FREE SHIPPING over $40
OVER 9000 FIVE-STAR REVIEWS
5% OFF ALL SUBSCRIPTIONS
100% HAPPINESS GUARANTEE
Analyze Diet
0
Home / Equine Research Bank / Acta Vet Scand / Acute rhabdomyolysis (“tying-up”) in standardbre...
Acta veterinaria Scandinavica1974; 15(3); 325-339; doi: 10.1186/BF03547462

Acute rhabdomyolysis (“tying-up”) in standardbred horses. A morphological and biochemical study.

Abstract: LINDHOLM, A., H.-E. JOHANSSON & P. KJÆRSGAARD: Acute rhabdomyolysis (“tying-up”) in standardbred horses. A morphological and biochemical study. Acta vet. scand. 1974, 15, 325–339. — Morphological, biochemical and histochemical changes were studied in muscle needle biopsy specimens (gluteus medius) from 59 standardbred trotters with acute clinical symptoms of the “tying-up” disease. All horses had increased levels of serum enzymes SGOT and SCPK. The biopsy specimens were taken at various intervals after onset of clinical symptoms (1–4 hrs., 18–24 hrs. and 2–20 days). Ry light microscopy it was shown that the muscular alterations had a focal distribution and were of the hyalin degeneration type with insignificant inflammatory reaction and slight calcification. The ultrastructural changes apparently commenced with myofibrillar waving, mitochondrial and sarcotubular alterations and terminated with myofibrillar degeneration and necrosis with invasion of inflammatory cells. The inflammatory cells were ultrastructurally similar to monocytes and macrophages. The degenerative changes mainly comprised fast twitch (FT and FTH) fibres as histochemically evidenced by myofibrillar ATPase and alkaline phosphatase staining. Riopsies from diseased muscle 1–4 hrs. after the onset of “tyingup” contained a low muscle concentration of glycogen, ATP and CP and a high concentration of lactate and glucose. Hence it is suggested that the described muscular alterations may be caused by a deranged carbohydrate metabolism caused by a local hypoxia. It was found that the “tying-up” disease resembled idiopathic rhabdomyolysis in man and was thus designated “equine rhabdomyolysis”. histochemistry; horse; rhabdomyolysis; skeletal muscle; “tying-up”; ultrastructure. Akut rhabdomyolys (korsförlamning) hos travhästar. En morfologisk och biokemisk undersökning. Morfologiska, biokemiska och histokemiska metoder användes för att studera förändringarna i muskelbiopsier, uttagna från m. gluteus médius från 59 varmblodiga travhästar med akuta kliniska symtom på sk “tying-up”. Samtliga bästar hade förhöjda serumvärden av enzymerna SGOT och SCPK. Biopsierna togs vid olika tidpunkter efter de kliniska symtomens insättande (1–4 tim., 18–24 tim. respektive 2–20 dagar). Ljusmikroskopiskt (LM) visades att muskelförändringarna hade en härdformig utbredning och att de var av typen hyalin degeneration med viss inflammatorisk reaktion och liten tendens till förkalkning. De ultrastrukturella förändringarna manifesterades först sàsom en vågighet av myofibrillerna och med förändringar i mitokondrier samt det sarkotubulära systemet. Senare utvecklades myofibrillär degeneration och nekros med invandring av inflammatoriska celler. De inflammatoriska cellerna liknade ultrastrukturellt monocyter och makrofager. De degenerativa förändringarna uppträdde huvudsakligen i de snabba fibrerna (FT och FTH), vilket kunde visas histokemiskt med myofibrillär ATPas- och alkalisk fosfatas-färgning. Muskelbiopsier uttagna 1–4 tim. efter de akuta symtomens insättande hade låg koncentration av glykogen, ATP och GP medan en hög koncentration av laktat och glykos förelåg. Mot denna bakgrund anses att de iakttagna muskelförändringarna orsakats av en störd kolhydratmetabolism, som i sin tur kan ha orsakats av en lokal hypoxi. Då muskelförändringarna vid “tying-up” liknar dem vid idiopatisk rhabdomyolysis hos människa, föreslår författarna att namnet “equine rhabdomyolysis” fortsättningsvis används för denna sjukdom.
Get Full Text
Publication Date: 1974-01-01 PubMed ID: 4411856PubMed Central: PMC8407238DOI: 10.1186/BF03547462Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
LinkedInCopy
  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This study examined the morphological and biochemical changes in the muscles of standardbred horses experiencing acute symptoms of “tying-up” disease, also known as equine rhabdomyolysis. The resulting data suggests that the muscle alterations seen in afflicted horses may be due to a disrupted carbohydrate metabolism caused by localized hypoxia.

