Intra-arterial injections of histamine, serotonin, or bradykinin: a topographic study of vascular leakage.
01 Nov 1970-Experimental Biology and Medicine (SAGE PublicationsSage UK: London, England)-Vol. 135, Iss: 2, pp 447-452
TL;DR: In certain organs (brain, cerebellum, testis, Gasserian ganglion) histamine-type mediators are apparently unable to cause vascular leakage, suggesting that the selective response of the venules depends on an intrinsic property of the Venular wall, and not on the route whereby the mediator reaches the vessel.
Abstract: SummaryHistamine, serotonin, and bradykinin, injected intra-arterially, cause (in susceptible organs) vascular leakage predominantly from the venules. The vascular segments affected are the same as when the mediators are injected locally. This suggests that the selective response of the venules depends on an intrinsic property of the venular wall, and not on the route whereby the mediator reaches the vessel. In certain organs (brain, cerebellum, testis, Gasserian ganglion) histamine-type mediators are apparently unable to cause vascular leakage.
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TL;DR: Among those peptides contained in perivascular afferent fibers and administered intravenously, substance P and neurokinin A (NKA), but not calcitonin gene-related peptide, caused a dose-dependent extravasation in the dura and conjunctiva of rats.
Abstract: Utilizing 125I-BSA administered intravenously, a simple, reliable, and sensitive method was established for the detection of plasma protein extravasation in the dura of rats and guinea pigs following chemical, electrical, or immunological stimulation. Extravasated 125I-BSA or Evans blue was noted in the dura and conjunctiva but not in the temporalis muscle of saline-perfused rats following intravenous capsaicin, 1 mumol/kg. Capsaicin-induced extravasation was mediated by unmyelinated and small myelinated fibers since leakage did not develop in adult animals in whom these fibers were destroyed by capsaicin pretreatment (50 mg/kg) as neonates. An ipsilateral increase in Evans blue and 125I-BSA was found in the dura, eyelids, lips and gingival mucosa, and snout following electrical stimulation of the rat trigeminal ganglion. This increase was also C-fiber dependent. Among those peptides contained in perivascular afferent fibers and administered intravenously, substance P (SP) and neurokinin A (NKA), but not calcitonin gene-related peptide, caused a dose-dependent extravasation in the dura and conjunctiva of rats. Neonatal capsaicin pretreatment did not attenuate SP- nor NKA-induced effects in the dura and actually increased extravasation in the conjunctiva. Intravenous administration of 5-HT or bradykinin to normal adult rats or adult rats pretreated as neonates with capsaicin increased levels of 125I-BSA in both the dura and the conjunctiva. Histamine and prostaglandin E2, on the other hand, caused protein leakage in the conjunctiva but not in the dura of rats; however, histamine did induce extravasation in the dura of guinea pigs.(ABSTRACT TRUNCATED AT 250 WORDS)
431 citations
Cites background from "Intra-arterial injections of histam..."
...Non-neurogenic plasma extravasation can be induced by the intravenous administration of substances such as 5-HT, histamine, and bradykinin (BK) (Gabbiani et al., 1970; Saria et al., 1983), which directly alter blood vessel permeability....
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...Similar mechanisms may take place in the dura since venules are the site of leakage in this tissue as well (Gabbiani et al., 1970)....
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TL;DR: Several substances including anaphylaxis induce protein leakage in many tissues with differing selective distribution patterns as well as SP, a likely mediator of neurogenic protein leaking in many organs.
