Anesthesia in horses is often associated with complications, including postoperative myopathies and colic, that contribute to the relatively high mortality rate in this species.1 The relevance of peripheral tissue perfusion and its association with these problems has gained increasing attention during the past few years. However, detailed information about the impact of various anesthetics on tissue perfusion is limited.
Horses are commonly anesthetized with volatile anesthetic agents for prolonged surgery. The very low blood-gas partition coefficient of desflurane2 (0.45) offers the potential for more precise control of anesthetic depth and more rapid recovery, compared with effects for other inhalation anesthetics.3 These properties make desflurane desirable for use in horses because rapid recovery is crucial in equine anesthesia. Like most volatile anesthetic agents, desflurane causes dose-related cardiopulmonary depression,4 which contributes to the high mortality rate associated with equine anesthesia.1 Therefore, it is preferable to minimize the amount of inhalation agent used by providing analgesia and muscle relaxation through other sources. Various α2-adrenoceptor agonists have been used in balanced anesthetic protocols that provide sedation and analgesia, which reduces the MAC of volatile anesthetic agents and improves the quality of recovery.5
Propofol is unsatisfactory as the sole agent for anesthesia of equids; the volume of drug required is too large to enable sufficiently rapid injection, and the quality of anesthetic induction is unpredictable. However, propofol results in a good quality of anesthetic induction after patients are sedated with α2-adrenoceptor agonists.6 A total intravenous anesthesia protocol that involved the use of medetomidine and propofol maintained good cardiovascular function in ponies that were anesthetized for ≥ 4 hours, and there was good recovery quality.7
Dexmedetomidine is a highly selective α2-adrenoceptor agonist that causes sedation, anxiolysis, and analgesia. Cardiopulmonary effects and pharmacokinetics of dexmedetomidine have been evaluated in ponies after IV administration. Although the cardiopulmonary effects are similar to those reported for other α2-adrenoceptor agonists, it has been determined that dexmedetomidine is rapidly redistributed and has short-acting effects in horses.8 These characteristics make it ideal for use in partial intravenous anesthesia protocols. A dexmedetomidine CRI of 1.75 μg•kg−1•h−1 significantly reduces the MAC of sevoflurane in ponies by 53%.9
Peripheral perfusion is also impaired during anesthesia, which can lead to a reduction of peripheral oxygenation. Postanesthetic myopathy, caused by impaired perfusion and oxygenation during anesthesia, is a recognized complication of equine anesthesia that has been identified as one of the principal causes of perioperative death in anesthetized horses.1 Although volatile anesthetics can impair muscle perfusion as well as intestinal perfusion,10,11 propofol has been found to improve peripheral perfusion in humans.12,13 One explanation for this phenomenon is that the anesthesia-induced vasodilatation in those studies12,13 might predominantly have involved small tissue venules when propofol was used.
The purpose of the study reported here was to determine global and peripheral perfusion and oxygenation during anesthesia with desflurane and propofol combined with a CRI of dexmedetomidine in horses. We hypothesized that the CRI of dexmedetomidine would reduce anesthetic requirements and that cardiovascular variables as well as peripheral perfusion and oxygenation would be maintained equally well during anesthesia with desflurane and propofol.
Materials and Methods
Animals
Six warmblood horses were used in the study. Horses had a mean ± SD body weight of 532 ± 65 kg and mean age of 8.7 ± 2.3 years. All horses were healthy as determined on the basis of results of clinical and laboratory examinations. Horses were maintained on pasture but were moved into stalls and fed hay beginning 12 hours before each experiment. Food, but not water, was withheld for 6 hours before anesthesia. The study was approved by the Ethical Committee of Lower Saxony, Germany (No. 33.12-42502-04-15/1780).
Study design
A complete crossover design was used. Horses were randomly allocated by means of a coin toss to initial anesthesia with propofol or desflurane. There was a washout period of 2 weeks between subsequent anesthetic episodes. The study was performed at sea level at the Clinic for Horses, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany.