Methods and study subjects

  • The study involved observing changes in muscle needle biopsy specimens from the gluteus medius muscle of 59 standardbred trotters showing acute clinical symptoms of “tying-up” disease.
  • The biopsies were conducted at various periods after the onset of clinical symptoms: 1–4 hrs., 18–24 hrs., and 2–20 days.
  • All horses included presented elevated levels of two serum enzymes, SGOT and SCPK, which are often found in higher concentrations in the bloodstream when muscle or liver damage occurs.

Observations and findings

  • The researchers found that muscle alterations exhibited a focal distribution and were identified as hyalin degeneration type with insignificant inflammatory reaction and slight calcification.
  • Microscopic observations indicated that the ultrastructural changes commenced with myofibrillar waving and alterations in the mitochondria and sarcotubules, evolving into myofibrillar degeneration and necrosis with the invasion of inflammatory cells.
  • The inflammatory cells were similar to monocytes and macrophages in their ultrastructure.
  • The observed degenerative changes predominantly affected fast twitch (FT and FTH) fibers, which was evidenced by myofibrillar ATPase and alkaline phosphatase staining.

Biochemical analysis

  • Biopsies from diseased muscle 1–4 hrs. after the onset of “tying-up” contained a low muscle concentration of glycogen, ATP and GP, contrasted with a high concentration of lactate and glucose.
  • The researchers suggested that the muscle alterations observed may be due to a deranged carbohydrate metabolism caused by local hypoxia (low oxygen).
  • The “tying-up” disease showed similarities to idiopathic rhabdomyolysis in humans, leading to the suggestion of the term “equine rhabdomyolysis” for this disease.

Cite This Article

APA
Lindholm A, Johansson HE, Kjaersgaard P. (1974). Acute rhabdomyolysis (“tying-up”) in standardbred horses. A morphological and biochemical study. Acta Vet Scand, 15(3), 325-339. https://doi.org/10.1186/BF03547462

Publication

Acta veterinaria Scandinavica
ISSN: 0044-605X
NlmUniqueID: 0370400
Country: England
Language: English
Volume: 15
Issue: 3
Pages: 325-339

Researcher Affiliations

Lindholm, A
    Johansson, H E
      Kjaersgaard, P

        MeSH Terms

        • Acute Disease
        • Adenosine Triphosphate / metabolism
        • Animals
        • Aspartate Aminotransferases / blood
        • Biopsy, Needle / veterinary
        • Creatine Kinase / blood
        • Female
        • Gait
        • Glucose / metabolism
        • Glucosephosphates / metabolism
        • Horse Diseases / metabolism
        • Horse Diseases / pathology
        • Horses
        • Lactates / metabolism
        • Male
        • Methods
        • Microscopy, Electron
        • Muscles / metabolism
        • Muscles / pathology
        • Myoglobinuria / metabolism
        • Myoglobinuria / pathology
        • Myoglobinuria / veterinary
        • Phosphocreatine / metabolism
        • Time Factors

