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Recurrent Airway Obstruction (view source)

Revision as of 11:56, 26 August 2010

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When a horse with a history of RAO is moved from pasture to a stable, the hay it is fed and the straw it is bedded on harbour organic dusts. These dusts contain components which are capable of causing inflammation of the lungs, such as specific allergens, endotoxin, moulds and small particulate matter<sup>1</sup>. Although small particles and endotoxin are known to cause pulmonary inflammation, there is evidence to suggest that there is an allergic component to recurrent airway obstruction. For example, bronchoalveolar lavage fluid in RAO has been shown to have increased levels of IgE specific for various moulds<sup>haliwell</sup>,  and the cytokine response appaears to be skewed towards TH2<sup>lavoi</sup>: both of these facts are suggestive of an allergic mechanism.
 
When a horse with a history of RAO is moved from pasture to a stable, the hay it is fed and the straw it is bedded on harbour organic dusts. These dusts contain components which are capable of causing inflammation of the lungs, such as specific allergens, endotoxin, moulds and small particulate matter<sup>1</sup>. Although small particles and endotoxin are known to cause pulmonary inflammation, there is evidence to suggest that there is an allergic component to recurrent airway obstruction. For example, bronchoalveolar lavage fluid in RAO has been shown to have increased levels of IgE specific for various moulds<sup>haliwell</sup>,  and the cytokine response appaears to be skewed towards TH2<sup>lavoi</sup>: both of these facts are suggestive of an allergic mechanism.
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On exposure to dust, neutrophils accumulate in the lung and quickly invade the lumen of the airway<sup>1</sup>. Aiway obstruction then develops due to several mechanisms. Mucus becomes more viscous and accumulates in the luman, and bronchospasm is initiated by the actions of inflammatory mediators on airway smooth muscle and cholinergic nerves. Oedema of the airway wall also contributes to narrowing, and in horses suffering chronic disease, the wall remodels to include smooth muscle hypertrophy and peribronchial fibrosis.
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On exposure to dust, neutrophils accumulate in the lung and quickly invade the lumen of the airway<sup>1</sup>. Aiway obstruction then develops due to several mechanisms. Mucus becomes more viscous and accumulates in the luman, and bronchospasm is initiated by the actions of inflammatory mediators on airway smooth muscle and cholinergic nerves<sup>Olszewski</sup>. Oedema of the airway wall also contributes to narrowing, and in horses suffering chronic disease, the wall remodels to include smooth muscle hypertrophy and peribronchial fibrosis.
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One of the characteristic features of horses with RAO is increased non-specific airway hyperresponsiveness [34,35]. This means that airways of RAO-affected horses narrow in an exaggerated fashion in response to a wide variety of stimuli including neurotransmitters [36], inflammatory mediators such as histamine [34,35,37], and non-specific stimuli such as citric acid [36]. The airway hyperresponsiveness is most pronounced during acute exacerbations of RAO when inflammation is most severe and hyperresponsiveness wanes when animals are out at pasture [34,36] and inflammation is less severe. Even quite brief exposure of a RAO-susceptible horse to a stable environment can induce hyperresponsiveness that persists for several days [38]. The causes of the hyperresponsiveness include airway wall thickening, smooth muscle hypertrophy, a reduction in some of the inhibitory mechanisms that limit smooth muscle contraction [39,40] and actions of inflammatory mediators on cholinergic nerves and smooth muscle to facilitate smooth muscle contraction [25,26]. Clinically, airway hyperresponsiveness is important because it means that RAO-susceptible horses are prone to develop bronchospasm in response to levels of stimuli that would not affect a normal horse. Reducing the level of airway inflammation best controls hyperresponsiveness.
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Many apparently normal horses develop low levels of airway inflammation when housed in the environment that causes a massive influx of neutrophils into the airways on RAO susceptible animal [41,42]. The reasons for the up-regulation of the inflammatory response following a dust challenge and the persistence of inflammation when RAO susceptible horses are returned to pasture are under active investigation. There is evidence for depletion of endogenous antioxidants in the airways of RAO susceptible animals [43,44] and for prolonged activation of NFkB, a transcription factor that initiates the production of many pro-inflammatory cytokines [22]. Activation of NFkB may be due to a positive feedback loop involving the persistent production of TNFa and IL-1b by neutrophils [45]. Inflammation also persists because apoptosis of neutrophils is delayed [46].
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Because of the diffuse obstruction of the peripheral airways, horses with RAO have a mismatching of ventilation and blood flow that leads to inefficient gas exchange and hypoxemia [47]. In order to compensate for the poor gas exchange, RAO-affected horses increase their minute ventilation by increasing respiratory rate [47,48]. Tidal volume does not change. Inhaling the same tidal volume in less time requires that the horse with RAO develop a higher mean airflow rates in the face of airway obstruction [47-49]. This is why, the horse adopts the breathing pattern characteristic of heaves.
      
==Signalment==
 
==Signalment==
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