Instrumentation
Lidocaine was infiltrated into the subcutaneous tissues over a jugular vein of each horse, and a 12-gauge catheter was placed aseptically. After horses were anesthetized, an arterial catheter was placed in a facial artery to measure blood pressure and blood gas concentrations. That catheter was connected to a pressure transducer placed at the level of the shoulder joint and zeroed to atmospheric pressure. The CO measurements were performed by use of the lithium dilution technique.14 Arterial blood samples were collected, and concentrations of sodium and hemoglobin were measured before CO measurement as required for the lithium dilution method for CO determination.
Anesthesia
Horses were sedated with dexmedetomidinea (3.5 μg•kg−1, IV), and anesthesia was induced with propofolb (2 mg•kg−1, IV) or ketamine hydrochloride (1 mg•kg−1, IV). Induction quality was scored on a scale of 1 to 5, as described elsewhere.15 After anesthesia was induced, the horses were endotracheally intubated and placed in lateral recumbency on a padded surgical table. Horses were mechanically ventilated with a large animal ventilator. Intermittent positive pressure was used (positive inspiratory pressure, 20 to 25 cm H2O), and the respiratory rate was adjusted to ensure horses remained normocapnic (Paco2, 35 to 45 mm Hg). All horses were allowed to breathe 100% oxygen.
Horses were randomly assigned to 2 treatment groups. Beginning approximately 5 minutes after induction, anesthesia was maintained for the propofol treatment by administration of an infusion of propofol (0.08 mg•kg−1•min−1) combined with a CRI of dexmedetomidine (7 μg•kg−1•h−1). Anesthesia was maintained for the desflurane treatment by administration of desfluranec (initial end-expiratory concentration, 5%) combined with the CRI of dexmedetomidine (7 μg•kg−1•h−1). Lactated Ringer solution was administered at a rate of 10 mL•kg−1•h−1 during anesthesia. Duration of anesthesia was defined as the time from connecting a horse to the large animal breathing circuit until disconnection for the desflurane treatment and from start of the propofol infusion until cessation of the infusion for the propofol treatment.
At the end of anesthesia, a hoist was used to move horses into a recovery stall. Recovery was assisted with ropes attached to the tail and head. For recovery, 5 mL of phenylephrine was sprayed into each nostril, and the endotracheal tube was replaced by a nasal tube. Oxygen was insufflated during the recovery period; the recovery period was defined as the interval from placing horses in the recovery stall until they achieved a standing position. Quality of recovery was scored on a 100-point scale, with a range between 11 and 100, as described elsewhere.16 A score of 11 indicated the best recovery possible, whereas a score of 100 represented the worst recovery possible. The score included values for 11 sections, each with variable emphasis.
Measurement of anesthetic requirements
A constant-current electrical stimulusd (which was described as a supramaximal stimulus in another study17) was used to evaluate anesthetic requirements. Response to the stimulus applied was assessed as defined elsewhere18 and was considered positive when there was gross purposeful movement (including movement of the limbs, head, and tail) or spontaneous movement. Nystagmus and alterations in physiologic variables were considered negative responses.
Horses were allowed to equilibrate to anesthesia for 60 minutes. Horses then were stimulated every 20 minutes, and equal depths of anesthesia (defined as MAC and MIR) were determined by use of the bracketing method.19 Each stimulus consisted of 25-millisecond train-of-five 1-millisecond constant current (40 mA) square-wave pulses. Voltage was continuously increased over a period of 30 seconds until 40 mA was reached; voltage of 40 mA was then maintained for an additional 20 seconds. The train-of-five pulses were delivered at a frequency of 5 Hz. Surface electrodese were placed at the lateral aspect over the proximal and middle phalanges. Interelectrode resistance was determined before each stimulus. If resistance exceeded 3 kΩ, the electrodes were replaced. In the case of a negative response, the end-expiratory concentration of desflurane was decreased by 0.5% and the infusion rate of propofol was reduced by 0.01 mg•kg−1•min−1. Stimulations were repeated until the horses had a positive response, after which the desflurane concentration was increased by 0.5% and the infusion rate of propofol was increased by 0.01 mg•kg−1•min−1; stimulations were repeated until the lowest anesthetic concentration that prevented movements was titrated. The MAC and MIR of each horse were defined as the mean desflurane concentration and propofol infusion rate for the lowest and highest desflurane concentration and propofol infusion rate that allowed and prevented movements, respectively. If horses moved spontaneously, a bolus of propofol (0.1 mg•kg−1) was administered promptly, and additional boluses were administered until the movement ceased.
