Eucalyptol, also known as 1,8-cineole, is a monoterpene traditionally used to treat respiratory disorders due to its secretolytic properties. In addition to its myorelaxant effects, it also has anti-inflammatory actions in vitro. In this study, we aimed to evaluate the efficacy of acute treatment with 1,8-cineole on reducing airway inflammatory parameters. Ovalbumin (OVA)-sensitized guinea pigs were submitted to antigenic challenge (OVA) with or without pre-treatment with a single dose of 1,8-cineole administered by inhalation. Airway inflammatory parameters were reduced or absent in 1,8-cineole-treated animals as compared with untreated guinea pigs. Acute treatment with 1,8-cineole impaired the development of airway hyperresponsiveness to carbachol in isolated tracheal rings. Levels of the pro-inflammatory cytokines TNFa and IL-1b was lower in bronchoalveolar lavage fluid (BALF) of 1,8-cineol-treated guinea pigs than in untreated animals. 1,8-Cineole impaired the OVA-induced increase of the myeloperoxidase activity in BALF. 1,8-Cineole also prevented the reduction of the mucociliary clearance induced by the antigen presentation. The present investigation provides evidence that inhaled 1,8-cineole prevents hyperresponsiveness and inhibits inflammation in airways of ovalbumin-challenged guinea pigs.
The antinociceptive and antispasmodic properties of the essential oil of OCIMUM micranthum (EOOM) were characterized. In mice, EOOM (15-100 mg · kg (-1), p. o.) reduced both the writhing responses induced by acetic acid and the licking-time induced by formalin, being inert on the hot plate test. In rat trachea, EOOM relaxed sustained contractions induced by KCl or carbachol (CCh). Its constituents, ( E)- [( E)-MC] and ( Z)-methyl cinnamate [( Z)-MC], reproduced several effects of EOOM. Inhaled as aerosol, EOOM prevented tracheal hyperresponsiveness to KCl or CCh in ovalbumin-sensitized animals after antigen challenge. Thus, EOOM exerts peripheral analgesia in nociception of inflammatory origin and has antispasmodic actions on rat airways under an inflammatory environment. Its effects are mainly due to ( E)-MC, which makes this substance potentially interesting for studies involving conjunctly smooth muscle cells, nociception, and inflammation. Other EOOM constituents also appear to be involved in its pharmacological actions.
1. 1,8-Cineole is a terpenoid constituent of essential oils with anti-inflammatory properties. It reduces the neural excitability, functions as an antinociceptive agent and has myorelaxant actions in guinea-pig airways. The aim of the present study was to investigate the mechanism underlying the myorelaxant effects of 1,8-cineole in guinea-pig isolated trachea from either naïve guinea-pigs or ovalbumin (OVA)-sensitized animals subjected to antigenic challenge. 2. Isometric recordings were made of the tone of isolated tracheal rings. Rings with an intact epithelium relaxed beyond basal tone in the presence of 1,8-cineole (6.5 x 10(-6) to 2 x 10(-2) mol/L) in a concentration-dependent manner (P < 0.001, anova) with a pD(2) value of 2.23 (95% confidence interval 2.10-2.37). Removal of the epithelium or pretreatment of intact tissue for 15 min with 50 micromol/L N(G)-nitro-l-arginine methyl ester, 5 mmol/L tetraethylammonium, 0.5 micromol/L tetrodotoxin or 5 micromol/L propranolol did not alter the potency (pD(2)) or the maximal myorelaxant effect (E(max)) of 1,8-cineole. 3. 1,8-Cineole also significantly decreased the Schultz-Dale contraction induced by OVA, mainly in preparations from OVA-sensitized animals submitted to antigen challenge. 1,8-Cineole decreased tracheal hyperresponsiveness to KCl and carbachol caused by antigen challenge and almost abolished the concentration-response curves to KCl, whereas it had little effect on the concentration-response curves to carbachol. Under Ca(2+)-free conditions and in the presence of 10(-4) mol/L acetylcholine, neither 1,8-cineole (6.5 x 10(-3) mol/L) nor verapamil (1 x 10(-5) mol/L) affected Ca(2+)-induced contractions, but they almost abolished Ba(2+)-induced contractions. 4. In conclusion, the findings of the present study show that 1,8-cineole is a tracheal myorelaxant that acts preferentially on contractile responses elicited electromechanically.
In the present study, a practical activity is proposed to adopt an experimental approach to demonstrate the relationship between the equilibrium potential for K(+) and transmembrane electrical potential without glass micropipettes. A conventional setup for recording contractile activity of isolated smooth muscle preparations was used based on the events elegantly described by Somlyo and Somlyo in the 1960s. They showed that, in response to a given stimulus, smooth muscle cells may contract, recruiting electromechanical or pharmacomechanical coupling by mechanisms that involve, or not, changes in transmembrane potential, respectively. By means of contractions and relaxations of a ring-like preparation from the rat mesenteric artery, it is possible to observe the functional consequences of handling K(+) concentration in the extracellular compartment and the effects caused by opening K(+) channels in that preparation, which are significant when the cell membrane establishes an electrical potential difference between intra- and extracellular compartments (driven mainly by K(+) permeability under resting conditions). The effects observed by students fit well with values predicted by Nernst and Goldman-Hodgin-Katz equations, and we demonstrated that the activity is able to improve students' comprehension regarding basic principles of bioelectricity.
Objective:To evaluate the effects of passive inhalation of cigarette smoke on the respiratory system of guinea pigs. Methods:Male guinea pigs were divided into two groups: control and passive smoking, the latter being exposed to the smoke of ten cigarettes for 20 min in the morning, afternoon and evening (30 cigarettes/day) for five days. After that period, inflammatory parameters were studied by quantifying mesenteric mast cell degranulation, as well as oxidative stress, in BAL fluid. In addition, we determined MIP, MEP, and mucociliary transport (in vivo), as well as tracheal contractility response (in vitro). Results:In comparison with the control group, the passive smoking group showed a significant increase in mast cell degranulation (19.75 ± 3.77% vs. 42.53 ± 0.42%; p < 0.001) and in the levels of reduced glutathione (293.9 ± 19.21 vs. 723.7 ± 67.43 nM/g of tissue; p < 0.05); as well as a significant reduction in mucociliary clearance (p < 0.05), which caused significant changes in pulmonary function (in MIP and MEP; p < 0.05 for both) and airway hyperreactivity. Conclusions:Passive inhalation of cigarette smoke caused significant increases in mast cell degranulation and oxidative stress. This inflammatory process seems to influence the decrease in mucociliary transport and to cause changes in pulmonary function, leading to tracheal hyperreactivity.
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