ABSTRACT. The bispectral index (BIS) was evaluated as an indicator of central nervous system (CNS) depression in horses anesthetized with propofol. Five non-premedicated horses were anesthetized with 7 mg/kg, IV propofol and the minimum infusion rate (MIR) of propofol required to maintain anesthesia was determined during intermittent positive pressure ventilation in each horse. The BIS was determined 20 min later and after stabilization at 2.0 MIR, 1.5 MIR, and 1.0 MIR. The BIS was also recorded after the cessation of propofol infusion when the horses regained spontaneous breathing and swallowing reflex. The MIR and plasma concentration (Cp) of propofol were 0.20  0.03 mg/kg/min and 17.5  4.0 g/ml, respectively. The BIS value and Cp were 59  13 and 26.7  8.6 g/ml at 2.0 MIR, 63  9 and 22.9  9.7 g/ml at 1.5 MIR, 64  13 and 20.1  5.9 g/ml at 1.0 MIR, 64  24 and 13.0  2.8 g/ml at return of spontaneous breathing, and 91  4 and 11.0  3.4 g/ml when the swallowing reflex returned, respectively. The BIS value was significantly less in anesthetized horses compared to horses once swallowing returned (p=0.025). The BIS value was significantly correlated with the propofol Cp (r=-0.625, p=0.001). There was not a significant difference in the BIS values during the MIR multiples of propofol. The BIS was a useful indicator of awakening but did not indicate the degree of CNS depression during propofol-anesthesia in horses.KEY WORDS: bispectral index (BIS), equine, propofol.

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We evaluated changes in cardiovascular and renal functions as well as arginine vasopressin (AVP) secretion, with remifentanil and dexmedetomidine administration alone or in combination in sevoflurane-anesthetized dogs. Six healthy adult Beagle dogs received one of the following four treatments in a randomized crossover study: saline (C), remifentanil alone at successively increasing doses (R; 0.15, 0.60, and 2.40 μg/kg/min), dexmedetomidine alone (D; 0.5 μg/kg intravenously for initial 10 min followed by a constant rate infusion at 0.5 μg/kg/hr), and a combination of remifentanil and dexmedetomidine at the above-mentioned doses (RD). Sevoflurane doses were adjusted to 1.5 times of minimum alveolar concentration (MAC) equivalent according to MAC-sparing effects with remifentanil and dexmedetomidine as previously reported. Cardiovascular measurements, renal function data, and plasma AVP concentrations were determined before and every 60 min until 180 min after drug administration as per each treatment. In the R, D and RD, heart rate significantly decreased and mean arterial pressure significantly increased from baseline or with C. Cardiac index significantly decreased and systemic vascular resistance index increased with D and RD.Oxygen extraction ratio, renal blood flow, and glomerular filtration rate were not affected. The plasma AVP concentrations significantly decreased in D and RD, but increased in R. Only in D, the natriuresis was elicited. The combination of remifentanil and dexmedetomidine in sevoflurane-anesthetized dogs was acceptable in terms of the hemodynamics, oxygenation, and renal function. Remifentanil may interfere with dexmedetomidine-induced diuresis and inhibition of AVP secretion. KEY WORDSarginine vasopressin, cardiovascular and renal effect, dexmedetomidine, dog, remifentanil noted above, no study has documented the combined effects of μ opioid and α2-adrenoreceptor agonists on renal functions.This study aimed to experimentally evaluate the changes in cardiovascular and renal functions as well as AVP secretion with the CRI of remifentanil and dexmedetomidine alone and in combination in dogs anesthetized with sevoflurane. MATERIALS & METHODS AnimalsSix healthy, adult neutered Beagle dogs (three males and three females), aged 3.0 ± 0.7 years (mean ± standard deviation [SD]) and weighing 10.2 ± 1.2 kg (mean ± SD), were included in this study. Health status was assessed before the study by physical examination, complete blood count, serum biochemical analysis, and urinalysis. The dogs were housed in cages; food, but not water, was withheld for 12 hr before anesthesia. This study was approved by the Animal Research Committee of Tottori University (no. 16-T-19). Study designEach dog was randomly anesthetized on four occasions with a ≥4-week washout period and received one of the following four treatments: CRI of saline at 2 ml/kg/min as control (C treatment); CRI of remifentanil (Ultiva, Janssen Pharmaceutical K.K., Tokyo, Japan) at successive dose rates of 0.15, 0.60, and 2.40 μg/kg/min (R treatm...

Remifentanil is an ultra-short-acting µ-opioid receptor agonist. The purpose of this study was to determine the relationship of the minimum alveolar concentration (MAC) of sevoflurane and other MAC derivatives, including the MAC for blocking adrenergic responses (MAC-BAR) and the MAC at which tracheal extubation is occurred (MAC-extubation), with or without remifentanil infusion. Six healthy adult beagle dogs were randomly anesthetized three times for determining the MAC-BAR (SEVMAC-BAR), MAC (SEVMAC), and MAC- extubation (SEVMAC-extubation) of sevoflurane under infusion of saline and remifentanil at rates of 0.15, 0.30, 0.60, 1.20, and 2.40 µg/kg/min. The ratio of the SEVMAC-BAR and SEVMAC and that of the SEVMAC-extubation and SEVMAC were not significantly different at baseline and during treatment. The MAC-BAR95 and MAC95 decreased in a dose-dependent manner until reaching 1.20 µg/kg/min, and the MAC-extubation5 decreased in a dose-dependent manner until reaching 0.60 µg/kg/min. The percentage reduction of SEVMAC-BAR, SEVMAC, and SEVMAC-extubation increased in a dose-dependent manner during remifentanil infusion. The heart rate significantly decreased in the MAC-BAR and MAC groups, and the systolic and mean arterial pressures increased after remifentanil infusion compared with the baseline values. Remifentanil infusion caused reduction of the SEVMAC-BAR, SEVMAC, and SEVMAC-extubation in a dose-dependent manner, and ceiling effects were observed in the dogs. Higher doses of remifentanil and sevoflurane were necessary for blocking the sympathetic response to the supramaximal stimulus to prevent movement and extubation in dogs.