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Acta veterinaria Scandinavica1986; 27(4); 548-559; doi: 10.1186/BF03548134

The use of atropine to control heart rate responses during detomidine sedation in horses.

Abstract: Detomidine is a sedative-analgesic which has a pharmacological profile similar to xylazine. There is evidence that the sedative effects are mediated through alpha-2 adrenoceptors. Cardiopulmonary responses were determined using detomidine as the principal agent and as a preanesthetic prior to the induction of general anesthesia. Compatibility with guaifenesin, sodium thia-mylal and halothane were determined. As in the case of xylazine, detomidine produces a slowing of heart rates. This was found to be either sinus bradycardia or heart block. There may be a corresponding increase in systolic blood pressures. The respiratory pattern is altered through the arterial blood gases and pH data supported evidence of adequate ventilation. The heart rate response to detomidine without anticholinergic treatment was transient and related to he duration of drug action. Atropine sulfate, 0.02 mg/kg i.v. was effective in preventing or treating bradycardia or heart block from detomidine. Heart rates also increased during the administration of guaifenesin and sodium thia-mylal when given 50 min poisit-detomidine. Detomidin är ett sedativt analgetikum med en farmakologisk profil lik xylazinets. De sedativa effekterna medieras uppenbarligen genom alfa-2 adrenoreceptorer. De kardiopulmonära effekterna av detomidin studerades med detomidin som den principiella faktorn och som ett preanestetikum före induktion av allmän anestesi med guaifenesin, natrium thiamylal och halotan. I likhet med xylazin förorsakar detomidin bradykardi, vilken befanns vare antingen sinus-bradykardi eller hjärtblock. En motsvarande ökning i systoliskt blodtryck kan inträffa. Respirationen kan vara förändrad även om arteriella blodgaser och pH tyder på adekvat ventilation. Effekten på hjärtfrekvensen av detomidin utan antikolinergisk behandling var tillfällig och berodde på längden av detomidinets verkan. Intravenös applicering av atropinsulfat, 0,02 mg/kg, förhindrade effektivt den av detomidin förorsakade bradykardin eller hjärtblocket. Hjärtfrekvensen ökade också efter administrering av guaifenesin och natrium thiamylal 30 min efter detomidin.
Publication Date: 1986-01-01 PubMed ID: 3604828PubMed Central: PMC8189396DOI: 10.1186/BF03548134Google Scholar: Lookup
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  • Journal Article

Summary

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This research studies the effects of detomidine, a sedative-analgesic similar to xylazine, in slowing horse heart rates, and the role of atropine in controlling this response.

About the Research

  • Detomidine is a sedative-analgesic drug often used in veterinary medicine. It has effects similar to xylazine, notably in the way it affects heart rate.
  • This study focuses on understanding the cardiopulmonary responses brought about by the use of detomidine in horses.
  • The research also looks into detomidine’s use as a preanesthetic prior to general anesthesia and its compatibility with other drugs such as guaifenesin, sodium thia-mylal, and halothane.

Key Findings

  • One of the findings is that detomidine slows down the heart rate in horses, either by producing sinus bradycardia (slowing of normal heartbeat) or heart block (interruption of electrical signal flow from upper to lower chambers of the heart).
  • Detomidine can also cause an increase in systolic blood pressure, and potentially affect the respiratory pattern, despite evidence suggesting adequate ventilation.
  • This altered heart rate response to detomidine is transient and is related to the duration of the drug’s action in the body.

The Role of Atropine

  • Atropine sulfate, injected intravenously at a dosage of 0.02 mg/kg, proved effective in either preventing or treating the bradycardia or heart block induced by detomidine.
  • Moreover, heart rates were found to increase during the administration of guaifenesin and sodium thia-mylal given 50 minutes post-detomidine.

Significance of the Study

  • These findings are important as they provide a better understanding of how detomidine impacts the heart rates of horses, offering insights into how its adverse effects can be controlled and minimized.
  • Understanding the role of atropine in effectively preventing or treating heart rate alterations caused by detomidine could be beneficial in the safe use of these drugs in veterinary medicine.

Cite This Article

APA
Short CE, Stauffer JL, Goldberg G, Vainio O. (1986). The use of atropine to control heart rate responses during detomidine sedation in horses. Acta Vet Scand, 27(4), 548-559. https://doi.org/10.1186/BF03548134

Publication

ISSN: 0044-605X
NlmUniqueID: 0370400
Country: England
Language: English
Volume: 27
Issue: 4
Pages: 548-559

Researcher Affiliations

Short, C E
    Stauffer, J L
      Goldberg, G
        Vainio, O

          MeSH Terms

          • Animals
          • Atropine / pharmacology
          • Drug Interactions
          • Female
          • Heart Rate / drug effects
          • Horses / physiology
          • Hypnotics and Sedatives / pharmacology
          • Imidazoles / pharmacology

          References

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          Citations

          This article has been cited 4 times.
          1. Jones DL. Clinical effects of detomidine with or without atropine used for arthrocentesis in horses. Can Vet J 1993 May;34(5):296-300.
            pubmed: 17424223
          2. Sinclair MD. A review of the physiological effects of alpha2-agonists related to the clinical use of medetomidine in small animal practice. Can Vet J 2003 Nov;44(11):885-97.
            pubmed: 14664351
          3. Gasthuys F, De Moor A, Parmentier D. Haemodynamic changes during sedation in ponies. Vet Res Commun 1990;14(4):309-27.
            doi: 10.1007/BF00350713pubmed: 2392824google scholar: lookup
          4. Gasthuys F, Parmentier D, Goossens L, De Moor A. A preliminary study on the effects of atropine sulphate on bradycardia and heart blocks during romifidine sedation in the horse. Vet Res Commun 1990;14(6):489-502.
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