A rat model of exercise-induced asthma: a nonspecific response to a specific immunogen

Abstract

Exercise-induced bronchoconstriction (EIB) is common; however, key aspects of its pathogenesis are still unclear. We investigated the feasibility of adapting an established animal model of asthma to investigate the earliest stages of EIB. The hypothesis was that a single exposure to a normally innocuous, and brief, exercise challenge could trigger EIB symptoms in rats previously sensitized to ovalbumin (OVA) but otherwise unchallenged. Brown-Norway rats were sensitized by intraperitoneal injection of OVA at 0 and 2 wk. At week 3, animals were exposed to either aerosolized OVA (SS) or exercise (EXS). A trained, blinded, clinical observer graded EIB by respiratory sounds. Plasma and lung cytokine levels were analyzed. No control rats with or without exercise (EX, CON) showed evidence of EIB. Eighty percent of the SS group demonstrated abnormal breath sounds upon exposure to aerosolized OVA. Approximately 30% of EXS rats sensitized to OVA but exposed only to exercise had abnormal breath sounds. Lung tissue levels of TNF-α, IL-1α, growth-related oncogene/keratinocyte/chemoattractant, and IFN-γ were significantly higher (P < 0.001) in the SS group, relative to all other groups. Changes in most of these cytokines were not notable in the EXS rats, suggesting a different mechanism of EIB. Remarkably, IFN-γ, but not the other cytokines measured, was significantly elevated following brief exercise in both sensitized and unsensitized rats. Exercise led to detectable breathing sound abnormalities in sensitized rats, but less severe than those observed following classical OVA challenge. Precisely how this immune crossover occurs is not known, but this model may be useful in elucidating essential mechanisms of EIB.

Lack of desensitization of the cough reflex in ovalbumin-sensitized rabbits during exercise

“…It is also able to trigger various and complex interacting mechanisms within the psycho-neuro-immune-endocrine pathways [ 36 ]. Exercise-induced bronchoconstriction (EIB) is common but key aspects of its pathogenesis are still lacking [ 37 ]. Regarding to the pathophysiological mechanisms involved, it is generally assumed that exercise-induced asthma/bronchoconstriction involves both osmolar (“airway drying”) and vascular (“thermal”) modifications of the airways, in addition to parasympathetic stimulation caused by the entrance of fresh air into the respiratory tract [ 38 ].…”

Diurnal, seasonal, and sex patterns of heart rate in grip-restrained African giant rats (Cricetomys gambianus, Waterhouse)

“…The HR of each restrained AGR was recorded as the number of heart beats per minute (bpm) by auscultation with the aid of a stethoscope (3M TM Littman â Classic II S.E. ), placed on the left ventro-lateral side of the thorax (Kodesh et al 2011;Ayo et al 2014). The HRs of the AGRs were measured in the morning (7-9 h), afternoon (12-14 h), and evening ( (Table 3).…”

Low-Intensity Aerobic Exercise Mitigates Exercise-Induced Bronchoconstriction by Improving the Function of Adrenal Medullary Chromaffin Cells in Asthmatic Rats

“…On day 56, rats were challenged with a single bout of 8-min progressive exercise (Kodesh et al 2011). During the first 4 min, the rats ran on a treadmill with the speed rapidly increasing to 30 m/min and continually running at that speed, until completion of the challenge.…”

“…Rats were examined three times both before and after exercise challenge (over a 10-min period), and each examination lasted for 1 min. The auscultated sounds were semi-quantitatively classified, as previously described (Kodesh et al 2011): 0, clear breath sounds with no abnormality; 1, increased breath sounds without elements of tone or pitch; and 2, increased breath sounds with elements of tone or pitch. Following the pulmonary auscultation, the rats were anesthetized by i.p.…”