Relevant bibliographies by topics / Lactic acidosis in ruminants

Academic literature on the topic 'Lactic acidosis in ruminants'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Lactic acidosis in ruminants.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Lactic acidosis in ruminants"

1

Dunlop, Robert H., and Paul B. Hammond. "D-LACTIC ACIDOSIS OF RUMINANTS*†." Annals of the New York Academy of Sciences 119, no. 3 (December 16, 2006): 1109–32. http://dx.doi.org/10.1111/j.1749-6632.1965.tb47466.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Lorenz, Ingrid, and Arcangelo Gentile. "d-Lactic Acidosis in Neonatal Ruminants." Veterinary Clinics of North America: Food Animal Practice 30, no. 2 (July 2014): 317–31. http://dx.doi.org/10.1016/j.cvfa.2014.03.004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Clayton, E. H., and G. P. D. Jones. "Preliminary observations of tumour necrosis factor-alpha in the faeces of sheep following acute lactic acidosis." Australian Journal of Agricultural Research 52, no. 9 (2001): 869. http://dx.doi.org/10.1071/ar00118.

Full text
Abstract:
Lactic acidosis resulting from excessive fermentation of starch by ruminants can lead to many deleterious effects on the animal including shock and death in severe cases. The exact mechanisms mediating this response are still relatively unknown and the present study has examined the influence of lactic acidosis in sheep on the production of tumour necrosis factor-alpha (TNFα), a pro-inflammatory cytokine. Lactic acidosis was induced in 6 Merino sheep by feeding 2 kg of barley-based pellets. Lactic acid levels rose in rumen fluid and faeces from 0.5 to 32.1 mmol/L and 0.5 to 48.0 mmol/L, respectively (P < 0.05); whereas, pH in both rumen fluid and faeces decreased from 8.22 to 5.18 and 7.05 to 5.00, respectively (P < 0.05), after lactic acidosis. TNF-· levels increased in faeces from 15 ng/g to 75 ng/g (P < 0.05) 24 h and 12 h after ruminal and hind gut lactic acidosis incidence, respectively. These preliminary findings suggest the possibility of an immune response in the body to lactic acidosis indicated by increasing TNFα levels. TNFα may be a mediator of lactic acidosis and its presence may explain many of the secondary effects observed after acidosis including laminitis and liver abscesses.
APA, Harvard, Vancouver, ISO, and other styles
4

Park, Seon Young, Mingyung Lee, Se Ra Lim, Hyemin Kwon, Ye Seul Lee, Ji Hyung Kim, and Seongwon Seo. "Diversity and Antimicrobial Resistance in the Streptococcus bovis/Streptococcus equinus Complex (SBSEC) Isolated from Korean Domestic Ruminants." Microorganisms 9, no. 1 (January 4, 2021): 98. http://dx.doi.org/10.3390/microorganisms9010098.

Full text
Abstract:
S. bovis/S. equinus complex (SBSEC) includes lactic acid-producing bacteria considered as the causative agent associated with acute rumen lactic acidosis in intensive ruminants. Considering the limited information on the detailed characteristics and diversity of SBSEC in Korea and the emergence of antimicrobial resistance (AMR), we investigated the diversity of SBSEC from domestic ruminants and verified the presence of antimicrobial resistance genes (ARGs) against several antimicrobials with their phenotypic resistance. Among 51 SBSEC isolates collected, two SBSEC members (S. equinus and S. lutetiensis) were identified; sodA-based phylogenetic analyses and comparisons of overall genome relatedness revealed potential plasticity and diversity. The AMR rates of these SBSEC against erythromycin, clindamycin, and tetracycline were relatively lower than those of other SBSEC isolates of a clinical origin. An investigation of the ARGs against those antimicrobials indicated that tetracycline resistance of SBSECs generally correlated with the presence of tet(M)-possessing Tn916-like transposon. However, no correlation between the presence of ARGs and phenotypic resistance to erythromycin and clindamycin was observed. Although a limited number of animals and their SBSEC isolates were examined, this study provides insights into the potential intraspecies biodiversity of ruminant-origin SBSEC and the current status on antimicrobial resistance of the bacteria in the Korean livestock industry.
APA, Harvard, Vancouver, ISO, and other styles
5

Valente, Tiago Neves Pereira, Cláudia Batista Sampaio, Erico da Silva Lima, Bruno Borges Deminicis, Andréia Santos Cezário, and Wallacy Barbacena Rosa dos Santos. "Aspects of Acidosis in Ruminants with a Focus on Nutrition: A Review." Journal of Agricultural Science 9, no. 3 (February 13, 2017): 90. http://dx.doi.org/10.5539/jas.v9n3p90.

Full text
Abstract:
An increased risk of acidosis in animals is associated with a high dry matter intake (DMI), which in turn results in the consumption of more fermentable organic matter (OM) in the rumen leading to a high production of volatile fatty acids (VFA). This is observed in lactating dairy cows and animals in a feedlot. Acute acidosis occurs when there is a severe drop in the pH of the rumen. A prolonged period when pH of in rumen remains low, it leads to sub-acute ruminal acidosis (SARA), which is a temporary imbalance between acid production and absorption. An associated change of an acute increase in the ruminal osmolarity and the accumulation of glucose and lactate in its stereoisomeric forms (D-lactate and L-lactate), is observed in the rumen fluid. However, in the sub-acute form, the accumulation of lactic acid occurs in the rumen. To a great extent, these changes in the rumen are due to high concentrations of VFA. The best way to avoid problems with ruminal acidosis is an adequate supply of neutral detergent fiber (NDF) in the diet, preferentially with large particle size and length to stimulate rumination and consequently greater buffering efficiency, thus maintaining the balance between pH and microorganisms in the rumen.
APA, Harvard, Vancouver, ISO, and other styles
6

Abeysekara, Saman, Jonathan M. Naylor, Andrew W. A. Wassef, Ulyana Isak, and Gordon A. Zello. "d-Lactic acid-induced neurotoxicity in a calf model." American Journal of Physiology-Endocrinology and Metabolism 293, no. 2 (August 2007): E558—E565. http://dx.doi.org/10.1152/ajpendo.00063.2007.

