Atipamezole Reverses Cardiovascular Changes Induced by High-Dose Medetomidine in Cats Undergoing Sedation for Semen Collection

Abstract

This study aimed at describing the change in echocardiographic variables after high-dose medetomidine and the reversal with atipamezole in six cats undergoing sedation for semen collection. Further cardiac Troponin I (cTnI) concentration and the effect of repeated sedation were assessed. Echocardiography was performed before and 20 min after sedation with 0.1 mg/kg medetomidine intramuscularly (IM) for urethral catheterisation. Prior to epididymectomy, S-ketamine was administered intravenously. Twenty minutes after reversal with 0.5 mg/kg atipamezole IM, the third echocardiography was performed. Sedation with medetomidine and reversal with atipamezole was repeated on day 7, 14, 21 and 28. Heart rate (HR) and rhythm were monitored throughout all sedations. On day 0 and 28 cTnI concentrations were measured before and after the procedure. After normality testing, the values were compared over time. The administration of medetomidine led to a marked reduction in HR, cardiac output and ventricular systolic function and a significant increase in left ventricular dimensions. Rhythm abnormalities, such as ventricular premature complexes and idioventricular rhythm, could be observed. The administration of atipamezole completely reversed sedation and the changes in haemodynamic variables. No significant increase in cTnI concentrations could be detected, although two out of six cats showed values above the reference range.

The Effect of a Subsequent Dose of Dexmedetomidine or Other Sedatives following an Initial Dose of Dexmedetomidine on Electrolytes, Acid–Base Balance, Creatinine, Glucose, and Cardiac Troponin I in Cats: Part II

“…Transient mild bradycardia has been reported after dexmedetomidine administration in dogs, and no intervention was required [45]. Similarly, in a crossover study in healthy cats by Diggelmann et al ( 2023), the administration of a high dose of medetomidine (100 µg/kg) in cats resulted in marked bradycardia and reduction in cardiac output but not a significant increase in cTnI concentrations [30]. In contrast, the administration of 40 µg/kg dexmedetomidine IM in healthy cats by Côté et al (2022) resulted in similar effects as in the study by Diggelmann et al; however, serum cTnI concentrations were significantly increased [31].…”

“…Cardiac troponin I (cTnI) is responsible for actin-myosin inhibition during calcium shortage; troponin T (cTnT) binds to tropomyosin and binds it, whereas troponin C (cTnC) binds calcium to inhibit contraction [27][28][29]. It has been reported that the administration of a 2 -agonists does not alter [30] or increase the concentration of cTnI [31,32] in small animals. Hence, the effect of dexmedetomidine and other commonly administered sedative drugs on myocardial function can be easily and non-invasively assessed by measuring specific cardiac biomarkers such as cTnI in cats [27,31].…”

Pharmacological semen collection in domestic and wild canids and felids: literature review

“…Furthermore, Romagnoli et al (2016) observed reduced heart rate, increased cardiac preload, and compromised systolic function in domestic cats after medetomidine administration (130 μg/kg; im). Diggelmann et al (2023) assessed cardiological changes in this species, focusing on cardiac troponin I (cTnI) levels, following medetomidine treatment (100 μg/kg; im). However, they found that atipamezole (5 μg/kg; im) effectively restored hemodynamic parameters without a significant increase in cTnI concentrations during sedation reversal.…”