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| ====Intrinsic ulcerogneic factors==== | | ====Intrinsic ulcerogneic factors==== |
| Hydrochloric acid (HCl) and a sustained gastric pH<4.0 are the most significant factors in gastric ulceration. Volatile fatty acids (VFAs), lactic acid and bile acids act synergistically with HCl to cause changes in squamous mucosal bioelectric properties (the first sign of acidic damage). VFAs and lactic acid are by-products of bacterial fermentation of sugars in concentrate diets. | | Hydrochloric acid (HCl) and a sustained gastric pH<4.0 are the most significant factors in gastric ulceration. Volatile fatty acids (VFAs), lactic acid and bile acids act synergistically with HCl to cause changes in squamous mucosal bioelectric properties (the first sign of acidic damage). VFAs and lactic acid are by-products of bacterial fermentation of sugars in concentrate diets. |
− | =====Hydrochloric acid=====
| + | *'''Hydrochloric acid''' damages the squamous mucosa by compromising the outer cell barrier. It then diffuses into the squamous cells of the ''stratum spinosum'', inhibiting cellular sodium transport and causing cell swelling, necrosis and eventual ulceration. (Argenzio and Eismann 1987; Nadeau et al. 2003a,b) |
− | HCl damages the squamous mucosa by compromising the outer cell barrier. It then diffuses into the squamous cells of the ''stratum spinosum'', inhibiting cellular sodium transport and causing cell swelling, necrosis and eventual ulceration. (Argenzio and Eismann 1987; Nadeau et al. 2003a,b)
| + | *'''Volatile Fatty Acids (VFAs)''' (acetic, propionic, butyric and valeric acids) are lipid soluble. They readily diffuse into the squamous mucosal cells of the ''stratum spinosum'' and immediately inhibit sodium transport leading to cell swelling, necrosis and ulceration. |
− | =====Volatile Fatty Acids (VFAs)=====
| + | *'''Lactic acid''' may increase the permeability of the squamous mucosa in the presence of VFAs and/or HCl (Andrews et al. 2008). |
− | Whereas, VFAs (acetic, propionic, butyric and valeric acids), because of their lipid solubility, induce damage by rapidly diffusing into the squamous mucosal cells of the stratum spinosum layer and immediately inhibit sodium transport which results in cell swelling and ulceration. Squamous mucosal cells are susceptible to HCl and VFA injury in pH, dose and time dependent manner (Andrews et al. 2006).
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− | =====Lactic acid=====
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− | Lactic acid has a similar chemical structure to VFAs. But lactic acid (pH 1.5 and 40 mmol/l) exposed to the nonglandular mucosa increased tissue permeability, as indicated by increased transepithelial conductance (Andrews et al. 2008).
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− | Furthermore, HCl and VFAs have been shown to cause disruption in bioelectric properties and barrier function of the NG mucosa of horses in an in vitro Ussing chamber system (Widenhouse et al. 2002; Nadeau et al. 2003a,b; Andrews et al. 2006). The proposed mechanism by which VFAs cause acid injury is as follows: at low pH (≤4.0), VFAs remain undisassociated (nonionic) and are highly lipid soluble. By penetrating the NG mucosal cells and acidifying cellular contents they disrupt cellular sodium transport, leading to cell swelling, cell death and ulceration (Argenzio and Eisemann 1996; Nadeau
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− | et al. 2003a,b).
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− | Lactic acid (LA), commonly found in the stomach of horses after eating, has a chemical structure and low pKa (3.8) similar to acetic acid, but LA is stronger. In previous studies, LA concentrations in the stomach were high (Wolter and Chaabouni 1979; Al Jassim 2006), compared to other regions of the digestive tract. Stomach LA is probably produced by resident acid-tolerant bacteria, such as Lactobacillus and Streptococcus spp., which have been found in abundance in the equine stomach (Al Jassim | |
− | et al. 2005; Varloud et al. 2007). Also, a recent study showed a3-fold increase in post prandial L-/D-lactate concentration (Varloud et al. 2007). Therefore, LA exposure to NG mucosa of horses in an acidic environment would be expected to cause similar acid injury to that caused by other VFAs.
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− | Lactic acid, produced in the stomach of horses fed a high-grain diet, does not significantly alter sodium transport or permeability in equine NG mucosal tissue. Lactic acid may require a longer exposure time or may need the presence of other VFAs in HCl to cause gastric ulcers.(Andrews 2008)
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| ==Risk Factors== | | ==Risk Factors== |