Full text
Abstract:
-Lactic acidosis (DAC) occurs as a complication of short-bowel syndrome in humans and in a variety of other gastrointestinal disorders in monogastrics and ruminants. DAC is associated with signs of impaired central nervous system (CNS) function including ataxia and coma. The objective of this experiment was to determine whether either acidification of nervous tissue or d-lactic acid is responsible for decreased neurological function. Eight Holstein calves (32 ± 11 days, 70 ± 10 kg) were surgically catheterized with indwelling intravenous jugular and atlanto-occipital space cerebrospinal fluid (CSF) catheters and infused for 6 h in random order with isomolar dl-lactic acid (dl-LA), l-lactic acid (l-LA), hydrochloric acid (HCl), or saline. dl-LA induced ataxia after 4 h of infusion and produced the greatest obtunding of CNS function (at 7 h, score 8.0 ± 0.4), whereas the other infusions caused neither ataxia nor scores over 1.5 ( P < 0.01 from dl-LA). dl-LA induced significantly less acidemia than HCl (at 6 h pH 7.13 ± 0.06 and 7.00 ± 0.04, base excess −16 ± 1 and −23 ± 3 mmol/l, bicarbonate 11 ± 1 and 8 ± 1 mmol/l respectively, all P < 0.01) but greater than l-LA and saline ( P < 0.01). CSF changes followed a similar but less pronounced pattern. Although HCl infusion produced a severe acidemia and CSF acidosis, only minor effects on neurological function were evident suggesting that d-lactate has a direct neurotoxic effect that is independent of acidosis. Conversely, l-LA produced only minor neurological changes.
APA, Harvard, Vancouver, ISO, and other styles
7

Ghali, M. B., P. T. Scott, G. A. Alhadrami, and R. A. M. Al Jassim. "Identification and characterisation of the predominant lactic acid-producing and lactic acid-utilising bacteria in the foregut of the feral camel (Camelus dromedarius) in Australia." Animal Production Science 51, no. 7 (2011): 597. http://dx.doi.org/10.1071/an10197.

Full text
Abstract:
The camel is emerging as a new and important animal in the Australian livestock industry. However, little is known regarding the microbial ecosystem of the gastrointestinal tract of this ruminant-like animal. This study was carried out to determine the diversity of lactic acid-producing and lactic acid-utilising bacteria in the foregut of the feral camel (Camelus dromedarius) in Australia. Putative lactic acid bacteria were isolated from the foregut contents of camels by culturing on De Man, Rogosa, Sharpe and lactic acid media. Identification of representative isolates was based on the analysis of 16S rRNA gene sequences. Fermentation end products of glucose (i.e. volatile fatty acids and lactate) were also measured in vitro. The key predominant bacteria identified in this study were closely related to Streptococcus bovis, Selenomonas ruminantium, Butyrivibrio fibrisolvens, Lachnospira pectinoschiza and Prevotella ruminicola. The main L-lactate producers were those isolates closely related to S. bovis, S. ruminantium and Lactococcus garvieae, while the efficient lactate utilisers were S. ruminantium-related isolates. D-lactate was produced by isolates closely related to either L. pectinoschiza or S. ruminantium. The predominant bacteria isolated and characterised in this study are identical and/or closely related to those typically found in true ruminants (e.g. S. ruminantium, B. fibrisolvens, S. bovis). In addition, some of the bacteria isolated represent novel species of Lachnospira and Clostridium in the context of lactic acid bacteria from a large herbivorous host. The results from this study have contributed to our understanding and provide opportunities to reduce foregut acidosis in the camel.
APA, Harvard, Vancouver, ISO, and other styles
8

Hutton, P., C. L. White, Z. Durmic, and P. E. Vercoe. "Eremophila glabra is an Australian plant that reduces lactic acid accumulation in an in vitro glucose challenge designed to simulate lactic acidosis in ruminants." Animal 3, no. 9 (2009): 1254–63. http://dx.doi.org/10.1017/s1751731109004789.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Bacha, Flávia Barbieri, Rayane Chitolina Pupin, Paula Velozo Leal, Nilton Marques Carvalho, Gumercindo Loriano Franco, Camila Celeste Brandão Ferreira Ítavo, Franklin Riet-Correa, and Ricardo Antônio Amaral de Lemos. "Experimental poisoning by Enterolobium contortisiliquum in sheep." Pesquisa Veterinária Brasileira 37, no. 1 (January 2017): 23–30. http://dx.doi.org/10.1590/s0100-736x2017000100004.

Full text
Abstract:
ABSTRACT: Ingestion of Enterolobium contortisiliquum pods causes digestive disturbances, secondary hepatogenous photosensitization and abortions in ruminants. Pods were administered to sheep via a ruminal cannula to characterize acute poisoning. In Experiment 1, a single dose of 12g/kg of body weight (BW) was administered to three sheep in one experiment. One sheep died, and the other two recovered after presenting clinical signs. In Experiment 2, 10g/kg BW were administered daily to 15 sheep until the onset of clinical signs or for three consecutive days. Fourteen sheep showed mild to severe signs after the ingestion of 1-3 doses. Two sheep died, and the others recovered. Clinical signs in both experiments were diarrhea, anorexia, rumen atony, apathy, dehydration and tachypnea. The main macroscopic findings were an orange, frothy ruminal content witch contained pods fragments. The intestinal content was liquid. Detachment of the mucosa from the submucosa and ballooning degeneration of mucosal cells were observed histologically in the forestomachs. Evaluation of ruminal contents revealed acute lactic ruminal acidosis (ALRA). Bromatological analysis of E. contortisiliquum pods revealed 537.8g/kg DM (dry matter) of non-fibrous carbohydrates, which is sufficient to cause ALRA. Only one sheep in Experiment 2 had liver failure, characterized by jaundice, elevated serum activity of liver enzymes and histological lesions in liver biopsies. It is concluded that the administration of E. contortisiliquum pods in forage-fed sheep at doses of 10g/kg BW or higher may cause ALRA. The induction of liver failure in one sheep suggests that liver damage may occur in those sheep that do not develop acidosis.
APA, Harvard, Vancouver, ISO, and other styles
10

McAllister, T. A., K. A. Beauchemin, A. Y. Alazzeh, J. Baah, R. M. Teather, and K. Stanford. "Review: The use of direct fed microbials to mitigate pathogens and enhance production in cattle." Canadian Journal of Animal Science 91, no. 2 (June 2011): 193–211. http://dx.doi.org/10.4141/cjas10047.

