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- Author or Editor: Eduardo R. Monteiro x
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Objective—To evaluate the postoperative analgesic effects of epidural administration of morphine and neostigmine, either alone or in combination, in dogs.
Animals—30 dogs undergoing orthopedic surgery on a pelvic limb.
Procedures—Anesthetic protocols were standardized. At the end of surgery, 10 dogs each received 1 of 3 epidural treatments: morphine (0.1 mg/kg), neostigmine (5 μg/kg), or morphine plus neostigmine (0.1 mg/kg and 5 μg/kg, respectively). Postoperative pain scores and the need for rescue analgesia were evaluated for 24 hours.
Results—Pain scores were higher in the neostigmine group, compared with scores for the morphine-neostigmine group, at 2 and 24 hours after surgery and higher in the morphine group than in the morphine-neostigmine group at 2 and 4 hours. During 24 hours, rescue analgesia was provided for 4, 7, and 2 of 10 dogs each in the morphine, neostigmine, and morphine-neostigmine groups, respectively. The number of dogs given rescue analgesia was significantly different among groups at 2, 3, 4, and 6 hours after surgery. Dogs in the morphine and morphine-neostigmine groups had a lower probability of receiving rescue analgesia within 24 hours than did dogs in the neostigmine group.
Conclusions and Clinical Relevance—When administered epidurally, morphine alone or in combination with neostigmine provided effective postoperative analgesia in most dogs after orthopedic surgery, whereas neostigmine alone did not. Findings for this study suggested a potential role for neostigmine as an adjuvant for epidural analgesia in dogs undergoing orthopedic surgeries on the pelvic limbs.
Objective—To evaluate the effects of epidural administration of 3 doses of dexmedetomidine on isoflurane minimum alveolar concentration (MAC) and characterize changes in bispectral index (BIS) induced by nociceptive stimulation used for MAC determination in dogs.
Animals—6 adult dogs.
Procedures—Isoflurane-anesthetized dogs received physiologic saline (0.9% NaCl) solution (control treatment) or dexmedetomidine (1.5 [DEX1.5], 3.0 [DEX3], or 6.0 [DEX6] μg/kg) epidurally in a crossover study. Isoflurane MAC (determined by use of electrical nociceptive stimulation of the hind limb) was targeted to be accomplished at 2 and 4.5 hours. Changes in BIS attributable to nociceptive stimulation and cardiopulmonary data were recorded at each MAC determination.
Results—With the control treatment, mean ± SD MAC values did not change over time (1.57 ± 0.23% and 1.55 ± 0.25% at 2 and 4.5 hours, respectively). Compared with the control treatment, MAC was significantly lower at 2 hours (13% reduction) but not at 4.5 hours (7% reduction) in DEX1.5-treated dogs and significantly lower at 2 hours (29% reduction) and 4.5 hours (13% reduction) in DEX3-treated dogs. The DEX6 treatment yielded the greatest MAC reduction (31% and 22% at 2 and 4.5 hours, respectively). During all treatments, noxious stimulation increased BIS; but changes in BIS were correlated with increases in electromyographic activity.
Conclusions and Clinical Relevance—In dogs, epidural administration of dexmedetomidine resulted in dose-dependent decreases in isoflurane MAC and that effect decreased over time. Changes in BIS during MAC determinations may not represent increased awareness because of the possible interference of electromyographic activity.
Objective—To evaluate the correlation between the bispectral index (BIS) and end-tidal isoflurane (ET ISO ) concentration and compare the use of 3 BIS sensor positions in dogs.
Animals—6 adult dogs.
Procedures—Mechanically ventilated dogs received pancuronium, and depth of anesthesia was altered by increasing ET ISO concentration from 1.5% to 2.3% and 3.0%. The BIS, suppression ratio (relative percentage of isoelectric electroencephalographic waveforms), and signal quality index (SQI) were recorded at each ET ISO concentration for each of 3 BIS sensor positions (frontal-occipital, bifrontal, and frontal-temporal positions).