Measurement of variables
Microperfusion and oxygenation were measured by use of a micro-lightguide spectrophotometer,f as described elsewhere.20 Micro-lightguide spectrophotometry is a validated method for use in assessing microperfusion and oxygenation in humans. This method has yielded reliable and reproducible results for horses.11,21 Two surface probes were used: a flat probeg for measurements of rectal and oral mucosa, and a vertical probeh for measurements of esophageal mucosa. The flat probe was placed on the buccal mucosa of the oral cavity and on the rectal mucosa. The vertical probe was inserted into the esophagus by the aid of a modified gastric tube. Depth of penetration was 2.5 mm for both the flat and vertical probes.
Baseline values for microperfusion and oxygenation of the 3 locations were determined. Measurements were repeated 5 minutes after IV administration of the bolus of dexmedetomidine (3.5 μg•kg−1; sedation measurement). After the desflurane MAC and propofol MIR were determined, microperfusion and oxygenation measurements were performed for anesthetized horses 4 times (measurements A1 to A4) with an interval of 20 minutes between successive measurements. Measurements were performed in the same order and by the same investigator (SN) and involved 4 complete respiratory cycles.
Cardiorespiratory variables were monitored throughout anesthesia. Data were recorded and analyzed for 60 minutes at the individual MIR and MAC. Heart rate, respiratory rate, Petco2, FIo2, end-expiratory partial pressure of O2, end-expiratory desflurane concentration, inspiratory desflurane concentration, MAP, and CO were recorded every 20 minutes during anesthesia (measurements A1 to A4). In addition, arterial blood samples were collected every 10 minutes and used for determination of Pao2 and Paco2.
End-expiratory desflurane concentration and Petco2 were measured continuously during anesthesia at the Y-piece by use of side-stream capnography and infrared absorption spectroscopy.i The monitor was calibrated before each experiment by means of 2-point calibrations at expected concentrations.j
Calculated variables
A simplified formula was used to calculate SVR22; SVR was calculated as (MAP × 80) • CO−1. Stroke volume was calculated as CO•heart rate−1. The Pao2-FIO2 quotient was calculated as Pao2 •FIO2−1. Alveolar dead space was calculated as (Paco2 - PETco2) • Paco2−1. The Pao2 - Pao2 was calculated as ([{barometric pressure - Ph2O}•Fio2] - [Paco2•R−1]) - Pao2, where R is the respiratory exchange ratio with a value of 0.8.
Stroke volume and CO were indexed to body weight.
Statistical analysis
Data analysis was performed with statistical software.k Perfusion (blood flow) and tissue oxygenation variables were recorded at a frequency of 2 Hz, which resulted in 20 to 25 data points for each variable and time point. Consecutively, the mean for each time point and location was calculated, which resulted in 1 value for each respective variable. Visual assessment of Q-Q plots and the Shapiro-Wilk test were used to confirm a normal distribution of model residuals for dependent variables. All data were reported as mean ± SD.
Analysis of global and tissue variables was conducted as a 2-factorial analysis of variance for repeated measurements to detect differences between treatments. A Dunnett post hoc test for multiple paired comparisons was used to assess differences among measurements at various time points within a treatment. For direct comparison between the 2 treatments, a t test was chosen. The Wilcoxon signed rank test was used to analyze nonparametric data to detect differences between the desflurane and propofol treatments. Significance was set at values of P < 0.05.
Results
Anesthesia
Induction of anesthesia was smooth and resulted in no complications. Quality of induction for the desflurane treatment was fair (median, 3; range, 1 to 4), whereas quality of induction for the propofol treatment was good (median, 4; range, 3 to 4). Mean ± SD duration of anesthesia was 256 ± 24 minutes and 244 ± 29 minutes for the desflurane and propofol treatments, respectively (Table 1).