Full text
Abstract:
McAllister, T. A., Beauchemin, K. A., Alazzeh, A. Y., Baah, J., Teather, R. M. and Stanford, K. 2011. Review: The use of direct fed microbials to mitigate pathogens and enhance production in cattle. Can. J. Anim. Sci. 91: 193–211. Direct-fed microbials (DFM) have been employed in ruminant production for over 30 yr. Originally, DFM were used primarily in young ruminants to accelerate establishment of the intestinal microflora involved in feed digestion and to promote gut health. Further advancements led to more sophisticated mixtures of DFM that are targeted at improving fiber digestion and preventing ruminal acidosis in mature cattle. Through these outcomes on fiber digestion/rumen health, second-generation DFM have also resulted in improvements in milk yield, growth and feed efficiency of cattle, but results have been inconsistent. More recently, there has been an emphasis on the development of DFM that exhibit activity in cattle against potentially zoonotic pathogens such as Escherichia coli O157:H7, Salmonella spp. and Staphylococcus aureus. Regulatory requirements have limited the microbial species within DFM products to organisms that are generally recognized as safe, such as lactic acid-producing bacteria (e.g., Lactobacillus and Enterococcus spp.), fungi (e.g., Aspergillus oryzae), or yeast (e.g., Saccharomyces cerevisiae). Direct-fed microbials of rumen origin, involving lactate-utilizing species (e.g., Megasphaera elsdenii, Selenomonas ruminantium, Propionibacterium spp.) and plant cell wall-degrading isolates of Butyrivibrio fibrisolvens have also been explored, but have not been commercially used. Development of DFM that are efficacious over a wide range of ruminant production systems remains challenging because[0] comprehensive knowledge of microbial ecology is lacking. Few studies have employed molecular techniques to study in detail the interaction of DFM with native microbial communities or the ruminant host. Advancements in the metagenomics of microbial communities and the genomics of microbial–host interactions may enable DFM to be formulated to improve production and promote health, responses that are presently often achieved through the use of antimicrobials in cattle.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Lactic acidosis in ruminants"

1

Hutton, Peter. "Antimicrobial plants of Australia have the potential to prevent lactic acidosis in ruminants." University of Western Australia. School of Animal Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0159.

Full text
Abstract:
[Truncated abstract] Antimicrobial growth promoters are added to feed to prevent lactic acidosis in ruminant animals by selectively inhibiting rumen bacteria that produce lactic acid. However, recently imposed or impending bans on the use of antimicrobial growth promoters in animal production have lead to a critical need to find practical alternatives that are safe for the animal and consumer and that obtain similar production benefits. I investigated bioactive plants of Australia for their potential to prevent lactic acidosis in ruminants. The unifying hypothesis tested was that plants would be identified that selectively inhibit lactic acid-producing bacteria and consequently protect against lactic acidosis. This hypothesis was tested in a three phase process: phase 1, plant selection and collection; phase 2, a three stage protocol for screening plants and essential oils; phase 3, in vivo experiments and chemical fractionation of the most promising plant. I developed an in vitro bioassay that simulated acidosis by adding glucose to rumen fluid in Bellco tubes and incubating for 5 h (Chapter 4). The pH and gas production were used as indicators of acidosis and fermentation activity. I used this bioassay to screen ninety-five plants (dried and ground material from 79 species) and ten essential oils and included a negative control (oaten chaff) and a positive control (virginiamycin). One plant, Eremophila glabra, produced a similar pH (5.63) to the positive control (5.43) although it inhibited gas production to a moderate extent (P < 0.05). ... Seven serrulatane diterpenes were identified to be the major secondary metabolites in E. glabra. The metabolites were screened using a broth dilution and microtitre spectrophotometry method and were selective against S. bovis at between 320 and 1077 [mu]g/ mL. The serrulatanes from E. glabra were probably responsible for the activity against acidosis that I observed in vitro, because they selectively inhibited lactateproducing bacteria. It is also possible that a synergy between serrulatanes and possibly other metabolites are responsible for the activity observed in vitro. The results from my experiments support the role that bioactive plants may have to replace the antibiotics that are added to livestock feed. Australian plants were identified containing compounds that were active against the bacterial processes responsible for ruminant acidosis. To my knowledge this is the first work undertaken to identify bioactive plants of Australia for their potential to prevent acidosis. I developed in vitro screening bioassays that targeted key indicators of acidosis. These bioassays enabled me to identify 5 plants from the 104 screened that could potentially control acidosis. One of these plants in particular, E. glabra, showed a level of activity in vitro that was comparable to antibiotic protection against acidosis. The exciting in vitro results were not demonstrated in vivo but only one dose level of E. glabra was used, which was based on the in vitro work. In contrast to the in vitro system the rumen is a continuous flow system with greater complexity and it is possible that the concentration of E. glabra that I used in vivo was not optimum. This places importance on future dose response experiments to confirm the efficacy of E. glabra in vivo.
APA, Harvard, Vancouver, ISO, and other styles
2

Wiryawan, I. Komang Gede. "Microbial control of lactic acidosis in grain-fed sheep." Title page, contents and summary only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phw799.pdf.

Full text
Abstract:
Bibliography: leaves 122-138. Investigates the use of microbial inoculants to prevent the onset of acidosis in acutely grain fed animals; and, the most effective combination of virginiamycin and lactic acid utilising bacteria (selenomonas ruminantium subsp. lactilytica and Megasphaera elsdenii) in controlling lactic acid accumulations in vitro.
APA, Harvard, Vancouver, ISO, and other styles
3

Nordin, Angelica. "Genetic and functional studies of hereditary myopathy with lactic acidosis." Doctoral thesis, Umeå universitet, Medicinsk och klinisk genetik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-50592.

