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Contribution of whole blood L-lactate, pyruvate, D-lactate, acetoacetate, and 3-hydroxybutyrate concentrations to the plasma anion gap in horses with intestinal disorders.

Abstract: Increased anion gap (AG) was due, in part, to L-lactic acidosis in 14 of 14 horses with intestinal disorders. In a few horses, increased whole blood concentrations of D-lactate made a minor contribution to the AG. However, the increase in AG was often greater than the sum of the increases in these 2 acid anions. This unexplained increase was not a result of increases in whole blood pyruvate, 3-hydroxybutyrate, or acetoacetate concentrations or serum albumin or phosphate concentrations. Identification of other anions causing increased AG could lead to better understanding, diagnosis, and treatment of metabolic imbalances in critically ill horses.
Publication Date: 1987-01-01 PubMed ID: 3826846
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research investigates what contributes to the increased anion gap (AG) — a measure of acid-base balance — in horses with intestinal problems, finding L-lactic acidosis as a significant factor in all examined cases, with other elements like D-lactate providing a minor but noteworthy contribution in some.

Overview

The study focuses on testing various possible contributors to an elevated anion gap (AG) in horses with intestinal disorders. An AG is a calculation used in medicine to help identify the cause of a patient’s acid-base imbalance. In this situation, horses were used as the patient model, and different substances present in their blood were measured to see which had a significant impact on the AG.

Main Findings

  • The primary finding was L-lactic acidosis which was responsible for an increased AG in every single of the 14 horses studied. L-lactic acidosis refers to an elevated level of L-lactate, a form of lactic acid, in the body. In horses with intestinal disorders, their bodies produce more lactic acid as a byproduct of the body’s energy production processes. This excessive accumulation acidifies the body’s internal environment, thereby increasing the AG.
  • In a few instances, an increase in the concentration of D-lactate in the whole blood also contributed to the AG. D-lactate is another form of lactic acid which is produced by bacterial fermentation in the colon and can be absorbed into the blood.

Other Element Findings

  • The increase in AG often surpassed the combined increases in L-lactate and D-lactate — which cannot be attributed to other measured elements like pyruvate, 3-hydroxybutyrate, acetoacetate, serum albumin, or phosphate. Pyruvate, 3-hydroxybutyrate, and acetoacetate play critical roles in the body’s energy metabolism processes, while serum albumin and phosphate help in maintaining the body’s acid-base balance.
  • With the data collected, the research team suggests that unidentified ions could be contributing to the increased AG, and their identification could enhance the understanding, diagnosis, and treatment of metabolic imbalances in critically ill horses.

Cite This Article

APA
Gossett KA, Cleghorn B, Adams R, Church GE, McCoy DJ, Carakostas MC, Flory W. (1987). Contribution of whole blood L-lactate, pyruvate, D-lactate, acetoacetate, and 3-hydroxybutyrate concentrations to the plasma anion gap in horses with intestinal disorders. Am J Vet Res, 48(1), 72-75.

Publication

ISSN: 0002-9645
NlmUniqueID: 0375011
Country: United States
Language: English
Volume: 48
Issue: 1
Pages: 72-75

Researcher Affiliations

Gossett, K A
    Cleghorn, B
      Adams, R
        Church, G E
          McCoy, D J
            Carakostas, M C
              Flory, W

                MeSH Terms

                • 3-Hydroxybutyric Acid
                • Acetoacetates / blood
                • Acid-Base Equilibrium
                • Animals
                • Horse Diseases / blood
                • Horses
                • Hydroxybutyrates / blood
                • Intestinal Diseases / blood
                • Intestinal Diseases / veterinary
                • Lactates / blood

                Citations

                This article has been cited 6 times.
                1. Gomez DE, Biermann NM, Sanchez LC. Physicochemical Approach to Determine the Mechanism for Acid-Base Disorders in 793 Hospitalized Foals. J Vet Intern Med 2015 Sep-Oct;29(5):1395-402.
                  doi: 10.1111/jvim.13590pubmed: 26256847google scholar: lookup
                2. Forni LG, McKinnon W, Hilton PJ. Unmeasured anions in metabolic acidosis: unravelling the mystery. Crit Care 2006;10(4):220.
                  doi: 10.1186/cc4954pubmed: 16879718google scholar: lookup
                3. Nappert G, Johnson PJ. Determination of the acid-base status in 50 horses admitted with colic between December 1998 and May 1999. Can Vet J 2001 Sep;42(9):703-7.
                  pubmed: 11565369
                4. Moore RM, Muir WW, Rush BR. Systemic and colonic venous plasma biochemical alterations in horses during low-flow ischemia and reperfusion of the large colon. Can J Vet Res 1998 Jan;62(1):14-20.
                  pubmed: 9442934
                5. Pascoe PJ, Ducharme NG, Ducharme GR, Lumsden JH. A computer-derived protocol using recursive partitioning to aid in estimating prognosis of horses with abdominal pain in referral hospitals. Can J Vet Res 1990 Jun;54(3):373-8.
                  pubmed: 2199007
                6. Giraldo AF, Carballo R, Serrenho RC, Tran V, Valverde A, Renaud DL, Gomez DE. Association of the type of metabolic acidosis and non-survival of horses with colitis. Can Vet J 2023 Nov;64(11):1044-1050.
                  pubmed: 37915775