Mean ± SD values for anesthesia of 6 horses sedated with a bolus of dexmedetomidine (3.5 μg•kg−1, IV) and then anesthetized at an equal depth of anesthesia with propofol plus a CRI of dexmedetomidine (7 μg•kg−1 •h−1) or desflurane plus the CRI of dexmedetomidine.
| Variable | Desflurane | Propofol | P value* |
|---|---|---|---|
| Duration of anesthesia (min) | 256 ± 23 | 244 ± 28 | 0.52 |
| Recovery period (min) | 38 ± 11 | 39 ± 16 | 0.93 |
| Additional dexmedetomidine (μg•kg−1) | 1.6 ± 1.7 | 1.2 ± 1.0 | 0.94 |
| Additional propofol (mg•kg−1) | 0.7 ± 0.9 | 1.0 ± 1.4 | 0.43 |
Duration of anesthesia was defined as the time from connecting a horse to the large animal breathing circuit until disconnection for the desflurane treatment and from starting the propofol infusion until cessation of the infusion for the propofol treatment. The recovery period was defined as the time from placing horses in the recovery stall until they achieved a standing position. Additional dexmedetomidine was the additional boluses of dexmedetomidine administered to provide sedation sufficient for induction of anesthesia. Additional propofol was the additional boluses of propofol administered during determination of MAC and MIR.
Values were considered significant at P < 0.05.
Depth of sedation after administration of the initial bolus of dexmedetomidine (3.5 μg•kg−1, IV) was insufficient in 4 horses for each treatment. These horses received additional boluses of dexmedetomidine to provide sedation sufficient for induction of anesthesia (Table 1). The interval between bolus administration of dexmedetomidine and anesthetic induction was always < 20 minutes. Mean ± SD recovery time was 38 ± 11 minutes and 39 ± 16 minutes for the desflurane and propofol treatments, respectively. All horses recovered with 1 attempt to stand, except for 1 horse when receiving the desflurane treatment (which required 2 attempts to stand). The recovery period was characterized as excellent for both the propofol (median score, 14; range, 11 to 24) and desflurane (median score, 21; range, 17 to 43) treatments.
Determination of equal depth of anesthesia
Mean ± SD MAC of desflurane was 2.6 ± 0.9%, and the mean MIR of propofol was 0.04 ± 0.01 mg•kg−1•min−1. Three horses for each treatment did not respond to the supramaximal stimulus applied; instead, those horses moved spontaneously. For 2 of the 3 horses, spontaneous movements were characterized by lifting the head and paddling the limbs. For all 3 horses, multiple additional boluses of propofol were needed to increase the depth of anesthesia, which resulted in a mean additional amount of propofol of 0.7 ± 0.9 mg•kg−1 for the desflurane treatment and 1.0 ± 1.4 mg•kg−1 for the propofol treatment (Table 1). End-expiratory concentrations of desflurane and the infusion rate of propofol were determined (Figure 1).
End-expiratory desflurane concentration (A) and infusion rate of propofol (B) for anesthesia of each of 6 horses. Each symbol represents results for 1 horse. Horses were allowed to equilibrate to anesthesia for 60 minutes before depth of anesthesia was determined. The horizontal gray line indicates the mean MAC for desflurane and mean MIR for propofol. Vol% = Volume percentage.
Citation: American Journal of Veterinary Research 79, 5; 10.2460/ajvr.79.5.487
Cardiopulmonary variables
The cardiac index was significantly (P = 0.01) higher for the desflurane treatment than for the propofol treatment (Table 2). By contrast, the SVR was significantly (P = 0.049) lower for the desflurane treatment than for the propofol treatment. The Pao2 (P = 0.004) and Pao2-FIO2 quotient (P < 0.001) were significantly higher and the alveolar dead space (P < 0.001) and Pao2 - Pao2 (P = 0.007) were significantly lower for the propofol treatment, compared with values for the desflurane treatment.
Tissue blood flow
Microperfusion and oxygenation measurements of the oral, esophageal, and rectal mucosa were tolerated well by the unsedated horses. Administration of the dexmedetomidine bolus caused a significant reduction of blood flow, compared with baseline values (Figure 2). Peripheral blood flow increased during anesthesia (measurements A1 to A4), compared with values for the sedation measurement, but remained lower than baseline values.