Full text
Abstract:
Hereditary myopathy with lactic acidosis (HML, OMIM#255125) is an autosomal recessive disorder which originates from Västerbotten and Ångermanland in the Northern part of Sweden. HML is characterized by severe exercise intolerance which manifests with tachycardia, dyspnea, muscle pain, cramps, elevated lactate and pyruvate levels, weakness and myoglobinuria. The symptoms arise from malfunction of the energy metabolism in skeletal muscles with defects in several important enzymes involved in the TCA cycle and the electron transport chain. All affected proteins contain iron-sulfur (Fe-S) clusters, which led to the suggestion that the disease was caused by malfunctions in either the transportation, assembly or processing of Fe-S clusters. The aim of my thesis was to identify the disease causing gene of HML and to investigate the underlying disease-mechanisms. In paper I we identified a disease-critical region on chromosome 12; a region containing 16 genes. One of the genes coded for the Fe-S cluster assembly protein ISCU and an intronic base pair substitution (g.7044G>C) was identified in the last intron of this gene. The mutation gave rise to the insertion of intron sequence into the mRNA, leading to a protein containing 15 abberant amino acids and a premature stop. In paper II we investigated why a mutation in an evolutionary well conserved protein with a very important cellular role, which in addition is expressed in almost all tissues, gives rise to a muscle-restricted phenotype. Semi-quantitative RT-PCR analysis showed that the mutant transcript constituted almost 80% of total ISCU mRNA in muscle, while in both heart and liver the normal splice form was dominant. We could also show that, in mice, complete absence of Iscu protein was coupled with early embryonic death, further emphasizing the importance of the protein in all tissues. These data strongly suggested that tissue-specific splicing was the main mechanism responsible for the muscle-specific phenotype of HML. In paper III the splicing mechanisms that give rise to the mutant ISCU transcript was further investigated. We identified three proteins; PTBP1, IGF2BP1 and RBM39, that could bind to the region containing the mutation and could affect the splicing pattern of ISCU in an in vitro system. PTBP1 repressed the inclusion of the intronic sequence, while IGF2BP1 and RBM39 repressed the total ISCU mRNA level though the effect was more pronounced for the normal transcript. Moreover, IGF2BP1 and RBM39 were also able to reverse the effect of PTBP1. IGF2BP1, though not a splicing factor, had higher affinity for the mutant sequence. This suggested that the mutation enables IGF2BP1 binding, thereby preventing the PTBP1 induced repression seen in the normal case. In conclusion, we have determined the genetic cause of HML, identifying a base pair substitution in the last intron of the ISCU gene that gives rise to abnormally spliced transcript. The muscle-specific phenotype was also analyzed and tissue-specific splicing was identified as the main disease-mechanism. Furthermore, nuclear factors with ability to affect the splicing pattern of the mutant ISCU gene were identified. This work has thoroughly investigated the fundamental disease mechanisms, thus providing deeper understanding for this hereditary myopathy.
APA, Harvard, Vancouver, ISO, and other styles
4

Osler, Meg. "Associations of severe hyperlactataemia and lactic acidosis in HIV-infected patients receiving antiretroviral theraphy." Master's thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/7438.

Full text
Abstract:
Includes bibliographical references (leaves 67-70).
Severe symptomatic hyperlactataemia and lactic acidosis (SHLA) are life-threatening events that are occurring at increasing incidence levels in South Africa. Globally, the rise in SHLA cases is closely correlated to the increased accessibility of anti retroviral (ARV) medication for human immunodeficiency virus (HIV). Although hyperlactataemia and lactic acidosis were once thought of as rare conditions, they are now being recognized as important concerns when administering antiretroviral therapy. A better understanding of the risk factors for SHLA is important in combating the morbidity and mortality associated with such an adverse event.
APA, Harvard, Vancouver, ISO, and other styles
5

Nlooto, Manimbulu. "Effect of stavudine dosage reduction on the incidence of symptomatic hyperlactataemia/lactic acidosis in adults female HIV/AIDS infected patients treated at Dr George Mukhari Hospital." Thesis, University of Limpopo (Medunsa Campus), 2010. http://hdl.handle.net/10386/216.

Full text
Abstract:
Theses (Msc.(Med.)(Pharmacy))--University of Limpopo, 2010.
With the availability of Highly Active Antiretroviral Therapy (HAART), one of the limitations of treatment safety is the occurrence of adverse events associated with antiretroviral agents. The aim of this study was to establish whether stavudine dosage reduction prevents toxicity from developing and minimizes the incidence of symptomatic hyperlactataemia/lactic acidosis (LA) in adults female HIV/AIDS infected patients. This retrospective study covered adult patients treated at the adult ARV clinic, Dr George Mukhari Hospital. The records of 88 patients aged between 27 and 59 years, initiated and treated from August 2004 to January 2006, were analyzed ( 67 females and 21 males). Twenty nine females started their treatment on a regimen containing 40 mg stavudine while 38 females were started on 30 mg stavudine. A group of male patients (n=21) were included for comparison. Seven males started on 40 mg stavudine and 14 were on 30 mg stavudine. Ten out of twenty nine females who started treatment on 40 mg stavudine developed elevated lactate levels while nineteen received 30 mg stavudine as reduced dose. Eight out of nineteen further developed elevated lactate levels when on 30 mg stavudine but eleven out of nineteen remained stable on treatment with 30 mg stavudine as reduced dose. In the group started on 30 mg stavudine, thirteen females out of thirty seven developed elevated lactate levels while twenty four were stable on their treatment. Key words: stavudine, dosage reduction, lactate levels, hyperlactataemia, lactic acidosis.
APA, Harvard, Vancouver, ISO, and other styles
6

Maruta, Celso Akio. "Comparação da susceptibilidade de bovinos das raças Jersey e Gir à acidose láctica ruminal, induzida experimentalmente com sacarose." Universidade de São Paulo, 2000. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-24072007-082404/.

