on changes in blood vascular endothelium in the living animal. Amer. J. Anat.57, 385–438 (1935).
Fawcett, D. W.: An experimental study of mast cell degranulation and regeneration. Anat. Rec.121, 29–51 (1955).
Hurley, J. V., Edwards, B., Ham, K. N.: The response of newly formed blood vessels in healing wounds to histamine and other permeability factors. Pathology2, 133–145 (1970).
Karnovsky, M. J.: A formaldehyde-glutaraldehyde fixative of high osmolarity for use in electron microscopy. J. Cell Biol.27, 137A-138A (1965).
Krogh, A.: The anatomy and physiology of capillaries. New York: Hafner Publishing Co., Inc. 1959 (Reprinting of “Revised and Enlarged Edition, 1930”).
Lane, B. P.: Alterations in the cytologic detail of intestinal smooth muscle cells in various stages of contraction. J. Cell Biol.27, 199–213 (1965).
Little, R. A.: Changes in the reactivity of the skin blood vessels of the rabbit with age. J. Path.99, 131–138 (1969).
Majno, G.: Mechanisms of abnormal vascular permeability in acute inflammation. In: Injury, inflammation and immunity (ed. L. Thomas, J. W. Uhr and L. Grant), p. 58–93. Baltimore: Williams & Wilkins, Co. 1964.
Majno, G., Gilmore, V., Leventhal, M.: On the mechanism of vascular leakage caused by histamine-type mediators. A microscopic study in vivo. Circulat. Res.21, 833–847 (1967).
Majno, G., Palade, G. E.: Studies on inflammation. I. The effect of histamine and serotonin on vascular permeability: an electron microscopic study. J. biophys. biochem. Cytol.11, 571–605 (1961).
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.11, 607–626 (1961).
Majno, G., Shea, S. M., Leventhal, M.: Endothelial contraction induced by histamine-type mediators. An electron microscopic study. J. Cell Biol.42, 647–672 (1969).
McCuskey, R. S.: A dynamic and static study of hepatic arterioles and hepatic sphincters. Amer. J. Anat.119, 455–478 (1966).
McCuskey, R. S., Chapman, T. M.: Microscopy of the living pancreas in situ. Amer. J. Anat.126, 395–408 (1969).
Reynolds, E. S.: The use of lead citrate at high pH as an electron-opaque stain in electron microscopy. J. Cell Biol.17, 208–212 (1963).
Rowley, D. A.: Venous constriction as the cause of increased vascular permeability produced by 5-hydroxytryptamine, histamine, bradykinin and 48/80 in the rat. Brit. J. exp. Path.45, 56–67 (1964).
Sanders, A. G., Ebert, R. H., Florey, H. W.: The mechanism of capillary contraction. Quart. J. exp. Physiol.30, 281–287 (1940).
Sandison, J. C.: Contraction of blood vessels and observations on the circulation in the transparent chamber in the rabbit’s ear. Anat. Rec.54, 105–127 (1932).
Stromberg, D.D., Phelps, P.C., Rushmer, R. F., Luft, J. H.: An index for quantitative measurement of vasoconstriction in histologic sections of blood vessels. Vasc. Surg.3, 68–80 (1969).
Wilhelm, D. L.: Increased vascular permeability in acute inflammation. Rev. canad. Biol.30, 153–172 (1971).
Zweifach, B.W.: A micro-manipulative study of blood capillaries. Anat. Rec.59, 83–108 (1934).
Zweifach, B. W.: General principles governing the behavior of the microcirculation. Amer. J. Med.23, 684–696 (1957).
Zweifach, B. W.: Functional behavior of the microcirculation. Springfield: Charles C. Thomas. 1961a.
Zweifach, B. W.: Biologic properties of vascular endothelium. Angiology12, 507–510 (1961b).
Author information
Authors and Affiliations
Additional information
This work was submitted by Miss Joris in partial fulfillment of the requirements for a Doctorate in Medical Biology, University of Geneva.
Rights and permissions
About this article
Cite this article
Joris, I., Majno, G. & Ryan, G.B. Endothelial contractionin vivo : A study of the rat mesentery. Virchows Arch. Abt. B Zellpath. 12, 73–83 (1972). https://doi.org/10.1007/BF02893987
Received:
Issue Date:
DOI: https://doi.org/10.1007/BF02893987