Abstract: Plasma extravasation was induced in rats or guinea-pigs by intravenous injections of (1) substance P (SP), (2) the C-terminal SP-hexapeptide SP(6--11), (3) serotonin (5-HT), (4) histamine, (5) bradykinin, (6) capsaicin and (7) by antigen challenge. Plasma extravasation induced by SP, SP(6--11), by 5-HT and by capsaicin was, with few exceptions, observed in the same tissues. The effect of SP was not blocked by H1 and H2 histamine receptor antagonists. The effect of i.v. capsaicin was absent in capsaicin desensitized animals. Plasma extravasation upon i.v. SP, SP(6--11), 5-HT and capsaicin was seen in the skin and in all organs containing mucous membranes except the intestinal mucosa. Plasma extravasation by histamine, bradykinin, and antigen challenge of sensitized guinea-pig was, in addition, also observed in the stomach and intestine. Plasma extravasation and bronchoconstriction by antigen challenge with 20 micrograms/kg ovalbumin was completely blocked by combined H1 and H2 histamine receptor blockade. Both responses were reduced to about the half capsaicin desensitized guinea-pigs, although the reduction of the permeability response was statistically not significant in all organs. In conclusion, several substances including anaphylaxis induce protein leakage in many tissues with differing selective distribution patterns. Anaphylactic histamine release leads to protein leakage partly via activation of sensory neurons. SP is a likely mediator of neurogenic protein leakage in many organs.
414 citations
Cites background from "Intra-arterial injections of histam..."
...It is unlikely that the route of administrat ion is responsible for the absence of protein leakage since also intra-arterial administrat ion of histamine failed to increase vascular permeabil i ty in the CNS (Gabbiani et al. 1970)....
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...1982), bradykinin (see Regoli and Barab6 1980), serotonin (5-HT) (Gabbiani et al. 1970), and leukotrienes (see Bach 1982)....
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TL;DR: The characteristics and mechanisms enabling the blood-brain barrier (BBB) to maintain the milieu of the brain and provide an optimally controlled exchange between blood and brain are reviewed in detail.
Abstract: The characteristics and mechanisms enabling the blood-brain barrier (BBB) to maintain the milieu of the brain have been reviewed in detail elsewhere (Banks and Kastin, 1987; Bradbury, 1985; Crone, 1986a, 1987; Cornford, 1985; Davson, 1976; Er misch et aI. , 1985; Fenstermacher, 1985; Gjedde, 1983; Goldstein and Betz, 1986; Meisenberg and Simmons, 1983; Oldendorf, 1974; Pardridge, 1983; Rapoport, 1976a; Rapoport and Robinson, 1986). Before discussing the possible role of mediators in BBB opening some pertinent aspects of the BBB will be discussed briefly. The morphological substrate of the BBB in cere bral vessels is the continuous layer of endothelial cells with tight junctions and no or minimal vesic ular transport. The functional characteristics of BBB are the same as of "tight epithelium" such as (a) low diffusional permeability for water-soluble compounds, (b) low hydraulic conductivity, (c) high reflection coefficient, and (d) high electrical resis tance. All these parameters are indicative of low diffusional exchange of water-soluble solutes. As well as by the restricted diffusion the penetration of several mediators is also inhibited by an enzymatic degradation at the endothelial border. Although li pophilic compounds can easily cross the BBB by simple diffusion, the trans cellular transport of hy drophilic solutes is made possible by facilitated dif fusion and active transport. All these mechanisms permit a highly selective exchange between blood and brain and provide an optimally controlled ho-
293 citations
TL;DR: Neurogenic inflammation in the trachea and bronchi of rats is characterized by increased permeability of postcapillary venules and collecting venules in specific regions of the respiratory mucosa as well as adherence of leucocytes, erythrocytes and platelets to the endothelium of these venule and prominent changes in the respiratory epithelium.
Abstract: This study was done to characterize the morphological changes in the respiratory mucosa that occur in neurogenic inflammation, which is a type of inflammation mediated by substances released from sensory nerves. Neurogenic inflammation was produced in the trachea and bronchi of atropine-treated Long-Evans rats by electrically stimulating the left or right superior laryngeal and vagus nerves. This procedure is known to increase vascular permeability in the airways, presumably as a consequence of antidromic activation of sensory vagal axons (Lundberg & Saria, 1982). By using a particulate tracer (Monastral blue, 30 mg kg-1 i.v.) that does not cross the walls of normal tracheal blood vessels but does cross the endothelium of abnormally permeable vessels, it was possible to identify which blood vessels were affected in neurogenic inflammation. Light and electron microscopic examination of tracheas prepared after 2 or 5 min of vagal stimulation revealed that postcapillary venules and collecting venules 7-80 micron in diameter were labelled by extravasated Monastral blue but capillaries, arterioles, and larger venules were not. Venules from which the extravasation occurred had gaps as wide as 1.5 micron between endothelial cells. Most of the abnormally permeable venules were located just beneath the airway epithelium in regions between the cartilaginous rings. Extravasation also occurred from venules in the mucosa overlying the posterior membrane of the extrathoracic trachea, but little occurred in the posterior membrane of the intrathoracic trachea. After unilateral vagal stimulation, vascular permeability was increased on both sides of the trachea; it was also increased in first through fourth order bronchi but only on the side of stimulation. Leucocytes (principally monocytes and neutrophils) were adherent to the endothelium of some of the abnormally permeable venules. Erythrocytes and platelets also were adherent to the walls of some venules. These changes in venules were accompanied by a degranulation of epithelial secretory cells, widening of the spaces between tracheal epithelial cells, and probably an increase in epithelial permeability. Neurogenic inflammation in the trachea and bronchi of rats is thus characterized by increased permeability of postcapillary venules and collecting venules in specific regions of the respiratory mucosa as well as adherence of leucocytes, erythrocytes and platelets to the endothelium of these venules and prominent changes in the respiratory epithelium.
178 citations
TL;DR: It is demonstrated that neurogenic inflammation develops within the dura mater in the rat and that ergot alkaloids prevent the process by a C-fiber-dependent mechanism.
Abstract: C-fiber-dependent neurogenic plasma extravasation developed in the dura mater but not the brain after electric stimulation of the rat trigeminal ganglion or after chemical stimulation of perivascular axons with intravenous capsaicin, a drug that depolarizes sensory nerve fibers. C-fiber-independent extravasation also developed in this tissue after intravenous injections of substance P or neurokinin A (two constituents of unmyelinated C fibers) and after serotonin, bradykinin, or allergic challenge in presensitized animals. Intravenous dihydroergotamine or ergotamine tartrate, in doses similar to those used to treat migraine and cluster headache, prevented the stimulation-induced leakage of plasma proteins within the dura mater. Not unexpectedly, the acute administration of methysergide, a drug effective in the prophylactic treatment of headache, was inactive in this acute model. Neither acute nor chronic administration of propranolol affected stimulation-induced leakage of plasma protein. These results demonstrate that neurogenic inflammation develops within the dura mater in the rat and that ergot alkaloids prevent the process by a C-fiber-dependent mechanism.
163 citations
Cites result from "Intra-arterial injections of histam..."
...The non-neurogenic extravasation induced by the injection of 5HT or BK is probably the result of a direct chemical effect on the endothelium of dural postcapillary venules and is in keeping with the findings from most vascular beds (23-25)....
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References
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TL;DR: Publisher Summary Mast cells are present wherever there is a connective tissue and are large mesenchymal cells containing granules and a substance with mucopolysaccharide characters in their cytoplasm.
Abstract: Publisher Summary Mast cells are present wherever there is a connective tissue. They are large mesenchymal cells containing granules and a substance with mucopolysaccharide characters in their cytoplasm. They are—like the fibroblasts and histiocytes—integral individuals of the cell population in normal connective tissue. The term “mast cell” was coined by Ehrlich and means an overnourished cell. Owing to common tinctorial properties (metachromatic staining of the granules with toluidine blue and other basic dyes), the basophile leukocytes of the blood are interpreted as “blood mast cells.” The basophile leukocytes may migrate into the tissues. The nucleus of the blood cells, however, is usually segmented, unlike that of the tissue mast cells. Apart from the metachromatic staining of the granules, the two cells have nothing in common, and a large number of workers repudiate the view that the two should represent the same type of cell. Mitotic figures are rarely seen in the mast cells of an adult organism. Pappenheim regarded the mast cell as a degenerating cell.
89 citations