Full text
Abstract:
Foram utilizados neste experimento quatro garrotes Jersey (J) e quatro Gir (G), providos de cânula ruminal. Dois meses antes da indução da acidose láctica ruminal (ALR), os animais foram alimentados com dieta padronizada a base de feno e concentrado. A ALR foi induzida experimentalmente por meio da administração de sacarose intraruminal, correspondente ao peso metabólico corrigido, segundo técnica descrita por ORTOLANI (l995). Colheitas de sangue, suco de rúmen, urina, fezes e exames clínicos foram realizados nos seguintes momentos após a indução: zero, 14, 16, 18, 20, 22 e 24 horas. O pH e as concentrações de ácido láctico total, D e L e de seus sais foram determinados em todos os materiais biológicos colhidos. No sangue foram avaliados o hematócrito, os exames gasométricos e a concentração de creatinina; esta última substância também foi determinada na urina. Após a última colheita, todo o conteúdo ruminal foi completamente retirado para a determinaçãodo seu volume. Os bovinos de ambas as raças apresentaram marcante e idêntica acidose ruminal, não ocorrendo diferença no pH e na concentração de ácido láctico total, L e D no suco de rúmen. A acidose metabólica sistêmica foi moderada em ambas as raças, porém esta foi mais intensa nos bovinos J, confirmada pelas menores concentrações médias de bicarbonato e TCO2 (P < 0,00001) e pelo menor pH sangüíneo, (p < 0,025). Os garrotes J absorveram maiores quantidades de ácido láctico total e do isômero D; este último apresentou correlação negativa com o pH sangüíneo nesta raça (r = -O,78). Os garrotes G apresentaram maior capacidade homeostática de manutenção de pH sangüíneo no final da indução, provavelmente pela maior metabolização do lactato-L. Entretanto, os mesmos animais tiveram maior grau de desidratação, evidenciado pelas maiores porcentagens de hematócrito e de déficit de volume plasmático (p < 0,00001). Nessa raça ocorreu uma menor filtração glomerular, demonstrada pela maior concentração sérica de creatinina (p < 0,00001), menor depuração deste catabólito (p < 0,003) e menor volume urinário estimado (p < 0,05). Não ocorreram diferenças significativas no pH fecal entre as raças estudadas. Houve correlação negativa entre a concentração de lactato total fecal e o correspondente pH (r = - 0,65).
Four Jersey (J) and four Gir (G) rumen-cannulated steers were used. The steers were fed, for two months before the beginning of the rumen lactic acidosis (RLA) induction, a standard diet of hay and concentrates. The RLA was induced experimentally through the administration of sucrose into the rumen, according to the corrected metabolic weight, after ORTOLANI (1995). Blood, rumen fluid, urine, and fecal samples were collected and clinical examination carried out in the following times after the induction: zero, 14, 16, 18, 20, 22 and 24 hours. The pH, the total lactic acid and its L and D isomers were determined in all samples. The hematocrit, acid-base variables and the creatinine concentration were determined in the blood samples; creatinine was also determined in the urine samples. All the rumen content was evacuated in order to evaluate its volume at the 24th h. A intense rumen acidosis was reached; no differences in the rumen fluid pH and in the concentration of the total lactic acid and its isomers were found in both studied breeds. A moderate level of systemic metabolic acidosis was reached in both breeds, but lower overall mean of bicarbonate and TCO2 (p < 0.0001) as well as blood pH (p < 0.025) were found in the J steers. These steers absorbed higher amounts of total lactic and its D isomer than the G animals; the higher the blood D-lactate concentration, the lower the blood pH (r = - O.78) in the former breed. Better blood pH homeostasis were kept, at the end of induction, by the G steers, probably by their higher efficiency to metabolize L-lactate. However, the G steers exhibited a higher level of dehydration as seen by the greater hematocrit and plasma volume deficit (p < 0.00001). They also presented a lower glomerular filtration as evidenced by the higher creatinine serum levels (p < 0.00001), its lower urinary clearance (p < 0.003) and the lower estimated urinary volume (p < 0.05). There were no differences in the fecal pH values presented by both breeds. There was a negative correlation between the fecal total lactate concentration and the fecal pH (r = - 0.65).
APA, Harvard, Vancouver, ISO, and other styles
7

Rojas, Jesus Antonio. "Evaluation of the pH-stat modified approach for the treatment of non-respiratory (lactic) acidosis and vascular hyporeactivity caused by hemorrhagic shock in dogs." Columbus, Ohio : Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5fnum=osu1063035811.

Full text
Abstract:
Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xvi, 246 p.; also contains graphics. Includes abstract and vita. Advisor: William W. Muir, Dept. of Veterinary Clinical Sciences. Includes bibliographical references (p. 229-246).
APA, Harvard, Vancouver, ISO, and other styles
8

Rojas, Jesus Antonio Sr. "Evaluation of the pH-stat modified approach for the treatment of non-respiratory (lactic) acidosis and vascular hyporeactivity caused by hemorrhagic shock in dogs." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1063035811.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Sarti, Luís Marcelo Nave [UNESP]. "Efeito da suplementação com anticorpos policlonais e/ou monensina sódica sobre a saúde ruminal de bovinos jovens confinados." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/95211.