        References

        This article includes 31 references
        1. Afifi A K, Bergman R A, Harvey J C. Steroid myopathy. Clinical, histologic and cytologic observations.. Johns Hopk. Med. J. 1968;123:158–174.
          pubmed: 5681186
        2. Cardinet G H, Littrell J F, Freedland R A. Comparative investigations of serum creatine phosphokinase and glutamic-oxalacetic transaminase activities in equine paralytic myoglobinuria.. Res. vet. Sci. 1967, 8, 219–226.
          pubmed: 6068600
        3. Carlström B. Über die Àtiologie und Pathogenese der Kreuzlähme des Pferdes (Haemoglobinaemia paralytica) The etiology and pathogenesis in horses with haemoglobinaemia paralytica).. Skand. Arch. Physiol. 1931;62:1–69.
        4. Carlström B. Über die Ätiologie und Pathogenese der Kreuzlähme des Pferdes (Haemoglobinaemia paralytica) (The etiology and pathogenesis in horses with haemoglobinaemia paralytica).. Skand. Arch. Physiol. 1932;63:164–212.
        5. De la Iglesia F A, Lumb G. Ultrastructural circulatory alterations of the myocardium in experimental coronary artery narrowing.. Lab. Invest. 1972;27:17–31.
          pubmed: 5034390
        6. Engel W K, Cunningham G G J. Alkaline phosphatase positive abnormal muscle fibers of humans.. J. Histochem. Cytochem. 1970;18:55.
          doi: 10.1177/18.1.55pubmed: 5415691google scholar: lookup
        7. Gomori B. Microtechnical demonstration of phosphatase in tissue sections.. Proc. Soc. exp. Biol. (N.Y.) 1939;42:23–26.
          doi: 10.3181/00379727-42-10786google scholar: lookup
        8. Jennings R B, Baum J H, Herdson P B. Fine structural changes in myocardial ischemic injury.. Arch. Path. 1965;79:135–143.
          pubmed: 14232929
        9. Jennings R B, Herdson P B, Sommers H M. Structural and functional abnormalities in mitochondria isolated from ischemic dog myocardium.. Lab. Invest. 1969;20:548–566.
          pubmed: 4306675
        10. Jubb K V F, Kennedy P C. Pathology of domestic animals. Vol. 2.. Acad. Press, New York and London 1963.
        11. Karlsson J, Diamant B, Saltin B. Muscle metabolites during sub-maximal and maximal exercise in man.. Scand. J. clin. Lab. Invest. 1970;26:385–394.
          doi: 10.3109/00365517009046250pubmed: 5486403google scholar: lookup
        12. Kontos H A, Harley E L, Wasserman A J, Kelly J J, Magee J H. Exertional idiopathic paroxysmal myoglobinuria. Evidence for a defect in skeletal muscle metabolism.. Amer. J. Med. 1963;35:283–292.
          pubmed: 14060030
        13. Kuby S A, Noda L, Hardy H A. Adenosine phosphate – creatine transphosphorylase. I. Isolation of the crystalline enzyme from rabbit muscle.. J. biol. Chem. 1954;209:191–201.
          pubmed: 13192073
        14. Lindholm A. Korsförlamning och serumenzymer hos travhästar. (“Tying-up” and serum enzymes in standardbred trotters).. Svensk Vet.-Tidn. 1972, 24, 871–897.
        15. Lindholm A. The possible relationship between corticosteroid treatment and acute rhabdomyolysis (“tying-up”) in standardbred trotters.. Nord. Vet.-Med. 1974. In press.
        16. Lindholm A, Piehl K. Fibre composition, enzyme activity and concentrations of metabolites and electrolytes in muscles of standardbred horses.. Acta vet. scand. 1974;15:287–303.
          pmc: PMC8407315pubmed: 4137664
        17. Linnarsson D, Karlsson J, Fagréus L, Saltin B. Muscle metabolites and oxygen deficit with exercise in hypo- and hyperoxia.. J. appl. Physiol. 1974. In press.
          pubmed: 4820319
        18. Mair W G P, Tomé F M S. Atlas at the ultrastructure of diseased human muscle.. Churchill Livingstone, Edinburgh and London 1972.
        19. McLean J G. Equine paralytic myoglobinuria (“Azoturia”) : A review.. Aust. vet. J. 1973, 49, 41–43.
          pubmed: 4570243
        20. Meginnis P. Myositis (Tying up) in race horses.. J. Amer. vet. med. Ass. 1957;130:237–239.
          pubmed: 13416094
        21. Novikoff A B, Shin W, Drucker J. Mitochondrial localisation of oxidative enzymes: staining results with two tetrazolium salts.. J. biophys. biochem. Cytol. 1961;9:47–61.
          doi: 10.1083/jcb.9.1.47pmc: PMC2224971pubmed: 13729759google scholar: lookup
        22. Okinaka S, Kumagi H, Ebashi S, Sugita H, Momoi H, Toyokura Y, Fujie Y. Serum creatine phosphokinase.. Arch. Neurol. (Chic.) 1961;4:520–525.
          doi: 10.1001/archneur.1961.00450110050006pubmed: 13730599google scholar: lookup
        23. Padykula H A, Herman E. The specificity of the histochemical method of adenosine triphosphatase.. J. Histochem. Cytochem. 1955;3:170–195.
          doi: 10.1177/3.3.170pubmed: 14381606google scholar: lookup
        24. Reitman S, Frankel S. A colormetric method for the determination of serum glutamic and glutamicpyruvic transaminases.. Amer. J. Path. 1957;28:56–63.
          doi: 10.1093/ajcp/28.1.56pubmed: 13458125google scholar: lookup
        25. Reznik M. Origin of myoblasts during skeletal muscle regeneration. Electron microscopic observations.. Lab. Invest. 1969;20:353–363.
          pubmed: 5776329
        26. Savage D C L, Forbes M, Pearce G W. Idiopathic rhabdomyolysis.. Arch. Dis. Childh. 1971;46:594–607.
          doi: 10.1136/adc.46.249.594pmc: PMC1647832pubmed: 4107384google scholar: lookup
        27. Scarpelli D G, Greider M H, Frajola W J. Idiopathic recurrent rhabdomyolysis. A clinical, chemical and morphological study.. Amer. J. Med. 1963;34:426–433.
          pubmed: 13976533
        28. Schutta H S, Kelly A M, Sacks S I. Necrosis and regeneration of muscle in paroxysmal idiopathic myoglobinuria: Electron microscopic observations.. Brain. 1969;92:191–202.
          doi: 10.1093/brain/92.1.191pubmed: 5774027google scholar: lookup
        29. Smith B. Histological and histochemical changes in the muscle of rabbits given the corticosteroid triamcinolone.. Neurology (Minneap.) 1964;14:857–863.
          doi: 10.1212/WNL.14.9.857pubmed: 14215603google scholar: lookup
        30. Smith H A, Jones T C. Veterinary Pathology. 3rd Ed.. Lea and Febiger, Philadelphia 1966.
        31. Stenger R J, Spiro D, Scully R E, Shannon J M. Ultrastructural and physiologic alterations in ischemic skeletal muscle.. Amer. J. Path. 1962;40:1–19.
          pmc: PMC1949565pubmed: 13916833

