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      Ruminal acidosis: strategies for its control

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          Abstract

          ABSTRACT: Ruminal acidosis in ruminants is a metabolic disorder of gastrointestinal origin that occurs in animals with a high feed intake of cereal grains diets, which affect the performance. According to clinical manifestations it can be classified as: a) acute lactic acidosis with prolonged exposure to ruminal pH ≤ 5.0, triggering a systemic acidosis, with clinical manifestations and changes in biochemical patterns, starting the first twelve hours of ruminal acidosis and it takes 48 to 120 hours to reestablish, b) subacute ruminal acidosis (SARA), it has no clinical manifestations, rumen pH decreases in a range of 5.5 to 5.0 and is held for 111 to 180 minutes in 24 hours, this decrease causes an imbalance in the ruminal metabolism, as well as the fluid balance. Ruminal acidosis can be prevented by adding sodium bicarbonate to the ration, or zootechnic additives such as Saccharomyces cereviseae and Megasphaera elsdenii as well as essential oils (cinnamaldehyde and eugenol). It is also important to consider the forage/concentrate ratio, the forage particle size, the NDF content of the ration, as well as the cereal's rate of degradation in the rumen. The objective of this review was to address the ruminal acidosis pathophysiology, its effects on animal welfare and control strategies to minimise the detrimental impact on animal production.

          Translated abstract

          RESUMEN: La acidosis ruminal es un trastorno metabólico de origen digestivo, que se presenta en los rumiantes al ingerir dietas altas en granos de cereales, y que afecta el rendimiento productivo. Según sus manifestaciones clínicas se clasifica en: a) acidosis láctica aguda en la que hay una exposición prolongada a un pH ruminal ≤ 5,0, lo que desencadena una acidosis sistémica con manifestaciones clínicas, así como cambios en los patrones bioquímicos que se inician en las primeras doce horas de la acidosis ruminal y tardan de 48 a 120 horas en restablecerse, y b) acidosis subaguda ruminal (ASR), donde no hay manifestaciones clínicas, el pH del rumen disminuye en un rango de 5,5 a 5,0 y se mantiene durante 111 a 180 minutos en 24 horas, este descenso provoca un desequilibrio tanto en el metabolismo ruminal como en el balance de líquidos. La acidosis ruminal se puede prevenir por la adición de bicarbonato de sodio, aditivos zootécnicos como la Sccharomyces cerevisiae y Megasphaera elsdenii, y aceites esenciales (cinamaldehído y eugenol). Es importante considerar la relación forraje/concentrado así como el tamaño de partícula del forraje, el contenido de FND de la ración, y la degradación del grano de cereal en el rumen. El objetivo de la presente revisión fue abordar la fisiopatología de la acidosis ruminal, los efectos que esta causa en el bienestar animal y las estrategias para su control, para minimizar su impacto detrimental en la producción animal.

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          Most cited references106

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          Bovine acidosis: implications on laminitis.

          J Nocek (1997)
          Bovine lactic acidosis syndrome is associated with large increases of lactic acid in the rumen, which result from diets that are high in ruminally available carbohydrates, or forage that is low in effective fiber, or both. The syndrome involves two separate anatomical areas, the gastrointestinal tract and body fluids, and is related to the rate and extent of lactic acid production, utilization, and absorption. Clinical manifestations range from loss of appetite to death. Lactic acid accumulates in the rumen when the bacteria that synthesize lactic acid outnumber those that utilize lactic acid. The systemic impact of acidosis may have several physiological implications, including laminitis, a diffuse aseptic inflammation of the laminae (corium). Although a nutritional basis for the disease exists, etiology includes a multitude of interactive factors, such as metabolic and digestive disorders, postpartum stress, and localized trauma, which lead to the release of vasoactive substances that trigger mechanisms that cause degenerative changes in the foot. The severity of laminitis is related to the frequency, intensity, and duration of systemic acidotic insults on the mechanisms responsible for the release of vasoactive substance. The critical link between acidosis and laminitis appears to be associated with a persistent hypoperfusion, which results in ischemia in the digit. Management of acidosis is critical in preventing laminitis. High producing dairy herds attempting to maximize energy intake are continually confronted with subclinical acidosis and laminitis. Management of feeding and husbandry practices can be implemented to reduce incidence of disease.
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            Starch utilization by ruminants: from basics to the bunk.

            Starch is the major energy component of grains. Wheat contains 77% of DM as starch, corn and sorghum contain 72%, and barley and oats contain 57 to 58%. In vitro systems have provided valuable data on kinetic aspects of starch digestion. Molecular biological techniques have provided a clearer picture of the ruminal microbial milieu. Proportions of starch fermented in the rumen can be predicted satisfactorily for a variety of grains and processing methods. Compared with dry rolling, steam processing (flaking or rolling) increases ruminal digestibility of starch (percentage of intake) from 52 to 78% for sorghum, from 75 to 85% for corn, and six percentage units or less for other grains. Recent research provides new insight into pancreatic function and intestinal glucose transport systems. The capacity to digest starch in the intestine ranges from 45 to 85% of starch entering the duodenum, with that capacity apparently limited by the supply of pancreatic amylase. There is evidence that amylase secretion may be enhanced by increasing duodenal entry of protein. Capacity for active transport of glucose across of gut wall does not seem to limit the amount of starch digested that is absorbed as glucose. For ruminants eating medium- to high-concentrate diets, about 30% of their total glucose need comes from glucose absorption, 50% from organic acid absorption (substrates for hepatic gluconeogenesis), and 20% from other sources. When glucose absorption from the gut increases, ruminants generally adjust (decrease) gluconeogenesis to meet their need; that need is directly linked to DE intake. In terms of overall ME yield, grain starch is best used when it is fermented in the rumen. However, close coordination of protein and starch supply to the duodenum may improve capture of starch in the form of glucose.
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              Ruminant Nutrition Symposium: Role of fermentation acid absorption in the regulation of ruminal pH.

              Highly fermentable diets are rapidly converted to organic acids [i.e., short-chain fatty acids (SCFA) and lactic acid] within the rumen. The resulting release of protons can constitute a challenge to the ruminal ecosystem and animal health. Health disturbances, resulting from acidogenic diets, are classified as subacute and acute acidosis based on the degree of ruminal pH depression. Although increased acid production is a nutritionally desired effect of increased concentrate feeding, the accumulation of protons in the rumen is not. Consequently, mechanisms of proton removal and their quantitative importance are of major interest. Saliva buffers (i.e., bicarbonate, phosphate) have long been identified as important mechanisms for ruminal proton removal. An even larger proportion of protons appears to be removed from the rumen by SCFA absorption across the ruminal epithelium, making efficiency of SCFA absorption a key determinant for the individual susceptibility to subacute ruminal acidosis. Proceeding initially from a model of exclusively diffusional absorption of fermentation acids, several protein-dependent mechanisms have been discovered over the last 2 decades. Although the molecular identity of these proteins is mostly uncertain, apical acetate absorption is mediated, to a major degree, via acetate-bicarbonate exchange in addition to another nitrate-sensitive, bicarbonate-independent transport mechanism and lipophilic diffusion. Propionate and butyrate also show partially bicarbonate-dependent transport modes. Basolateral efflux of SCFA and their metabolites has to be mediated primarily by proteins and probably involves the monocarboxylate transporter (MCT1) and anion channels. Although the ruminal epithelium removes a large fraction of protons from the rumen, it also recycles protons to the rumen via apical sodium-proton exchanger, NHE. The latter is stimulated by ruminal SCFA absorption and salivary Na(+) secretion and protects epithelial integrity. Finally, SCFA absorption also accelerates urea transport into the rumen, which via ammonium recycling, may remove protons from rumen to the blood. Ammonium absorption into the blood is also stimulated by luminal SCFA. It is suggested that the interacting transport processes for SCFA, urea, and ammonia represent evolutionary adaptations of ruminants to actively coordinate energy fermentation, protein assimilation, and pH regulation in the rumen.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                australjvs
                Austral journal of veterinary sciences
                Austral j. vet. sci.
                Universidad Austral de Chile. Facultad de Ciencias Veterinarias (Valdivia, , Chile )
                0719-8000
                0719-8132
                September 2017
                : 49
                : 3
                : 139-148
                Affiliations
                [1] Chihuahua orgnameUniversidad Autónoma de Ciudad Juárez México
                Article
                S0719-81322017000300139
                10.4067/S0719-81322017000300139
                2a16d2de-bc0e-4278-b48e-d22c55bcf2f6

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 107, Pages: 10
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                SciELO Chile


                metabolic disorder,ruminal subacute acidosis,trastorno metabólico,acidosis subaguda ruminal

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