Mean ± SD blood flow measured in the rectal (A), oral (B), and esophageal (C) mucosa of 6 horses at various time points before and after horses were sedated with a bolus of dexmedetomidine (3.5 μg•kg−1, IV) and then anesthetized at an equal depth of anesthesia with propofol plus a CRI of dexmedetomidine (7 μg•kg−1 •h−1; squares) or desflurane plus the CRI of dexmedetomidine (circles). Time points were as follows: B = baseline (before administration of any drugs), S = sedation measurement at 5 minutes after IV administration of the bolus of dexmedetomidine, and A1 to A4 = time points at 20-minute intervals during anesthesia beginning 60 minutes after induction of anesthesia. *Within the propofol treatment, value differs significantly (P < 0.05) from the baseline value. †Within the desflurane treatment, value differs significantly (P < 0.05) from the baseline value. AU = Arbitrary units.
Citation: American Journal of Veterinary Research 79, 5; 10.2460/ajvr.79.5.487
Tissue oxygenation
Tissue So2 decreased at all sites after the administration of dexmedetomidine (Figure 3). During anesthesia, tissue So2 values returned to approximately baseline values.
Mean ± SD So2 measured in the rectal (A), oral (B), and esophageal (C) mucosa of 6 horses at different time points before and after being sedated with a bolus of dexmedetomidine (3.5 μg•kg−1, IV) and then anesthetized at an equal depth of anesthesia with propofol plus a CRI of dexmedetomidine (7 μg•kg−1 •h−1; squares) or desflurane plus the CRI of dexmedetomidine (circles). See Figure 2 for remainder of key.
Citation: American Journal of Veterinary Research 79, 5; 10.2460/ajvr.79.5.487
Discussion
Hemodynamic variables, microperfusion, and So2 were well maintained during anesthesia with propofol and dexmedetomidine as well as during anesthesia with desflurane and dexmedetomidine. The dexmedetomidine premedication bolus decreased microperfusion after administration. To the authors’ knowledge, the study reported here was the first in which rectal, oral, and esophageal microperfusion in horses anesthetized with desflurane and propofol has been evaluated.
Depth of anesthesia was measured by determining the MAC and MIR for each horse. Despite some differences from standard MAC determination evaluations23 with respect to gas sampling technique, site of sample collection, and induction of anesthesia, use of the same methods for both treatments allowed the determination of an equal depth of anesthesia on the basis of immobility in response to electrical stimulation. The MAC of desflurane is reportedly 7.0% for ponies24 and 8.06% for horses,25 and the mean ± SD MIR of propofol is 0.1 ± 0.02 mg•kg−1•min−1 in horses premedicated with xylazine.26 The MIR of propofol with a CRI of medetomidine at a rate of 3.5 mg•kg−1•min−1 for horses7 is 0.06 to 0.1 mg•kg−1•min−1, which is much higher than the MIR for propofol reported here. One explanation for the lower MIR in the present study was the higher dose of dexmedetomidine, which resulted in more pronounced sedative and analgesic effects. In the present study, dexmedetomidine decreased the requirement for desflurane and propofol by 48% and 50%, respectively, compared with the original concentration, which is comparable to results for other studies7,9 of horses. However, most of the aforementioned studies were conducted with lower doses of dexmedetomidine; the dose used here was based on results of a study27 in which it was determined that 7 μg of dexmedetomidine•kg−1•h−1 caused sedative effects equivalent to those for 1 mg of xylazine•kg−1•h−1 in standing horses. Administration of a CRI of 1 mg of xylazine•kg−1•h−1 resulted in stable cardiovascular variables in another study.28
Constant-current electrical stimulation is a common and superior method for determining MAC and MIR in horses because it ensures tissue integrity and leads to reproducible responses.17 However, 3 horses did not have any response to the stimulus applied; instead, they moved spontaneously, which indicated a light plane of anesthesia and insufficient hypnosis, which is in accordance with results of another study29 in which desflurane and medetomidine were used. An explanation could be the strong analgesic, muscle relaxant, and hypnotic effects of dexmedetomidine. Results from the present study indicated that hypnosis may have been the limiting factor for responsiveness, which also has been reported in other studies.7,9 Caution is advised if these doses are used in clinical settings. The stepwise decrease in the desflurane concentration in intervals of 20 minutes appeared to be appropriate for reaching steady-state conditions because of a very short elimination half-life of 4.3 minutes.30 The context-sensitive short half-life of propofol was 5.8 minutes after a CRI of propofol at a rate of 0.136 mg•kg−1•min−1 in another study31; thus, the adjustment of the dose of propofol in the present study also appeared to be appropriate.