Results—The BIS and ET ISO concentration were poorly correlated; regardless of sensor positioning, mean BIS values did not change significantly as ET ISO was increased. At 3% isoflurane, regardless of sensor positioning, there was an increase in suppression ratio coincident with BIS < 40 in some dogs, whereas paradoxic increases in BIS (> 60) were recorded in others. Furthermore, at 3.0% isoflurane, the SQI was significantly lower for the bifrontal sensor position (compared with values for the other positions), but low SQI values prevented recording of BIS values from the frontal-occipital sensor position in 2 dogs. Overall, BIS values derived from the 3 sensor positions did not differ.
Conclusions and Clinical Relevance—In dogs, BIS values may not reflect changes in depth of isoflurane anesthesia in the absence of noxious stimulation. Of the 3 sensor positions, frontal-temporal positioning provided better correlation with changes in depth of anesthesia induced via changes in isoflurane concentrations. However, the sensor placements yielded similar results at SQI values > 50.
Objective—To compare hemodynamic effects in dogs anesthetized with remifentanilisoflurane and with isoflurane alone.
Animals—6 adult dogs.
Procedures—Mechanically ventilated, isoflurane-anesthetized dogs received increasing constant rate infusions (CRIs) of remifentanil (0.15, 0.30, 0.60, and 0.90 μg/kg/min) or physiologic saline (0.9% NaCl) solution (control treatment), with a 1-week washout interval between treatments. Each CRI of remifentanil or saline solution was maintained for 60 minutes with equipotent end-tidal isoflurane concentrations that corresponded to 1.3 times the minimum alveolar concentration. Hemodynamic measurements and plasma vasopressin concentrations were determined before and at the end of each CRI and 60 minutes after the end of the infusion regimen.
Results—Compared with the control treatment, remifentanil CRIs significantly decreased heart rate (HR) and cardiac index (CI) and significantly increased systemic vascular resistance index (SVRI) and plasma vasopressin concentration. Greatest differences in mean values between treatments were recorded for remifentanil at 0.60 μg/kg/min (HR and Cl were 55% and 47% lower, respectively, and SVRI was 91% higher than for the control treatment). Mean arterial pressure increased significantly during the highest remifentanil CRI (9% higher than for the control treatment). The increase in vascular resistance was positively correlated with increases in vasopressin concentrations (coefficient of determination, 0.65) during anesthesia with remifentanil-isoflurane.
Conclusions and Clinical Relevance—Anesthesia maintained with remifentanil-isoflurane may decrease tissue perfusion as a result of a decrease in Cl. However, hypotension may not develop because of systemic vasoconstriction. An increase in plasma vasopressin concentration was associated with the vasoconstriction observed in dogs anesthetized with remifentanil-isoflurane. (Am J Vet Res 2010;71:1133-1141)
Objective—To evaluate the effects of remifentanil on isoflurane minimum alveolar concentration (ISOMAC) in dogs.
Animals—6 adult mixed-breed dogs.
Procedures—Dogs were anesthetized with isoflurane on 2 occasions. During the first set of experiments, ISOMAC was determined before remifentanil infusion (baseline), during constant rate infusion (CRI) of remifentanil (0.15, 0.30, 0.60, and 0.90 μg/kg/min), and 80 minutes after remifentanil infusion. After a 1-week washout period, dogs received a CRI of remifentanil (0.15 μg/kg/min) and ISOMAC was redetermined 2, 4, and 6 hours after commencing the infusion.
Results—Mean ± SD baseline ISOMAC was 1.24 ± 0.18%. Remifentanil infusion (0.15, 0.30, 0.60, and 0.90 μg/kg/min) decreased ISOMAC by 43 ± 10%, 59 ± 10%, 66 ± 9%, and 71 ± 9%, respectively. The ISOMAC values determined during the 0.30, 0.60, and 0.90 μg/kg/min infusion rates did not differ from each other, but these values were significantly lower, compared with the 0.15 μg/kg/min infusion rate. The ISOMAC recorded after remifentanil infusion (1.09 ± 0.18%) did not differ from baseline ISOMAC. There was no change in ISOMAC throughout the 6-hour period of a CRI of remifentanil.
Conclusions and Clinical Relevance—Remifentanil decreased ISOMAC in a dose-related fashion; the reduction in ISOMAC was stable over the course of a prolonged CRI (6 hours). A dose of 0.30 μg of remifentanil/kg/min resulted in nearly maximal isoflurane-sparing effect in dogs; a ceiling effect was observed at higher infusion rates.