PubMed · 4690521
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O Hjalmarson. 1973. Intrathoracic tracheal collapse--a pathophysiological study.. https://doi.org/10.1136/adc.48.2.162-f
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We evaluated roles of kinins in allergen-induced nasal blockage and sneezing, and development of nasal hyperresponsiveness to leukotriene D4 in a Japanese cedar pollen-induced allergic rhinitis model of guinea pigs. Sensitised guinea pigs were repeatedly challenged by pollen inhalation once every week. Neither a bradykinin B1 receptor antagonist, des-Arg9-[Leu8]bradykinin nor a bradykinin B2 receptor antagonist, icatibant suppressed allergen-induced sneezing and nasal blockage. However, development of nasal hyperresponsiveness to leukotriene D4 was significantly suppressed by them. The amount of bradykinin in nasal cavity lavage fluid was immediately increased after the challenge. In non-sensitised animals, hyperresponsiveness to leukotriene D4 was developed by a bradykinin B2 receptor agonist, bradykinin, but not by a bradykinin B1 receptor agonist, des-Arg10-kallidin, while in the sensitised-challenged animal, both agonists developed hyperresponsiveness. In conclusion, the nasal hyperresponsiveness appeared to be induced by kinins produced in response to the antigen challenge through activation of not only bradykinin B2 but also B1 receptors.
Horses display remarkable aerobic capabilities, attaining during muscular exercise a maximal rate of oxygen consumption about 30-fold higher than the resting value, and 2.5-fold higher than that of other mammals of similar body mass. Under these circumstances an enormous mechanical burden is expected to impinge on the equine respiratory pump and regulatory mechanisms aiming to minimize this load may play an important role in determining the adequacy of the respiratory system to the metabolic requirements. The behaviour of the respiratory system has been investigated in horses at rest and during treadmill locomotion at different velocities and gaits. During exercise hyperpnoea, horses exhibit a significant reduction in the lung viscous resistance not observed in other mammals, such as dogs and humans. Therefore, the exercise-dependent increase in the rate of mechanical work of breathing is lower in the horse than in other mammals. This increase in the equine airway patency during exercise appeared to be mainly determined by the pattern of laryngeal movements. In fact, during exercise, the laryngeal cross-sectional area, determined with a video-endoscopic imaging technique at the level of rima glottidis (CSArg), undergoes during inspiration an increase averaging up to over 4 times the resting expiratory values. Although a significant linear correlation was found between CSArg and minute ventilation (VE), the laryngeal activation contributes to increase lung conductance only when CSArg is narrower than the tracheal section. It appears therefore that in exercising horses pulmonary resistive features are finely controlled to reduce the mechanical load supported by the respiratory muscles and to counterbalance the increase in the ventilatory energetic requirements inherent in the remarkably enhanced aerobic performance observed in this species.
Carbon monoxide (CO) in expired gas has been shown to be elevated with asthma; however, its function is not known, and there is some potential that it may serve a bronchoprotective role to decrease airway hyperresponsiveness (AHR). Thus the ability of CO to reverse methacholine (MCh)-induced bronchoconstriction was evaluated in C57BL/6 (C57) and A/J mice with and without airway inflammation produced by ovalbumin (OVA). Acutely administered CO (1% in air, 10 min) reduced MCh-driven increases in lung resistance in OVA-challenged C57 mice by an average of 50% (from 14.5 to 7.1 cmH2O.ml-1.s-1), whereas no effect was observed in naïve C57 mice or OVA-challenged C57 mice inhaling air alone. Acutely inhaled CO (500 ppm = 0.05%, for 10 min) reduced MCh-induced airway reactivity (AR) by 20-60% in airway hyperresponsive naïve A/J mice, whereas repeated 10-min administrations of 500 ppm CO over a 5-day period decreased AR by 50%. Repeated administration of low-dose CO [250 (0.025%) and (0.05%) 500 ppm, 1 h/day, 5 days] to A/J mice with airway inflammation likewise resulted in a drop of AR by 50%, compared with those not receiving CO. Inhibition of guanylyl cyclase/guanosine 3',5'-cyclic monophosphothioate (cGMP) using 1H-[1,2,4] oxydiazolo[4,3-a]quinoxalin-1-one or a competitive inhibitor, Rp diastereomers of 8-bromo-cGMP, resulted in inhibition of the effect of CO on AHR, suggesting that the effects of CO were mediated through this mechanism. These results indicate that low-dose CO can effectively reverse AHR in the presence and absence of airway inflammation in mice and suggest a potential role for CO in the modulation of AHR.