Influence of the drugs used for induction on the determination of MAC and MIR cannot be completely excluded. Nevertheless, an equilibration time of 60 minutes would appear to be adequate to ensure a decrease of the ketamine plasma concentration to below a threshold value that would have anesthetic-sparing properties.32,33 Propofol also has anesthetic-sparing effects,34 although its elimination and context-sensitive half-life is very short31; therefore, a major influence on anesthetic requirements is unlikely. Time to reach MAC and MIR was similar between treatments; therefore, there was no influence of anesthesia time on cardiovascular variables.
Blood flow and So2 decreased after administration of a bolus of dexmedetomidine. Activation of α2-adrenoreceptors causes a significant reduction of tissue perfusion in horses.35 Administration of a dexmedetomidine bolus results in a decrease in CO, increase in SVR, and mild bradycardia, although these effects are short lasting.8 Tissue perfusion is directly related to CO and MAP,10,11,35 which could have been 1 explanation for the reduced blood flow detected in the present study. Furthermore, α2B-adrenoreceptor-mediated vasoconstriction is also associated with a reduction in blood flow.35 Dexmedetomidine reduces oxygen delivery to tissues and leads to an increase in oxygen extraction,36 which could explain the lower So2 measured in the 3 tissues. Tissues with reduced oxygen delivery normally counteract with an increase in oxygen extraction to prevent hypoxia until the threshold is exceeded, at which point the tissues become supply-dependent and hypoxia occurs.37,38
In the present study, global perfusion and microperfusion were well maintained during anesthesia for both treatments. No differences were detected between the treatments with regard to microperfusion, and microperfusion was preserved better during anesthesia (when it almost reached baseline values) than immediately after administration of dexmedetomidine. The mild vasodilation caused by desflurane and propofol could have led to a partial reversal of the vasoconstriction mediated by dexmedetomidine. In humans, both propofol and desflurane cause an increase in blood flow during anesthesia, compared with baseline values, because of their vasodilative effects.12,39
The propofol treatment resulted in a higher Pao2 and Pao2-FIO2 quotient as well as lower values for alveolar dead space and Pao2 - Pao2, probably because propofol impaired hypoxic pulmonary vasoconstriction to a lesser extent than did desflurane. This is the situation for most injectable anesthetics.40 A maintained hypoxic pulmonary vasoconstriction is linked to better lung perfusion with less venous admixture, less ventilation-perfusion mismatch, less alveolar dead space, and a smaller Pao2 - Pao2, which maintains better arterial oxygenation.
Induction of anesthesia was smooth and not associated with any complications. Low doses of ketamine were added to the dose of propofol to improve the quality of the induction.15 After a mean duration of anesthesia of approximately 256 and 244 minutes for the desflurane and propofol treatments, respectively, the quality of recovery was excellent and comparable to that reported for recovery after anesthesia with desflurane4,30 or propofol.7 However, 2 of the horses used in the present study were anesthetized previously, so a positive influence on recovery quality attributable to a learning effect cannot be completely ruled out.
Sedation quality was sufficient after administration of a bolus of 3.5 μg of dexmedetomidine•kg−1 to enable data (measurements) to be collected. However, the same 4 horses for each treatment needed additional boluses of dexmedetomidine to achieve sedation sufficient for induction of anesthesia. Investigators of another study5 that involved the same dose of dexmedetomidine also reported sedation was insufficient for induction of anesthesia. The interval between bolus administration and induction of anesthesia was always < 20 minutes, and the most intense sedative effect of dexmedetomidine is considered to last 20 to 30 minutes.41 Therefore, a higher dose might be preferable in future studies if dexmedetomidine is to be administered before induction of anesthesia. However, the interval between the first bolus and induction of anesthesia was extended in the study reported here because of experimental conditions and would typically be shorter in clinical settings.