        Citations

        This article has been cited 5 times.
        1. El-Deeb WM, El-Bahr SM. Investigation of selected biochemical indicators of Equine Rhabdomyolysis in Arabian horses: pro-inflammatory cytokines and oxidative stress markers. Vet Res Commun 2010 Dec;34(8):677-89.
          doi: 10.1007/s11259-010-9439-5pubmed: 20830520google scholar: lookup
        2. Isgren CM, Upjohn MM, Fernandez-Fuente M, Massey C, Pollott G, Verheyen KL, Piercy RJ. Epidemiology of exertional rhabdomyolysis susceptibility in standardbred horses reveals associated risk factors and underlying enhanced performance. PLoS One 2010 Jul 14;5(7):e11594.
          doi: 10.1371/journal.pone.0011594pubmed: 20644724google scholar: lookup
        3. Friend SC. Postanesthetic myonecrosis in horses. Can Vet J 1981 Dec;22(12):367-71.
          pubmed: 7337914
        4. Armstrong RB. Muscle damage and endurance events. Sports Med 1986 Sep-Oct;3(5):370-81.
          doi: 10.2165/00007256-198603050-00006pubmed: 3529285google scholar: lookup
        5. Van Vleet JF, Ferrans VJ. Myocardial diseases of animals. Am J Pathol 1986 Jul;124(1):98-178.
          pubmed: 3524254
        Subscribe to our newsletter
        Join 99,357 horse owners like you who receive our email updates on horse health and nutrition.