title: Vascular and cellular responses to pro-inflammatory stimuli in rat dental pulp.
abstract: Dental pulp reactivity to various pro-inflammatory stimuli was independently evaluated in rats in terms of a vascular permeability increase and leukocyte recruitment. Substance P, calcitonin-gene related peptide (CGRP) and prostaglandin E(2) (in the picomol range) were applied to the exposed pulp from anesthetised animals and the plasma extravasation measured by the Evans blue content in the tissue following 10 min of administration. Leukocyte recruitment was evaluated morphometrically by counting the cell number present in serial sections of 1:3 4 microm pulp tissue 6 h after bacterial endotoxin (LPS; 0.06-1.2 microg/site) administration. Increase in pulp vascular permeability and cellular recruitment due to the injection of mentioned mediators in the skin or LPS in the peritoneal cavity were used as positive controls. Increase in vascular permeability in the pulp occurred in the same dose-range as observed in the skin, being CGRP the most active substance in both cases. However, it was necessary a higher dose of LPS (1.2 microg) to induce a similar cell recruitment in the pulp as that observed in the rat peritoneal cavity (0.3 microg). These data indicate that dental pulp reactivity presents the same pattern of increase in vascular permeability to other tissues in the rat, being CGRP the most potent mediator in this respect. In addition, they suggest the presence of CGRP receptors in the dental pulp. However, an adequate leukocyte recruitment response to bacterial endotoxin was not mounted, suggesting a deficiency in adhesion molecules in blood vessels in the rat dental pulp.
authors.affiliation: Departamento de Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, Brazil.
authors.forename: Kátia L M
authors.initials: KL
authors.lastname: Maltos
authors.forename: Gustavo B
authors.initials: GB
authors.lastname: Menezes
authors.forename: Marcelo V
authors.initials: MV
authors.lastname: Caliari
authors.forename: Orivaldo A
authors.initials: OA
authors.lastname: Rocha
authors.forename: Júlia M M
authors.initials: JM
authors.lastname: Santos
authors.forename: Dalton L F
authors.initials: DL
authors.lastname: Alves
authors.forename: Igor D G
authors.initials: ID
authors.lastname: Duarte
authors.forename: Janetti N
authors.initials: JN
authors.lastname: Francischi
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology*; D002199:Capillary Permeability / Q000187:drug effects*; D000068579:Celecoxib; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003782:Dental Pulp / Q000098:blood supply / Q000187:drug effects* / Q000473:pathology; D003907:Dexamethasone / Q000494:pharmacology; D015232:Dinoprostone / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D007962:Leukocytes / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D011671:Pulpitis / Q000473:pathology*; D011720:Pyrazoles; D051381:Rats; D012867:Skin / Q000098:blood supply; D013373:Substance P / Q000494:pharmacology*; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D016861:Cyclooxygenase Inhibitors; D008070:Lipopolysaccharides; D011720:Pyrazoles; D013449:Sulfonamides; D013373:Substance P; D003907:Dexamethasone; D000068579:Celecoxib; D015740:Calcitonin Gene-Related Peptide; D015232:Dinoprostone