Full text
Abstract:
Made available in DSpace on 2014-06-11T19:27:28Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-06-12Bitstream added on 2014-06-13T19:15:02Z : No. of bitstreams: 1 sarti_lmn_me_botfmvz.pdf: 903641 bytes, checksum: 047f7d8f364a869975bf468d835307c3 (MD5)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Universidade Estadual Paulista (UNESP)
O objetivo deste estudo foi avaliar os efeitos dos anticorpos policlonais, preparados contra as bactérias ruminais Streptococcus bovis, Fusobacterium necrophorum, Lactobacillus e endotoxina, ou monensina sódica sobre perfil metabólico sanguíneo e variações na ingestão diária de matéria seca de bovinos jovens confinados com diferentes níveis de concentrado. Foram utilizados 72 animais Brangus, machos, não castrados, desmamados com nove meses de idade, com peso vivo médio inicial de 261,04 ± 34,73 kg divididos em 24 baias (3 animais/baia), com 6 repetições (baias) em cada tratamento. Todos os animais foram submetidos à mesma dieta (ad libitum), tipo de alojamento e manejo. As dietas apenas foram diferentes no tocante aos aditivos alimentares utilizados: controle (sem aditivo), monensina sódica - MON, anticorpos policlonais – PAP ou mistura de monensina sódica com anticorpos policlonais – MIX, estes, na forma de pó. O delineamento experimental foi inteiramente casualizado em arranjo fatorial 2 x 2 com medidas repetidas no tempo, sendo os fatores: inclusão ou não de monensina sódica e inclusão ou não de anticorpos policlonais. Medidas de tempo foram tomadas de acordo com o período: adaptação, crescimento e terminação. Os dados de gasometria foram avaliados após 21 dias do início de cada período. A ingestão e a variação diária de matéria seca (IDMS e VIDMS, respectivamente) foram obtidas nos quatro primeiros dias após mudança do período de adaptação para crescimento e de crescimento para terminação. Não houve efeito (P<0,05) de aditivos para IDMS e VIDMS, apenas interação entre período e os 4 dias para as duas variáveis, com maior IDMS no dia 3 seguido de queda no dia 4 durante o período de crescimento e VIDMS nos quatro dias após mudança de dieta. Durante a terminação houve menor IDMS no dia 2 mas não foi observado VIDMS nos quatro primeiros...
The aim of this study was to evaluate the effects of polyclonal antibodies preparation (PAP) or monensin (MON) against rumen bacteria (Streptococcus bovis, Fusobacterium necrophorum, Lactobacillus and endotoxin) on blood metabolic profile and variations in daily dry matter intake (DM) of feedlot cattle fed high concentrate diets. Seventy-two 9-mo-old bullocks (261.04 ± 34.73 kg) were housed in 24 pens (3 bullocks/pen) and assigned to a completely randomized with 2 x 2 factorial arrangement with 6 replications per treatment. All animals received the same diet (ad libitum), type of accommodation and management. The diets treatments were different only about feed additives used: control (no additive), MON, PAP or MON + PAP (MIX). Factors were inclusion or not of PAP or MON, at a dose of 300 mg/kg DM or at 30 mg/ kg DM, respectively. Measures over time were taken according to the phase: adaptation, growing and finishing. Blood samples were collected and evaluated after 21 days of the beginning of each phase. The intake and daily variation of dry matter (IDMS and VIDMS, respectively) were obtained in the first four days of each phase. There was no effect (P < 0.05) additive for IDMS and VIDMS, only interaction between phase and four days for both variables, with higher IDMS on day 3 and then decreased on day 4 during the growth phase and VIDMS during four days after changing the diet. During the finishing, IDMS was lower on day 2, but was not observed VIDMS the first four days after change of diet. PAP and MON treatments had higher blood pH compared to MIX, but not different from control. In the finishing phase was observed lower blood pH compared with other phases... (Complete abstract click electronic access below)
APA, Harvard, Vancouver, ISO, and other styles
10

Rafael, Arenas-Pinto A. "Studies on clinical and epidemiological factors associated with peripheral neuropathy and severe hyperlactatemia or lactic acidosis in HIV-infected adults exposed to nucleoside analogues reverse transcriptase inhibitors." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444011/.

Full text
Abstract:
Studies on mitochondrial dysfunction in HIV-infected adults exposed to anti-retroviral therapy. A significant proportion of HIV-infected patients who require anti-retroviral therapy are or have been exposed to nucleoside analogue reverse transcriptase inhibitors (NRTIs). It has been consistently suggested that most of the NRTI-attributed adverse drug reactions (ADR) are due to mitochondrial dysfunction. In a sub-analysis of a large randomised clinical trial (Delta) the incidence of peripheral neuropathy (PN) was constant over time in all study arms, which does not support the hypothesis of cumulative toxicity previously proposed for NRTI-induced ADR. Patients taking zidovudine (AZT)/zalcitabine (ddC) combination were more likely to develop PN than patients on AZT monotherapy (RH= 2.30 95%CI= 1.62 - 3.28). The incidence of PN among patients exposed to zidovudine/didanosine (AZT/ddl) combination was not different from that observed in patients on AZT. In a multi-centre case-control study including 110 cases of lactic acidosis (LA) or severe hyperlactataemia (HL) patients with < 200 CD4 cell/pl were more likely to develop HL/LA than patients with higher levels of CD4 cells (OR=3.44 95%CI= 1.64 - 7.22). Female patients were found to be at higher risk for HULA than men (OR= 4.75 95%CI= 1.96 - 11.53). Patients exposed to either d4T, ddl or the combination of these two were four to six times more likely to develop HL/LA than patients taking other NRTIs based combinations. Interestingly, cases of HL/LA were exposed to d4T for shorter periods of time than controls. Almost 10 % of the cases included in the study were asymptomatic at the time of diagnosis. All these symptom-free cases had blood lactate ranging between 5 and 7 mmol/l. Therefore, case definitions for HL or LA based on clinical presentation may underestimate the magnitude of the problem.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Lactic acidosis in ruminants"

1

Publications, ICON Health. Lactic Acidosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Janssen, Mirian C. H., and Shamima Rahman. Pyruvate Dehydrogenase Complex Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0006.

Full text
Abstract:
Pyruvate dehydrogenase complex (PDHc) deficiency usually first manifests at a young age and is rarely diagnosed in adulthood. The clinical picture varies from neonatal death with overwhelming lactic acidosis to a relatively benign course early in life. The three main presentations are congenital lactic acidosis, Leigh syndrome, and episodic ataxia. Treatment consists of a ketogenic diet and cofactor supplementation with thiamine. Successful therapy is rare.
APA, Harvard, Vancouver, ISO, and other styles
3

Neligan, Patrick J., and Clifford S. Deutschman. Management of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0256.

Full text
Abstract:
Metabolic acidosis (MA) commonly complicates critical illness, usually manifesting as a fall in arterial pH (<7.4) accompanied by a concomitant fall in serum bicarbonate concentration. Acidosis caused by unmeasured anions (UMA), can be distinguished from Hyperchloraemic acidosis by demonstrating a widening of the anion gap (AG). AG should be corrected for albumin and lactate. The base deficit (BD) calculates degree of metabolic acidosis and represents the amount of strong cation required to restore the pH to 7.4. Neither the AG nor the BD specify the cause of acidosis, and are unhelpful in the setting of mixed disorders. The base deficit gap (BDG) is used to calculate the effect of free water, sodium, chloride and albumin on the BD. It is the difference between BDcalc and BDmeasured (on a blood gas) and represents UMA. The strong ion gap more robustly calculates the amount of UMA than AG or BDG, and may be more accurate at predicting outcomes in the emergency room. Lactic acidosis is due to hypovolaemia until otherwise proven. In the majority of cases aggressive fluid resuscitation is warranted. In the presence of normal tissue blood flow regional hypoperfusion, poisoning or exogenous catecholamines should be considered. Ketoacidosis is due to intracellular glucose deficiency, caused by hypoinsulinaemia or starvation. The former is treated with isotonic crystalloid and insulin. Renal acidosis is treated with renal replacement therapy or recovery of renal function.
APA, Harvard, Vancouver, ISO, and other styles
4

Neligan, Patrick J., and Clifford S. Deutschman. Pathophysiology and causes of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0255.