Three horses for each treatment had spontaneous movements during determination of MAC and MIR. The initial bolus of 0.1 mg of propofol•kg−1 was not sufficient to stop movement in the horses, and a total dose of 0.8 to 1 mg•kg−1 was necessary. This is higher than has been reported7 and could have been related to slow blood-brain circulation time, rapid redistribution of propofol, or an overall insufficient dose. The additional propofol boluses were not included in MIR and MAC determinations owing to the fact that electrical stimulation was performed again 20 minutes after spontaneous movements occurred. In case of a negative response, the mean desflurane concentration or propofol infusion rate was used, and horses were provided another 20 minutes of equilibration time until measurement of global and peripheral perfusion variables. It can be assumed that the additional propofol boluses had no or only minor influence on determination of MAC and MIR because of the rapid elimination of propofol and short context-sensitive half-life.31
For the present study, measurements of CO were performed by use of a lithium dilution method because it is less invasive than most other techniques. The influence of various drugs on the accuracy of lithium dilution measurements is related to changes in sensor voltage.42,43 The α2-adrenoreceptor agonists can potentially influence sensor voltage and lead to erroneous results.43,44 However, an in vivo study44 revealed that sensor voltage is less likely to be influenced when dexmedetomidine is used. Thus, sensor voltage was constantly monitored during the experiment and remained unaffected by dexmedetomidine, which indicated that there was no influence of the anesthesia treatments on CO measurements.
Another limitation of the study was the use of a laser Doppler ultrasonographic technique, which only allowed conclusions to be made about relative blood flow. Therefore, baseline measurements were performed for each horse to assess the influence of the various drugs on microvascular blood flow. Also, the investigator was aware of the treatments when scoring induction and recovery quality; however, the same investigator always performed the scoring.
The study reported here revealed that dexmedetomidine administered as a bolus decreased blood flow and So2 in peripheral tissues. However, during anesthesia with desflurane and propofol combined with a CRI of dexmedetomidine, So2 was well maintained and peripheral perfusion only mildly reduced. Dexmedetomidine reduced the anesthetic requirements, which led to low doses of desflurane and propofol and resulted in steady cardiovascular conditions.
Acknowledgments
This manuscript represents a portion of a thesis submitted by Dr. Neudeck to the Clinic for Horses, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany, as partial fulfillment of the requirements for a Doctor medicinae veterinariae degree.
Presented in abstract form at the Association of Veterinary Anaesthetists Spring Meeting, Lyon, France, April 2016.
ABBREVIATIONS
| CO | Cardiac output |
| CRI | Constant rate infusion |
| Flo2 | Fraction of inspired oxygen |
| MAC | Minimal alveolar concentration |
| MAP | Mean arterial blood pressure |
| MIR | Minimal infusion rate |
| Paco2 | Alveolar partial pressure of carbon dioxide |
| Pao2-Pao2 | Alveolar-arterial difference in partial pressure of oxygen |
| Petco2 | End-expiratory partial pressure of carbon dioxide |
| Ph2O | Partial pressure of water vapor |
| So2 | Oxygen saturation |
| SVR | Systemic vascular resistance |
Footnotes
Dexdomitor, 0.5 mg/mL, Orion Pharma, Espoo, Finland.
Propofol 2%, 20 mg/mL, Fresenius Kabi, Langenhagen, Germany.
Suprane, Baxter Deutschland GmbH, Höchstadt, Germany.
Grass stimulator S48, Grass Instrument Company, Quincy, Mass.
Ambu neuroline 70005-K/12, Ambu GmbH, Bad Nauheim, Germany.
O2C Oxygen to See device, LEA Medizintechnik, Gießen, Germany.
LF-2, LEA Medizintechnik, Gießen, Germany.
LF-17, LEA Medizintechnik, Gießen, Germany.
GE Datex-Ohmeda S/5 compact anesthesia monitor, GE Healthcare, München, Germany.
Quick Cal calibration gas, GE Healthcare Finland OY, Helsinki, Finland.
SAS, version 9.3, SAS Institute Inc, Cary, NC.
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