Liberation of histamine and serotonin and vascular permeability in an acute aseptic inflammatory focus

Lipshits, R. U.; Klimenko, N. A.

doi:10.1007/bf00804808

Cited by 3 publications

(4 citation statements)

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“…Biologically active agents like histamine, serotonin, heparin, bradikinine, and others are migrating into intracellular spaces during mast cells degranulation [106,107]. Mast cells degranulation evokes local immediate hyperergic reaction [108,109].…”

Section: Methodsmentioning

confidence: 99%

Aetiology and Pathogenesis of Trigeminal Neuralgia: a Comprehensive Review

Sabalys¹,

Juodžbalys²,

Wang

2012

JOMR

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ObjectivesThe aim of present paper was to discuss issues related to trigeminal neuralgia with strong emphasis on the aetiology and pathogenesis of this problem.Material and MethodsAn electronic search of 5 databases (1965 - Oct 2012) and a hand search of peer-reviewed journals for relevant articles were performed. In addition, experience acquired from treating 3263 patients in the Department of Maxillofacial Surgery, Lithuanian University of Health Sciences, were also summarized.ResultsGenerally, aetiological factors can be classified into 3 most popular theories that were based on: 1) Related to other disease, 2) Direct injury to the trigeminal nerve, and 3) Propagates the polyetiologic origin of the disease. In addition, two pathogenesis mechanisms of trigeminal neuralgia were proposed. First: the peripheral pathogenetic mechanism that is often induced by progressive dystrophy around the peripheral branches of the trigeminal nerve. Second, central pathogenetic mechanism which often triggered by peripheral pathogen that causes long-lasting afferent impulsation and the formation of a stable pathologic paroxysmal type irritation focus on the central nerve system (CNS).ConclusionsPatients with susceptive trigeminal neuralgia should be examined carefully by specialists who have expertise in assessing and diagnosing of possible pathological processes and be able to eliminate the contributing factors so the trigeminal neuralgia can be properly managed.

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Section: Methodsmentioning

confidence: 99%

Aetiology and Pathogenesis of Trigeminal Neuralgia: a Comprehensive Review

Sabalys¹,

Juodžbalys²,

Wang

2012

JOMR

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“…At present, mast ceils (MC) are considered to be the source of the main transmitters of initial vascular and exudative processes, in particular the immediate phase of the increase of vascular permeability [8,9] underlying exudation. Recently, a modulatory effect of MC on infdtration processes during inflammation has been shown and mechanisms of this effect dependent on the main products of MC, histamine, serotonin, and heparin, have been studied [6,7].…”

Section: Abstract: Inflammation; Mast Cells; Repairmentioning

confidence: 99%

“…The isotopes were injected intramuscularly (37 MBq/kg body weight in 0.5 ml isotonic NaC1 solution) in the hind paw 1, 2, and 3 hours before decapitation [3,4]. MC were removed from the peritoneal cavity by injecting 10 ml/100 g body weight distilled water 10 days before peritonitis was induced [5,8,9].…”

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confidence: 99%

Role of mast cells in reparative processes in inflammation

Klimenko¹,

Татарко²

1995

Bull Exp Biol Med

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Using the model of acute infectious peritonitis in rats, it is shown that inflammation induced in the absence of mast cells is characterized by marked inhibition of reparative processes. The most significant accumulation of functionally active fibroblasts and the development of granulations and young connective tissue in the mesentery occur 5-10 days after flogogen injection in the natural development of inflammation and after 10-20 days in the absence of mast cells. The data suggest that under natural conditions mast cells directly or indirectly stimulate reparative processes. Key Words: inflammation; mast cells; repairAt present, mast ceils (MC) are considered to be the source of the main transmitters of initial vascular and exudative processes, in particular the immediate phase of the increase of vascular permeability [8,9] underlying exudation. Recently, a modulatory effect of MC on infdtration processes during inflammation has been shown and mechanisms of this effect dependent on the main products of MC, histamine, serotonin, and heparin, have been studied [6,7].The aim of the present study was to investigate the role of MC in reparative processes during inflammation. MATERIALS AND METHODSThe experiments were performed on 396 male Wistar rats weighing 180-200 g. Acute infectious peritonitis was induced by intraperitoneal injection of 2x109 cells (0.5 LDs0 ) of a one-day-old E. coli culture, isolated from a patient with peritonitis, in 1 ml isotonic NaC1 [5,7,8]

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“…Conditioned media were obtained by culturing adherent or nonadherent myelokaryocytes (2 x 106 cells/ml) in complete RPMI-1640 medium supplemented with 10% fetal bovine serum for 24 h in the presence of 10 gg/ml lipopolysaccharide from E. coli serotype 01 l l:B4 (Sigma) or 5 gg/ml concanavalin A (ConA, Sigma). Mast cells were eliminated by intraperitoneal injection of 1.8-2 ml distilled water 10 days before peritonitis [7,11]. …”

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confidence: 99%

Role of mast cells in regulation of erythropoiesis during inflammation

et al. 1997

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Using the mouse model of acute infectious peritonitis caused by Escherichia coli, we have shown that preliminary osmotic elimination of peritoneal mast cells markedly affects the erythron reaction and its mechanisms during inflammation. Activation of local regulatory mechanisms of erythropoiesis (hemopoiesis-inducing microenvironment) and less pronounced hyperplasia of the erythron in the bone marrow were noted. Key Words: inflammation; erythropoiesis; mast cellsOur previous studies show that must cells modulate the intensity of granulomonocytopoiesis during inflammation [4]. It was also shown that inflammation characterized by marked stimulation of erythropoiesis and on days 6-9 of inflammation by hyperplasia of erythron in_ the bone marrow due to activation of proliferation and differentiation of committed erythropoiesis precursors, hemopoiesis-inducing microenvironment (HIM) of the bone marrow, and the erythropoietin system [2].The aim of the present study was to evaluate the role of mast ceils in the regulation of erythropoiesis in inflammation. MATERIALS AND METHODSExperiments were carried out on 204 male CBA mice weighing 18-20 g. The model of inflammation was infectious peritonitis caused by Escherichia coli strain ATCC 25922 inoculated intraperitoneally in 0.3 ml isotonic NaC1 solution in a dose of 0.5 LDs0 [4]. The mice were decapitated at various times of the inInstitute of Pharmacology, Tomsk Research Center, Russian Academy of Medical Sciences; *State Medical University, Kharkov flammatory process, and the total number of myelokaryocytes per femur and myelogram were counted. In the bone marrow, committed erythropoietic precursors, erythroid colony-forming units (CFU-E) [10], and hemopoietic islets [1,9] were counted, and erythropoietic activity of blood serum and conditioned media of adherent and nonadherent bone marrow cells was determined [12]. Conditioned media were obtained by culturing adherent or nonadherent myelokaryocytes (2 x 106 cells/ml) in complete RPMI-1640 medium supplemented with 10% fetal bovine serum for 24 h in the presence of 10 gg/ml lipopolysaccharide from E. coli serotype 01 l l:B4 (Sigma) or 5 gg/ml concanavalin A (ConA, Sigma). Mast cells were eliminated by intraperitoneal injection of 1.8-2 ml distilled water 10 days before peritonitis [7,11]. RESULTSNatural inflammation was characterized by a shortterm rise of erythroid elements in the bone marrow by hour 12 and hyperplasia of the erythron on days 6-9. In the absence of mast cells, the number of erythrokaryocytes rose considerably on day 1 (Fig. 1, a), i.e., erythron hyperplasia practically did not develop.

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Liberation of histamine and serotonin and vascular permeability in an acute aseptic inflammatory focus

Cited by 3 publications

References 5 publications

Aetiology and Pathogenesis of Trigeminal Neuralgia: a Comprehensive Review

Aetiology and Pathogenesis of Trigeminal Neuralgia: a Comprehensive Review

Role of mast cells in reparative processes in inflammation

Role of mast cells in regulation of erythropoiesis during inflammation

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