Full text
Abstract:
Critical illness is typically characterized by changes in the balance of water and electrolytes in the extracellular space, resulting in the accumulation of anionic compounds that manifests as metabolic acidosis. Metabolic acidosis manifests with tachypnoea, tachycardia, vasodilatation, headache and a variety of other non-specific symptoms and signs. It is caused by a reduction in the strong ion difference (SID) or an increase in weak acid concentration (albumin or phosphate). Increased SID results from hyperchloraemia, haemodilution or accumulation of metabolic by-products. A reduction in SID results in a corresponding reduction is serum bicarbonate. There is a corresponding increase in alveolar ventilation and reduced PaCO2. Lactic acidosis results from increased lactate production or reduced clearance. Ketoacidosis is associated with reduced intracellular glucose availability for metabolism, and is associated with insulin deficiency and starvation. Hyperchloraemic acidosis is associated with excessive administration of isotonic saline solution, renal tubular acidosis and ureteric re-implantation. Renal acidosis is associated with hyperchloraemia, hyperphosphataemia, and the accumulation of medley nitrogenous waste products.
APA, Harvard, Vancouver, ISO, and other styles
5

Pereira, Luis F., Harold W. Goforth, Esteban Martínez, Joseph Z. Lux, Maria Ferrara, and Michael P. Mullen. Cardiovascular Disease, Metabolic Complications and Lipodystrophy in Persons with HIV. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0046.

Full text
Abstract:
The introduction of effective antiretroviral therapy has contributed to a dramatic reduction in HIV-related mortality. As patients live longer, evidence suggests an increased incidence of cardiovascular disease in persons with HIV over that among individuals who do not have HIV, thus early detection and treatment of multimorbidities and modifiable cardiovascular disease risk factors particularly in persons with HIV are needed. Several mechanisms have been proposed to explain the increased risk of cardiovascular disease, including the virus itself, antiretroviral therapy, and traditional risks factors. This chapter discusses detection and treatment of cardiovascular disease in persons with HIV, as well as metabolic complications involved, including dyslipidemia, insulin resistance, and lactic acidosis. The pathogenesis and management of HIV-associated lipodystrophy as well as its psychosocial impact are also addressed.
APA, Harvard, Vancouver, ISO, and other styles
6

D’Mello, Ajay. Mitochondrial Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0047.

Full text
Abstract:
Mitochondrial disease is now considered to be an important cause for a diverse range of neurological, muscular, cardiac and endocrine disorders. Initially thought to be a rare group of disorders, it is now increasingly common for children with mitochondrial disease to present for a surgical procedure. While the mitochondrial respiratory chain is the essential finally common pathway for aerobic metabolism, mitochondria also play a role in a several important cellular processes. A variety of anesthetic techniques have been successfully used for this group of patients. However, the possibility of complications due to inhibition of mitochondrial function by anesthetic agents and surgical stress is a worry for the physician managing these patients. Anesthetic management focuses on disease symptoms at presentation, maintaining normoglycemia, while preventing further metabolic stress and complications that worsen lactic acidosis.
APA, Harvard, Vancouver, ISO, and other styles
7

Sedel, Frédéric, and Carla E. M. Hollak. Disorders of Thiamine Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0028.

Full text
Abstract:
Thiamine is a water-soluble vitamin acting in the mitochondria as a cofactor for energy metabolism and, in the cytoplasm, in the pentose phosphate biosynthetic pathway. Its transport through the plasma membrane requires two transporters with overlapping functions: THTR1 encoded by SLC19A2, and THTR2 encoded by SLC19A3. Thiamine is transformed into its active form, thiamine pyrophosphate (TPP) by a kinase encoded by the TPK1 gene. Then it may enter the mitochondria through a TPP transporter encoded by SLC25A19. Mutations in SLC19A2 cause thiamine-responsive megaloblastic anemia (TRMA). Mutations in SLC19A3 cause biotin/thiamine–responsive basal ganglia disease. Mutations in SLC25A19 may cause early microcephaly with death in infancy (also called Amish microcephaly) or a later-onset bilateral striatal necrosis with progressive peripheral neuropathy. Recently, mutations in the TPK1 gene have been associated with recurrent encephalopathy with mild lactic acidosis.
APA, Harvard, Vancouver, ISO, and other styles
8

Tuxen, David V. Pathophysiology and causes of airflow limitation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0110.

Full text
Abstract:
Exacerbations of asthma or chronic obstructive pulmonary disease (COPD) can be life-threatening emergencies, and require careful management to minimize the risks of morbidity and mortality. Prompt, full bronchodilator therapy, careful observation and appropriate mechanical ventilation technique is required. Dynamic hyperinflation of the lungs occurs in all patients, and must be careful assessed and regulated. Excessive dynamic hyperinflation can result in respiratory tamponade, hypotension, circulatory failure, pneumothoraces and, in severe cases, cardiac arrest. Intravenous or continuous nebulized salbutamol commonly causes lactic acidosis that should be detected and managed. Prolonged paralysis during difficult mechanical ventilation can result in severe necrotizing myopathy. Pneumothoraces in ventilated patients with asthma are usually under tension, redistribute ventilation to the contralateral lung, and risk a second tension pneumothorax. Patients surviving mechanical ventilation for asthma and COPD have an increased risk of recurrence and death. All these problems require awareness, avoidance or detection and management
APA, Harvard, Vancouver, ISO, and other styles
9

Bower, Mark, Louise Robinson, and Sarah Cox. Endocrine and metabolic complications of advanced cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0142.

