Xylazine and xylazine-ketamine in dogs

The cardiopulmonary consequences of IV administered xylazine (1.0 mg/kg) followed by ketamine (10 mg/kg) were evaluated in 12 dogs. Xylazine caused significant decreases in heart rate, cardiac output, left ventricular work, breathing rate, minute ventilation, physiologic dead space, oxygen transport, mixed venous partial pressure of oxygen, and oxygen concentration. It caused significant increases in systemic blood pressure, central venous pressure, systemic vascular resistance, tidal volume, and oxygen utilization ratio. The subsequent administration of ketamine was associated with significant increases in heart rate (transient increase), cardiac output, the alveolar-arterial PO2 gradient and venous admixture (transient increase), and arterial PCO2 (transient increase). It caused significant decreases in stroke volume (transient decrease), left ventricular stroke work (transient decrease), effective alveolar ventilation, arterial PO2 and oxygen content (transient decrease).     

Cardiopulmonary and anesthetic effects of ketamine and its enantiomers in dogs

Dogs were used to determine cardiopulmonary and chemical restraining effects of racemic ketamine and its enantiomers. Levorotatory ketamine induced the shortest duration of unconsciousness and recumbency when compared with effects of dextrorotatory and racemic ketamine. Administration of racemic ketamine or either of its enantiomers (30 mg/kg of body weight, IV) to dogs recovering from isoflurane anesthesia induced transient, but significant (P less than 0.05), decreases in arterial blood pressure, left ventricular contractility, cardiac output, and total peripheral vascular resistance. Arterial blood pressure and left ventricular contractility significantly (P less than 0.05) increased at later times after ketamine administration. Arterial pH and the PO2 values decreased after IV administration of racemic ketamine or its enantiomers. Significant differences in cardiopulmonary variables were not observed between groups given ketamine or its enantiomers.     

Alterations in epinephrine-induced arrhythmogenesis after xylazine and subsequent yohimbine administration in isoflurane-anesthetized dogs

Effects of xylazine (1.1 mg/kg of body weight, IV bolus, plus 1.1 mg/kg/h infusion) and subsequent yohimbine (0.125 mg/kg, IV bolus) administration on the arrhythmogenic dose of epinephrine (ADE) in isoflurane (1.8% end-tidal)-anesthetized dogs were evaluated. The ADE was defined as the total dose of epinephrine that induced greater than or equal to 4 premature ventricular contractions within 15 seconds during a 3-minute infusion period or within 1 minute after the end of infusion. Total ADE values during isoflurane anesthesia, after xylazine administration, and after yohimbine injection were 36.6 +/- 8.45 micrograms/kg, 24.1 +/- 6.10 micrograms/kg, and 45.7 +/- 6.19 micrograms/kg, respectively. Intravenous xylazine administration significantly (P less than 0.05) increased blood pressure and decreased heart rate, whereas yohimbine administration induced a significant (P less than 0.05) decrease in blood pressure. induced a significant (P less than 0.05) decrease in blood pressure. After yohimbine administration, the ADE significantly (P less than 0.05) increased above that after isoflurane plus xylazine administration. After yohimbine administration, blood pressure measured immediately before epinephrine-induced arrhythmia was significantly (P less than 0.05) less than the value recorded during isoflurane plus xylazine anesthesia. Heart rate was unchanged among treatments immediately before epinephrine-induced arrhythmia. Seemingly, yohimbine possessed a protective action against catecholamine-induced arrhythmias in dogs anesthetized with isoflurane and xylazine.     

Duration of etomidate-induced adrenocortical suppression during surgery in dogs

Plasma cortisol concentrations were compared in canine surgical patients given etomidate (2 mg/kg of body weight, IV) or thiopental sodium (12 mg/kg, IV) for anesthetic induction. Blood samples to determine plasma concentrations of etomidate were obtained at 0, 5, 10, 15, and 30 minutes and 1, 2, 3, 4, 5, 6, 8, 12, and 24 hours after induction. Adrenocortical function was evaluated before surgery by use of adrenocorticotropic hormone stimulation tests. Dogs in both induction groups had high plasma cortisol concentrations after induction. Dogs given thiopental had a significant increase (P less than 0.05) in plasma cortisol concentration from baseline at 2, 3, 4, 5, 6, 8, and 12 hours after induction. Dogs given etomidate had a significant increase (P less than 0.05) in plasma cortisol concentration from baseline at 5, 6, and 8 hours after induction. A comparison of plasma cortisol concentrations determined at 2, 3, 4, 5, and 6 hours after induction with thiopental or etomidate revealed a higher (P less than 0.05) concentration in dogs given thiopental. The disposition of etomidate was best described by a 2-compartment model, with a redistribution half-life of 0.12 +/- 0.04 minute and a terminal half-life of 1.70 +/- 0.27 minute. Plasma cortisol concentrations did not correlate with plasma etomidate concentrations. We conclude that, compared with thiopental, a single bolus injection of etomidate reduces the adrenocortical response to anesthesia and surgery from 2 to 6 hours after induction. Because cortisol concentrations were significantly higher than baseline, and because cardiopulmonary function is maintained after a single bolus injection of etomidate, it can be considered a safe induction agent in dogs.     

Cardiopulmonary effects of acepromazine and of the subsequent administration of ketamine in the dog

Cardiopulmonary consequences of acepromazine (0.2 mg/kg of body weight, IV) followed by IV administration of ketamine (10 mg/kg) were evaluated in 13 dogs. Acepromazine caused significant decreases in arterial blood pressure, stroke volume, left ventricular work, left ventricular stroke work, breathing rate, minute ventilation, and oxygen consumption. Subsequent administration of ketamine caused significant increases in heart rate, effective alveolar volume, alveolar-arterial Po2 gradient (transient increase), venous admixture (transient increase), and PaCO2 and PVCO2 (transient increases), and caused significant decreases in stroke volume, minute ventilation, physiologic dead space, and arterial and venous PO2 (transient decreases).     

Influence of preinduction methoxamine, lactated Ringer solution, or hypertonic saline solution infusion or postinduction dobutamine infusion on anesthetic-induced hypotension in horses

A controlled study of the cardiovascular responses in horses anesthetized with acepromazine (0.05 mg/kg of body weight, IV), guaifenesin (100 mg/kg, IV), thiamylal (5.0 mg/kg, IV), and halothane in O2 (1.2 to 1.4% end-expired concentration) was performed to determine whether hypotension could be prevented by use of various treatments. Six horses were given 5 treatments in a randomized sequence: no treatment (control), methoxamine (0.04 mg/kg, IV), lactated Ringer solution (20.0 ml/kg, IV), 7.5% hypertonic saline solution (4.0 ml/kg, IV), or constant infusion of dobutamine (5.0 mg/kg/min, IV) during anesthesia. Heart rate, ECG, blood pressure, central venous pressure, cardiac output, blood gas analysis, PVC, and plasma total protein concentration were measured during the study. Compared with the control value, an increase in blood pressure during halothane administration was observed after administration of lactated Ringer solution, hypertonic saline solution, or dobutamine (P less than 0.05). The improved blood pressure response to hypertonic saline solution and dobutamine was related to an increase in cardiac output, which was statistically significant (P less than 0.05). Other statistically significant differences in cardiopulmonary responses among treatments were not observed during anesthesia. The PCV was increased in response to dobutamine infusion, and plasma total protein concentration was reduced in response to administration of hypertonic saline or lactated Ringer solution.     

Cardiorespiratory Effects of the Intravenous Administration of Tiletamine-zolazepam to Cats

The hemodynamic and respiratory effects of three doses (9.7, 15.8, and 23.7 mg/kg intravenous [IV]) of a 1:1 combination of tiletamine and zolazepam were studied after isoflurane anesthesia in cats instrumented for the recording of hemodynamic data. Systolic, mean, and diastolic arterial blood pressures were decreased 1 minute after drug administration but then increased above baseline with all three doses. Cardiac output was decreased briefly at 1 minute with the 15.8 and 23.7 mg/kg doses. The rate of development of left ventricular pressure and peripheral vascular resistance decreased at 1 minute but returned to baseline or above by 10 minutes. There were no significant changes in heart rate, central venous pressure, or left ventricular end diastolic pressure. The arterial pH and blood gas measurements reflected the development of respiratory acidosis after administration of 23.7 mg/kg. These results support the conclusions that tiletamine-zolazepam administered intravenously is a useful and comparatively safe anesthetic agent in the cat.     

Cardiorespiratory Effects of Four Opioid-Tranquilizer Combinations in Dogs

The cardiorespiratory effects of four opioid-tranquilizer combinations were evaluated in six dogs. The four combinations were administered to each dog in a randomized order. Buprenorphine (BUP; 0.01 mg/kg IV) or oxymorphone (OXY; 0.1 mg/kg IV) was followed in 10.4 ± 1.3 minutes by midazolam (MID; 0.3 mg/kg IV) or acepromazine (ACE; 0.05 mg/kg IV). Nalbuphine (0.16 mg/kg IV) was administered 94.1 ± 2.3 minutes after the tranquilizer was given. Heart rate (HR) and mean arterial blood pressure (MAP) decreased significantly ( P < .05) after each combination. MAP was significantly lower with combinations using ACE. Most dogs panted after opioid administration; this was associated with increased minute volume (V_M) and decreased tidal volume (V_T). After administration of the tranquilizer, mean breathing rate and V_M index (V_MI) were significantly lower with ACE combinations. There were no significant changes in pH and blood gas variables after BUP-ACE. The other three combinations were associated with significant ( P < .05) decreases in pH and increases in Paco₂. Mean Pao₂ decreased significantly ( P < .05) with OXY combinations but not BUP combinations. Dysrhythmias (atrial or ventricular escape complexes) were seen with each combination. HR increased significantly ( P < .05) after nalbuphine in dogs receiving OXY, but not BUP. Dogs receiving OXY became more alert after nalbuphine on six of 12 occasions, whereas dogs receiving BUP became less alert on six of 12 occasions. OXY-ACE provided the most chemical restraint/sedation and BUP-MID provided the least.     

Anesthetic potency and cardiopulmonary effects of sevoflurane in goats: comparison with isoflurane and halothane.

The anesthetic potency and cardiopulmonary effects of sevoflurane were compared with those of isoflurane and halothane in goats. The (mean +/- SD) minimal alveolar concentration (MAC) was 0.96 +/- 0.12% for halothane, 1.29 +/- 0.11% for isoflurane, and 2.33 +/- 0.15% for sevoflurane. Cardiopulmonary effects of sevoflurane, halothane and isoflurane were examined at end-tidal concentrations equivalent to 1, 1.5 and 2 MAC during either spontaneous or controlled ventilation (SV or CV). During SV, there were no significant differences in respiration rate, tidal volume and minute ventilation between anesthetics. Dose-dependent decreases in both tidal volume and minute ventilation induced by halothane were greater than those by either sevoflurane or isoflurane. Hypercapnia and acidosis induced by sevoflurane were not significantly different from those by either isoflurane or halothane at 1 and 1.5 MAC, but were less than those by halothane at 2 MAC. There was no significant difference in heart rate between anesthetics during SV and CV. During SV, all anesthetics induced dose-dependent decreases in arterial pressure, rate pressure product, systemic vascular resistance, left ventricular minute work index and left ventricular stroke work index. Systemic vascular resistance with isoflurane at 2 MAC was lower than that with sevoflurane. During CV, sevoflurane induced dose-dependent circulatory depression (decreases in arterial pressure, cardiac index, rate pressure product, systemic vascular resistance, left ventricular minute work index and right ventricular minute work index), similar to isoflurane. Halothane did not significantly alter systemic vascular resistance from 1 to 2 MAC.     

Cardiovascular and respiratory effects of three rapidly acting barbiturates in dogs

The cardiovascular and respiratory effects of 3 rapidly acting barbiturates, thiopental sodium, thiamylal sodium, and methohexital sodium, were studied in dogs from completion of injection until 12.5 minutes after injection. The doses administered were 19.4 mg of thiopental/kg of body weight, 18.4 mg of thiamylal/kg, and 9.7 mg of methohexital/kg, which were chosen as equipotent doses necessary to inhibit the laryngoscopic reflex in 50% of the population. To determine the cardiovascular and respiratory effects for each drug, the values at each measurement time following injection were compared with baseline values (T0). At the 15- and 30-second measurement times following thiopental administration, stroke volume (SV) decreased; heart rate (HR), left atrial pressure, and mean pulmonary arterial pressure increased; and cardiac index (CI), myocardial contractility, and systemic and pulmonary vascular resistances were not different from baseline values. Mean arterial pressure (MAP) was not different from the baseline value at 15 seconds, but was increased from 30 seconds to 2 minutes. All values except HR had returned to baseline values by 7.5 minutes. At all measurement times, arterial oxygen tension and arterial pH were decreased, and arterial carbon dioxide tension increased from baseline values. Although the cardiovascular and respiratory changes following administration of thiamylal and methohexital were similar to those described for thiopental, some differences were found. Following thiamylal administration, systemic vascular resistance increased at 1 minute, pulmonary vascular resistance increased at 1 and 2 minutes, and myocardial contractility increased at 1 and 2 minutes. Following methohexital administration, MAP decreased at 15 seconds, and SV decreased at all measurement times.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of high-frequency oscillatory ventilation in halothane-anesthetized dogs

Hemodynamic effects of spontaneous ventilation, intermittent positive-pressure ventilation (IPPV), and high-frequency oscillatory ventilation (HFOV) were compared in 6 dogs during halothane anesthesia. Anesthesia was induced with IV thiamylal Na and was maintained with halothane (end-tidal concentration, 1.09%). During placement of catheters, dogs breathed spontaneously through a conventional semiclosed anesthesia circuit. Data were collected, and dogs were mechanically ventilated, using IPPV or HFOV in random order. Ventilation was adjusted to maintain PaCO2 between 38 and 43 mm of Hg during IPPV and HFOV. Cardiac index, aortic blood pressure, and maximum rate of increase of left ventricular pressure were significantly (P less than 0.05) less during HFOV than during spontaneous ventilation, whereas right atrial and pulmonary artery pressure were significantly greater during HFOV than during spontaneous ventilation. During IPPV, only the maximum rate of increase of left ventricular pressure was significantly less than that during spontaneous ventilation.     

Doxapram: cardiopulmonary effects in the horse

The cardiopulmonary effects of 3 dosages of doxapram hydrochloride (0.275 mg/kg, 0.55 mg/kg, and 1.1 mg/kg, IV) were studied in 6 adult horses. Doxapram given IV significantly (P less than 0.05) decreased PaCO2 and increased respiratory rate, cardiac output arterial blood pressures (systolic, mean, and diastolic) arterial pH, and PaO2 at 1 minute after each dose was administered. Heart rate and mean and diastolic pulmonary arterial blood pressure were significantly (P less than 0.05) increased 1 minute after the 2 larger dosages of doxapram were given (0.55 mg/kg and 1.1 mg/kg, IV), but not after the smallest dosage was given. All measurements, except heart rate and cardiac output, had returned to base line by 5 minutes after each dosing. Heart rate remained significantly (P less than 0.05) increased 10 minutes after the 0.55 mg/kg dosage was given and 30 minutes after the 1.1 mg/kg dosage. Cardiac output remained significantly (P less than 0.05) increased at 10 minutes, 5 minutes, and 30 minutes after the 0.275, 0.55, and 1.1 mg/kg dosages, respectively, were given.     

Arrhythmias in dogs associated with epinephrine and thiamylal anesthesia.

Sinus tachycardia bigeminy, ventricular rhythm, ventricular tachycardia, and ventricular fibrillation are produced by relatively small intravenous doses of epinephrine in nonanesthetized dogs and in dogs anesthetized with thiamylal sodium. Origin of the abnormal beat in coupled bigeminal rhythms generated from the bundle o of His or above. Increases in arterial blood pressure may predispose to arrhythmia formation during thiamylal anesthesia.     

Hemodynamic effects of unilateral segmented lumbar epidural analgesia in cattle.

Hemodynamic measurements, arterial and mixed venous blood gas tensions, and pH were determined in 12 adult cows (mean weight 538 kg) following the injection of 8 ml of 5% procaine between the first and the second lumber vertebra into the epidural space. Comparison of base-line data with obtained during unilateral segmented lumbar analgesia between T(13) and L(3) segments indicated significant decreases (P is less than 0.05) in total peripheral resistance and diastolic and mean arterial blood pressures, and significant increases (P is less than 0.05) in heart rate and cardiac output. Arterial and mixed venous blood gas tensions and pH, O(2)-uptake, stroke volume, left ventricular stroke work, left ventricular minute work and hematocrit did not change significantly (P is less than 0.05). Cardiovascular and respiratory values in two cows (mean weight 700 kg) given xylazine (50 mg, IM), were depressed from base-line data, but did not change significantly (P is less than 0.05) during unilateral segmental epidural analgesia of segments T(13 to L(3). The nonsedated healthy cow tolerates sympathetic vasomotor blockade between T(13) and L(3) segments well and is able to mobilize circulatory mechanisms effectively.     

Effects of xylazine on ventilation in horses.

The effects of 3 commonly used dosages (0.3, 0.5, and 1.1 mg/kg of body weight, IV) of xylazine on ventilatory function were evaluated in 6 Thoroughbred geldings. Altered respiratory patterns developed with all doses of xylazine, and horses had apneic periods lasting 7 to 70 seconds at the 1.1 mg/kg dosage. Respiratory rate, minute volume, and partial pressure of oxygen in arterial blood (PaO2) decreased significantly (P less than 0.001) with time after administration of xylazine, but significant differences were not detected among dosages. After an initial insignificant decrease at 1 minute after injection, tidal volume progressively increased and at 5 minutes after injection, tidal volume was significantly (P less than 0.01) greater than values obtained before injection. Partial pressure of carbon dioxide in arterial blood (PaCO2) was insignificantly increased. After administration of xylazine at a dosage of 1.1 mg/kg, the mean maximal decrease in PaO2 was 28.2 +/- 8.7 mm of Hg and 22.2 +/- 4.9 mm of Hg, measured with and without a respiratory mask, respectively. Similarly, the mean maximal increase in PaCO2 was 4.5 +/- 2.3 mm of Hg and 4.2 +/- 2.4 mm of Hg, measured with and without the respiratory mask, respectively. Significant interaction between use of mask and time was not detected, although the changes in PaO2 were slightly attenuated when horses were not masked. The temporal effects of xylazine on ventilatory function in horses should be considered in selecting a sedative when ventilation is inadequate or when pulmonary function testing is to be performed.     

Analgesic and cardiopulmonary effects of premedication with tramadol in calves anesthetized with the infusion of guaifenesin and thiamylal

This study examined the analgesic and cardiopulmonary effects of intravenous (IV) tramadol during general intravenous anesthesia in calves. Calves were premedicated with diazepam (0.2 mg/kg, IV) with tramadol (2 mg/kg, IV) (group T) or saline (group S). Anesthesia was induced by thiamylal sodium (4 mg/kg, IV) and maintained with an infusion (2 ml/kg/hr) of 5% guaifenesin containing thiamylal sodium (2 mg/ml). Additional thiamylal sodium (1–2 mg/kg, IV) was administered when interference from the calves was observed during surgery. The total counts of additional thiamylal sodium administration, analgesia score using a visual analog scale, recovery time, and cardiopulmonary function in the different groups were assessed and compared. Group T showed significantly fewer counts of additional drug administration and a significantly higher analgesia score. Tramadol may provide adequate analgesia with minimal cardiopulmonary changes in calves during general anesthesia.     

Cardiovascular effects of vasopressors in halothane-anesthetized dogs before and after hemorrhage

Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP, with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR.     

Hemodynamic response of endotoxemic calves to treatment with small-volume hypertonic saline solution

The hemodynamic effects of hypertonic saline solution (HSS) resuscitation on endotoxic shock were examined in pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli (055:B5) endotoxin was infused IV at dosage of 0.1 microgram/kg of body weight for 30 minutes. Endotoxin induced large decreases in cardiac index, stroke volume, maximal rate of change of left ventricular pressure (+dP/dtmax), femoral and mesenteric arterial blood flow, glomerular filtration rate, urine production, and mean aortic pressure. Severe pulmonary arterial hypertension and increased pulmonary vascular resistance were evident at the end of endotoxin infusion. Treatment with HSS (2,400 mosm of NaCl/L, 4 ml/kg) or an equivalent sodium load of isotonic saline solution (ISS: 300 mosm of NaCl/L, 32 ml/kg) was administered 90 minutes after the end of endotoxin administration. Both solutions were infused IV over a 4- to 6-minute period. Administration of HSS induced immediate and significant (P less than 0.05) increase in stroke volume and central venous pressure, as well as significant decrease in pulmonary vascular resistance. These effects were sustained for 60 minutes, after which all variables returned toward preinfusion values. The hemodynamic response to HSS administration was suggestive of rapid plasma volume expansion and redistribution of cardiac output toward splanchnic circulation. Plasma volume expansion by HSS was minimal 60 minutes after resuscitation. Administration of ISS induced significant increase in cardiac index, stroke volume, femoral arterial blood flow, and urine production. These effects were sustained for 120 minutes, at which time, calves were euthanatized. Compared with HSS, ISS induced sustained increase in mean pulmonary arterial pressure and only a small increase in mesenteric arterial blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of cardiopulmonary effects of isoflurane and halothane after atropine-guaifenesin-thiamylal anesthesia for rumenotomy in steers

Cardiopulmonary effects were assessed in 12 yearling steers anesthetized with guaifenesin and thiamylal sodium, intubated, and allowed to breathe isoflurane or halothane in oxygen spontaneously. Light surgical anesthesia, determined using eye position as a clinical indication of anesthetic depth, was maintained during surgical placement of a rumen cannula. Heart rate and respiratory rate were measured while the steers were standing quietly (baseline). Atropine (0.06 mg/kg of body weight, IM) was given after baseline measurements were taken. Heart rate, respiratory rate, arterial blood pressures, pHa, PaCO2, PaO2, arterial [HCO3-], esophageal temperature, and end-tidal anesthetic concentration were measured every 15 minutes for 90 minutes after induction of anesthesia. Mean heart rate increased significantly (P less than 0.05) above baseline in the isoflurane group at 15 and 30 minutes. Mean respiratory rate increased significantly (P less than 0.05) above baseline in the halothane group at 45 minutes. At 45 minutes, mean respiratory rate was lower (P less than 0.05) in the isoflurane group, compared with that in the halothane group. Mean values for arterial blood pressures and arterial gases were similar for both agents at comparable times. Mean end-tidal isoflurane concentrations were less than mean end-tidal halothane concentrations at each comparable time during maintenance of similar anesthetic depth. Maintenance of anesthesia with isoflurane resulted in higher heart rates and lower respiratory rates, compared with maintenance of anesthesia with halothane in these steers.     

Yohimbine/flumazenil antagonism of hemodynamic alterations induced by a combination of midazolam, xylazine, and butorphanol in dogs.

Reversal of hemodynamic alterations induced by midazolam maleate (1.0 mg/kg of body weight), xylazine hydrochloride (0.44 mg/kg), and butorphanol tartrate (0.1 mg/kg) with yohimbine (0.1 mg/kg) and flumazenil (0.25 mg/kg) was evaluated in 5 dogs. The dogs were anesthetized with isoflurane for instrumentation. With return to consciousness, baseline values were recorded, and the midazolam/xylazine/butorphanol mixture with glycopyrrolate was administered IV. Hemodynamic data were recorded for 60 minutes, and then a reversal mixture of yohimbine and flumazenil was administered IV. All variables were measured 1 minute from beginning of the reversal injection. Mean arterial pressure, pulmonary arterial pressure, systemic vascular resistance, and right ventricular stroke work index increased significantly (P < 0.05) above baseline at 60 minutes. Cardiac index and central venous pressure significantly decreased below baseline at 60 minutes. After reversal, mean arterial pressure and central venous pressure significantly decreased from baseline, whereas cardiac index, pulmonary arterial pressure, and right ventricular stroke work index increased significantly above baseline. Heart rate, cardiac index, and right ventricular stroke work index increased significantly above the 60-minute value after reversal. Mean arterial pressure and systemic vascular resistance decreased significantly (P < 0.05) below the 60-minute value after reversal. The hemodynamic alterations accompanying midazolam/xylazine/butorphanol sedation-anesthesia may be rapidly reversed with a combination of yohimbine and flumazenil.