Full text
Abstract:
Cancer produces endocrine and metabolic complications in two ways. Firstly, the primary tumour or its metastases may interfere with the function of endocrine glands, kidneys, or liver by invasion or obstruction. Secondly, tumours may give rise to remote effects without local spread and these actions are termed paraneoplastic manifestations of malignancy. Generally, these paraneoplastic syndromes arise from secretion by tumours of hormones, cytokines, and growth factors, but also occur when normal cells secrete products in response to the presence of tumour. This chapter reviews the pathogenesis, epidemiology, and management of the commonest paraneoplastic endocrinopathies including hypercalcaemia, Cushing’s syndrome, the syndrome of inappropriate antidiuresis, non-islet cell tumour hypoglycaemia, enteropancreatic hormone syndromes, Carcinoid syndrome, phaeochromocytoma, gonadotrophin secretion syndromes, prolactin and oxytocin secretion, and paraneoplastic pyrexia. The chapter concludes with a brief discussion of the management of metabolic disease in the context of advanced malignancy including hyperglycaemia, thyroid dysfunction, metabolic bone disease, renal failure, liver failure, and lactic acidosis.
APA, Harvard, Vancouver, ISO, and other styles
10

Staitieh, Bashar S., and Greg S. Martin. Therapeutic goals of fluid resuscitation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0070.

Full text
Abstract:
Optimizing tissue perfusion by administering intravenous fluids presents a special challenge to the intensive care unit (ICU) clinician. Recent studies have drastically altered how we assess a patient’s fluid responsiveness, particularly with regard to upstream surrogates of tissue perfusion. Central venous pressure and pulmonary capillary wedge pressure have been found to be inaccurate markers of fluid responsiveness and have given way to methods such as cardiac output as assessed by echocardiography and the various forms of arterial waveform analysis. These newer techniques, such as stroke volume variation, systolic pressure variation, and pulse pressure variation, have been found to better delineate which patients will respond to a fluid challenge with an increase in cardiac output, and which will not. In addition, traditional methods of assessing the consequences of excessive fluid administration, such as pulmonary oedema and the non-anion gap acidosis of saline administration, have given way to more sophisticated measurements of extravascular lung water, now available at the bedside. Downstream markers of tissue perfusion, such as base deficit, central venous oxygen saturations, and lactic acid, continue to be useful in particular clinical settings, but are all relatively non-specific markers, and are therefore difficult to use as resuscitation targets for ICU patients in general. Finally, recent data on septic shock and ARDS have demonstrated the importance of conservative fluid strategies, while data in surgical populations have emphasized the need for judicious fluid administration and attention to the balance of blood products used in resuscitation efforts.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Lactic acidosis in ruminants"

1

Hutton, Peter G., T. G. Nagaraja, Colin L. White, and Philip E. Vercoe. "Screening Plants for the Antimicrobial Control of Lactic Acidosis in Ruminant Livestock." In In vitro screening of plant resources for extra-nutritional attributes in ruminants: nuclear and related methodologies, 159–89. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3297-3_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Backer, Daniel De. "Lactic acidosis." In Applied Physiology in Intensive Care Medicine, 89–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01769-8_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

De Backer, Daniel. "Lactic acidosis." In Applied Physiology in Intensive Care Medicine, 69–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-37363-2_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Perret, Cl. "Lactic Acidosis." In Update in Intensive Care and Emergency Medicine, 287–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70309-6_60.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Reddi, Alluru S. "Lactic Acidosis." In Acid-Base Disorders, 63–83. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28895-2_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Schmidt, G. A. "Lactic Acidosis." In Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E., 695–705. Milano: Springer Milan, 2002. http://dx.doi.org/10.1007/978-88-470-2099-3_58.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

De Backer, Daniel. "Lactic acidosis." In Applied Physiology in Intensive Care Medicine 1, 111–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28270-6_25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Levy, B. "Lactic Acidosis and Hyperlactatemia." In Yearbook of Intensive Care and Emergency Medicine, 88–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-33396-7_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Lalau, Jean-Daniel. "Metformin and Lactic Acidosis." In Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants, 559–61. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119329725.ch37.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Tentolouris, Nikolaos, and Nikolaos Katsilambros. "Lactic Acidosis in Diabetes." In Diabetic Emergencies, 133–47. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119971825.ch6.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Lactic acidosis in ruminants"

1

Raoof, S. "Metformin Associated Lactic Acidosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4805.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Tsay, Junchieh J., Derrick Raptis, and David R. Schwartz. "Lactic Acidosis In Metastatic Melanoma." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4609.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ganta, Ashwin, Ratna Priya Gangi, Wilson Gonsalves, Sonica Saini, and Tammy Wichman. "Inhalational Beta Agonist Induced Lactic Acidosis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1343.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Hamarshi, Majdi. "Severe Lactic Acidosis In A Hemodynamically Stable Patient." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3177.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sharma, N., D. C. Kazmierski, S. Li, and P. O. Ochieng. "The Occult Culprit: Lactic Acidosis Due to Corticosteroids." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2908.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Annan, Dorcas A., Nako Maishi, Tomoyoshi Soga, Randa Dawood, Yasuhiro Hida, and Kyoko Hida. "Abstract 2054: Tumor endothelial cells survive under lactic acidosis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2054.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Khan, A. A., F. Chaudhary, and S. Sarkar. "Metformin Induced Lactic Acidosis - A Rare but Treatable Entity." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1740.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ahmed, R., W. Illyas, and Y. Hiltzik. "Profound Lactic Acidosis from Metformin Toxicity Confounded by Septic Shock." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5179.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Soni, P., V. Ponnusamy, S. Sharma, A. Sinha, C. Seneviratne, and Y. Kupfer. "A Case of Severe Lactic Acidosis Due to Metformin Toxicity." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4849.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Price, J. D., and K. El-Kersh. "Thyroid Storm Presenting with Multiorgan Failure and Severe Lactic Acidosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1712.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Lactic acidosis in ruminants"

1

Rodriquez, Fernando, Mark A. Rasmussen, and Milton J. Allison. Discovery of a Probiotic to Reduce the Risk of Lactic Acidosis in Cattle. Ames (Iowa): Iowa State University, January 2007. http://dx.doi.org/10.31274/ans_air-180814-563.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Lactic acidosis in ruminants' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography