Comparison of isoflurane and halothane as inhalation anaesthetics in the dog

Summary

A number of clinically important features of isoflurane anaesthesia were studied in comparison to those of halothane. Two groups of dogs were used. After light premedication, anaesthesia was induced by mask, and both groups of dogs were maintained for 30 minutes at 1.5 × MAC value of either halothane or isoflurane in a combination of oxygen and nitrous oxide (50:50). All animals were ventilating spontaneously.

There was no difference in the speed of induction of the halothane and isoflurane groups. Blood pressure in both groups dropped to approximately 7.5 kPa (56 mm Hg) during maintenance anesthesia (1.5 MAC), while the heart rate was significantly higher in the isoflurane group. Individual respiratory variables were not significantly different between the two groups, however the differences between the trends of the mean values were significant (Sign‐test). In general, with isoflurane, respiration rates were lower, with the tidal volume and end tidal CO₂ being greater.

The trends in pH and arterial pCO₂ showed a slightly more severe respiratory acidosis in the isoflurane group. However, neither group showed values corresponding to any expected clinical problems. Speed of recovery (determined by times to head‐lift and righting‐reflex) was greater in the isoflurane group. Previously known important features of isoflurane are low biodegradability, low blood: gas partition coefficient, and decreased myocardial sensitivity to catecholamines. It is concluded from this study that isoflurane deserves a place in canine anesthesia whenever these specific pharmacologic properties are desired.     

Effect of medetomidine on respiration and minimum alveolar concentration in halothane- and isoflurane-anesthetized dogs

OBJECTIVE: To evaluate the effect of medetomidine on minimum alveolar concentration (MAC), respiratory rate, tidal volume, minute volume (V(M)), and maximum inspiratory occlusion pressure (IOCP(max)) in halothane- and isoflurane-anesthetized dogs. ANIMALS: 6 healthy adult dogs (3 males and 3 females). PROCEDURE: The MAC of both inhalants was determined before and 5, 30, and 60 minutes after administration of medetomidine (5 microg/kg, IV). Dogs were subsequently anesthetized by administration of halothane or isoflurane and administered saline (0.9% NaCl) solution IV or medetomidine (5 microg/kg, IV). Respiratory variables and IOCP(max) were measured at specific MAC values 15 minutes before and 5, 30, and 60 minutes after IV administration of medetomidine while dogs breathed 0% and 10% fractional inspired carbon dioxide (FICO2). Slopes of the lines for VM/FICO2 and IOCP(max)/FICO2 were then calculated. RESULTS: Administration of medetomidine decreased MAC of both inhalants. Slope of V(M)/FICO2 increased in dogs anesthetized with halothane after administration of medetomidine, compared with corresponding values in dogs anesthetized with isoflurane. Administration of medetomidine with a simultaneous decrease in inhalant concentration significantly increased the slope for V(M)/FICO2, compared with values after administration of saline solution in dogs anesthetized with halothane but not isoflurane. Values for IOCP(max) did not differ significantly between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Equipotent doses of halothane and isoflurane have differing effects on respiration that are most likely attributable to differences in drug effects on central respiratory centers. Relatively low doses of medetomidine decrease the MAC of halothane and isoflurane in dogs.     

Hepatic effects of halothane, isoflurane or sevoflurane anaesthesia in dogs

The effects of halothane, isoflurane and sevoflurane anaesthesia on hepatic function and hepatocellular damage were investigated in dogs, comparing the activity of hepatic enzymes and bilirubin concentration in serum. An experimental study was designed. Twenty-one clinically normal mongrel dogs were divided into three groups and accordingly anaesthetized with halothane (n = 7), isoflurane (n = 7) and sevoflurane (n = 7). The dogs were 1-4 years old, and weighed between 13.5 and 27 kg (18.4 +/- 3.9). Xylazine HCI (1-2 mg/kg) i.m. was used as pre-anaesthetic medication. Anaesthesia was induced with propofol 2 mg/kg i.v. The trachea was intubated and anaesthesia maintained with halothane, isoflurane or sevoflurane in oxygen at concentrations of 1.35, 2 and 3%, respectively. Intermittent positive pressure ventilation (tidal volume, 15 ml/kg; respiration rate, 12-14/min) was started immediately after intubation and the anaesthesia lasted for 60 min. Venous blood samples were collected before pre-medication, 24 and 48 h, and 7 and 14 days after anaesthesia. Serum level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT), lactate dehydrogenase (LDH GGT) activities and bilirubin concentration were measured. Serum AST, ALT and GGT activities increased after anaesthesia in all groups. In the halothane group, serum AST and ALT activities significantly increased all the time after anaesthesia compared with baseline activities. But in the isoflurane group AST and ALT activities increased only between 2 and 7 days, and in the sevoflurane group 7 days after anaesthesia. GGT activity was increased in the halothane group between 2 and 7 days, and in the isoflurane and sevoflurane groups 7 days after anaesthesia. All dogs recovered from anaesthesia without complications and none developed clinical signs of hepatic damage within 14 days. The results suggest that the use of halothane anaesthesia induces an elevation of serum activities of liver enzymes more frequently than isoflurane or sevoflurane from 2 to 14 days after anaesthesia in dogs. The effects of isoflurane or sevoflurane anaesthesia on the liver in dogs is safer than halothane anaesthesia in dogs.     

Effects of Halothane, Enflurane, and Isoflurane on Supraventricular and Ventricular Rate in Dogs With Complete Atrioventricular Block

Complete atrioventricular (AV) block was produced in 32 chloralose-anesthetized autonomically intact dogs to determine the effects of halothane, enflurane, and isoflurane on supraventricular and ventricular rate. Halothane (n = 17), enflurane (n = 6), and isoflurane (n = 9) were administered in three separate experiments in sequential minimum alveolar concentration (MAC) multiples of 0.5, 1.0, 1.5, 2.0, 1.5, and 1.0. Supraventricular rate, ventricular rate, and mean arterial blood pressure (MAP) were measured and recorded at baseline and after a 20-minute equilibration period of each inhalation anesthetic at each MAC multiple. Increasing concentrations of enflurane and isoflurane significantly decreased supraventricular rate ( P < .05). Ventricular rate was not significantly changed by sequential MAC multiples of halothane, enflurane, and isoflurane. Increasing concentrations of halothane, enflurane, and isoflurane significantly decreased MAP with enflurane producing the most significant decrease ( P < .05). Ventricular arrhythmias occurred in 5 of 17 dogs anesthetized with halothane and 1 of 9 dogs anesthetized with isoflurane. Inhalation anesthesia can significantly decrease supraventricular rate and MAP, does not alter ventricular rate, and can produce ventricular arrhythmias in dogs with complete AV block.     

The effect of hypovolemia due to hemorrhage on the minimum alveolar concentration of isoflurane in the dog

OBJECTIVE: To determine the effect of hypovolemia on the minimum alveolar concentration (MAC) of isoflurane in the dog. STUDY DESIGN: Randomized, cross-over trial. ANIMAL POPULATION: Six healthy intact mixed breed female dogs weighing 18.2-29.0 kg. METHODS: Dogs were randomly assigned to determine the MAC of isoflurane in a normovolemic or hypovolemic state with a minimum of 18 days between trials. On both occasions, anesthesia was initially induced and maintained for 40 minutes with isoflurane delivered in oxygen while vascular catheters were placed in the cephalic vein and dorsal metatarsal artery. In dogs assigned to the hypovolemic group, 30 mL kg(-1) of blood was removed at 1 mL kg(-1) minute(-1) from the arterial catheter. All dogs were allowed to recover from anesthesia. Thirty minutes after the discontinuation of isoflurane, anesthesia was re-induced with isoflurane in oxygen delivered by face mask. The tracheas were intubated, and connected to an anesthetic machine with a Bain anesthetic circuit. Mechanical ventilation was instituted at a rate of 10 breaths minute(-1) with the tidal volume set to deliver 10-15 mL kg(-1). Airway gases were monitored continuously and tidal volume was adjusted to maintain an end-tidal carbon dioxide level of 35-40 mmHg (4.67-5.33 kPa). Body temperature was maintained at 37-38 degrees C (98.6-100.4 degrees F). The MAC determination was performed using an electrical stimulus applied to the toe web and MAC was defined as the mean value of end-tidal isoflurane between the concentrations at which a purposeful movement did and did not occur in response to the electrical stimulus. The MAC values were compared between groups using a Student's t-test. RESULTS: The MAC of isoflurane was significantly less in hypovolemic dogs (0.97 +/- 0.03%) compared with normovolemic dogs (1.15 +/- 0.02%) (p < 0.0079). CONCLUSIONS AND CLINICAL RELEVANCE: The MAC of isoflurane is reduced in dogs with hypovolemia resulting from hemorrhage. Veterinarians should be prepared to deliver a lower percentage of isoflurane to maintain anesthesia in hypovolemic dogs during diagnostic and therapeutic procedures.     

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.     

Recovery times and evaluation of clinical hemodynamic parameters of sevoflurane, isoflurane and halothane anaesthesia in mongrel dogs

In the present study the influence of three volatile agents (halothane, isoflurane and sevoflurane) in oxygen at two concentrations [1.5 and 2 minimum alveolar concentration (MAC)] on non-invasive cardio-respiratory parameters (heart and respirators rates, non-invasive blood pressures at 15, 30, 60 min and after extubation) and on the recovery times (appearance of the first eyelid reflex, emergence time) after clinical anaesthesia was studied. After premedication with fentanyl-droperidol (5 microg/kg and 0.25 mg/kg, intramuscularly) and induction with propofol (5 mg/kg, intravenously) six dogs were randomly anaesthetized for 1 h for a standard neurologic stimulation test. A wide individual variation in respiration rate (induced by an initial hyperpnea) was observed in the 1.5 MAC protocols, without significant differences. Heart rate was significantly lower during 1.5 and 2 MAC halothane when compared to isoflurane and sevoflurane. An increase from 1.5 to 2 MAC induced significant decreases in diastolic (DAP) and mean arterial blood pressure in all groups without significant changes in the systolic arterial pressures. Only DAP in sevoflurane protocol was significantly different at 1.5 and 2 MAC compared to halothane. Time had no significant influences in the non-invasive blood pressures in all protocols. Extubation induced a significant increase of all parameters in all protocols. The time for a first eyelid reflex was significantly longer after 2 MAC compared to the 1.5 MAC protocol. There was no significant difference between the three anaesthetic agents. Although emergence time was longest for halothane at both anaesthetic concentrations, no significant difference in emergence time was observed for the three volatile agents.     

Effect of halothane, isoflurane, and pentobarbital anesthesia on myocardial irritability in chickens

The relative myocardial irritant properties of halothane, isoflurane, and pentobarbital were evaluated in chickens. Sixteen adult male broiler chickens were randomly assigned to 1 of 3 groups: group-1 chickens were anesthetized with pentobarbital (30 mg/kg, IV), group-2 chickens were anesthetized with halothane (end tidal halothane 1.2%), and group-3 chickens were anesthetized with isoflurane (end tidal isoflurane 2.1%). Birds in any 2 of the 3 treatment groups were tested on any 1 day. Local anesthesia was induced, and blood pressure, heart rate, ECG, and blood gas variables were measured before general anesthesia was induced. Positive-pressure ventilation with an inspired O2 fraction greater than 0.95 was adjusted to result in an end tidal CO2 concentration that reflected a Paco2 similar to that obtained prior to anesthesia and ventilation. All measurements were repeated. The threshold for ventricular fibrillation in response to electrical stimulation of the heart was then determined for all birds. Effects of anesthesia on hemodynamic and blood gas variables were similar in all 3 groups. Compared with halothane or pentobarbital, isoflurane anesthesia resulted in a significantly (P less than 0.05) lower threshold for electrical fibrillation of the heart.     

Electroencephalography of Detomidine-Ketamine-Halothane and Detomidine-Ketamine-lsoflurane Anesthetized Horses During Orthopedic Surgery A Comparison

This study was done to compare the electroencephalographic (EEG) response evoked by orthopedic surgery in halothane- and isoflurane-anesthetized horses. Eight horses scheduled for bilateral arthroscopic surgery of the stifle were premedicated with detomidine (20 μg/kg) intravenously and five minutes later induced to anesthesia with ketamine (2.2 mg/kg) intravenously. Anesthesia was maintained with either halothane or isoflurane. Assignment of inhalation anesthetic was done randomly. The multiple of minimal alveolar concentration (MAC) of halothane required for anesthesia was significantly higher than the multiple of MAC of isoflurane (p < .05) required. Total amplitude of the EEG with halothane was smaller than with isoflurane (p < .05), but 13.0 to 32.0 Hz high frequency/0.0 to 3.9 Hz low frequency (|3/A) ratio was greater for halothane (p < .05). Arterial partial pressure of oxygen (PaO₂) was significantly (p < .05) higher with isoflurane than with halothane. The differences in EEG frequency shift observed suggest that isoflurane provided better analgesia than halothane for this group of horses.     

Effect of medetomidine administration on bispectral index measurements in dogs during anesthesia with isoflurane

OBJECTIVE: To determine the relationship between bispectral index (BIS) and minimum alveolar concentration (MAC) multiples of isoflurane after IM injection of medetomidine or saline (0.9% NaCl) solution in anesthetized dogs. ANIMALS: 6 dogs. PROCEDURE: Each dog was anesthetized 3 times with isoflurane. First, the MAC of isoflurane for each dog was determined by use of the tail clamp method. Second, anesthetized dogs were randomly assigned to receive an IM injection of medetomidine (8 microg x kg(-1)) or an equal volume of isotonic saline (0.9% NaCl) solution 30 minutes prior to beginning BIS measurements. Last, anesthetized dogs received the remaining treatment (medetomidine or isotonic saline solution). Dogs were anesthetized at each of 4 MAC multiples of isoflurane. Ventilation was controlled and atracurium (0.2 mg/kg followed by 6 microg/kg/min as a continuous infusion, IV) administered. After a 20-minute equilibration period at each MAC multiple of isoflurane, BIS data were collected for 5 minutes and median values of BIS calculated. RESULTS: BIS significantly decreased with increasing MAC multiples of isoflurane over the range of 0.8 to 2.0 MAC. Mean (+/- SD) MAC of isoflurane was 1.3 +/- 0.2%. During isoflurane-saline anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 65 +/- 8, 60 +/- 7 52 +/- 3, and 31 +/- 28, respectively. During isoflurane-medetomidine anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 77 +/- 4, 53 +/- 7, 31 +/- 24, and 9 +/- 20, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: BIS monitoring in dogs anesthetized with isoflurane has a predictive value in regard to degree of CNS depression. During isoflurane anesthesia, our results support a MAC-reducing effect of medetomidine.     

Effects of morphine,lidocaine, ketamine,and morphine-lidocaine-ketamine drug combination on minimum alveolar concentration in dogs anesthetized with isoflurane

OBJECTIVE: To determine the effects of constant rate infusion of morphine, lidocaine, ketamine, and morphine-lidocaine-ketamine (MLK) combination on end-tidal isoflurane concentration (ET-Iso) and minimum alveolar concentration (MAC) in dogs anesthetized with isoflurane and monitor depth of anesthesia by use of the bispectral index (BIS). ANIMALS: 6 adult dogs. PROCEDURE: Each dog was anesthetized with isoflurane on 5 occasions, separated by a minimum of 7 to 10 days. Individual isoflurane MAC values were determined for each dog. Reduction in isoflurane MAC, induced by administration of morphine (3.3 microg/kg/min), lidocaine (50 microg/kg/min), ketamine (10 microg/kg/min), and MLK, was determined. Heart rate, mean arterial blood pressure, oxygen saturation as measured by pulse oximetry (Spo2), core body temperature, and BIS were monitored. RESULTS: Mean +/- SD isoflurane MAC was 1.38 +/- 0.08%. Morphine, lidocaine, ketamine, and MLK significantly lowered isoflurane MAC by 48, 29, 25, and 45%, respectively. The percentage reductions in isoflurane MAC for morphine and MLK were not significantly different but were significantly greater than for lidocaine and ketamine. The Spo2, mean arterial pressure, and core body temperature were not different among groups. Heart rate was significantly decreased at isoflurane MAC during infusion of morphine and MLK. The BIS was inversely related to the ET-Iso and was significantly increased at isoflurane MAC during infusions of morphine and ketamine, compared with isoflurane alone. CONCLUSIONS AND CLINICAL RELEVANCE: Low infusion doses of morphine, lidocaine, ketamine, and MLK decreased isoflurane MAC in dogs and were not associated with adverse hemodynamic effects. The BIS can be used to monitor depth of anesthesia.     

Anesthetic indices of sevoflurane and isoflurane in unpremedicated dogs

OBJECTIVE: To compare the anesthetic index of sevoflurane with that of isoflurane in unpremedicated dogs. DESIGN: Randomized complete-block crossover design. ANIMALS: 8 healthy adult dogs. PROCEDURE: Anesthesia was induced by administering sevoflurane or isoflurane through a face mask. Time to intubation was recorded. After induction of anesthesia, minimal alveolar concentration (MAC) was determined with a tail clamp method while dogs were mechanically ventilated. Apneic concentration was determined while dogs were breathing spontaneously by increasing the anesthetic concentration until dogs became apneic. Anesthetic index was calculated as apneic concentration divided by MAC. RESULTS: Anesthetic index of sevoflurane (mean +/- SEM, 3.45 +/- 0.22) was significantly higher than that of isoflurane (2.61 +/- 0.14). No clinically important differences in heart rate; systolic, mean, and diastolic blood pressures; oxygen saturation; and respiratory rate were detected when dogs were anesthetized with sevoflurane versus isoflurane. There was a significant linear trend toward lower values for end-tidal partial pressure of carbon dioxide during anesthesia with sevoflurane, compared with isoflurane, at increasing equipotent anesthetic doses. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that sevoflurane has a higher anesthetic index in dogs than isoflurane. Sevoflurane and isoflurane caused similar dose-related cardiovascular depression, but although both agents caused dose-related respiratory depression, sevoflurane caused less respiratory depression at higher equipotent anesthetic doses.     

Effect of adenosine infusion on isoflurane MAC in dogs.

Adenosine is a potent analgesic in people and reduces the MAC of halothane in dogs. The purpose of this study was to determine whether adenosine reduces the MAC of isoflurane in dogs. Seven beagles (four males and three females) were anesthetized and randomly assigned to receive adenosine (0.3 mg kg^–1 minute^–1; 6 mL kg^–1 hour^–1, IV) or saline (0.9%, 6 mL kg^–1 hour^–1IV). After an interval of ≥7 days, each dog was reanesthetized and treated with the alternate infusion. Anesthesia was induced and maintained with isoflurane in oxygen. Dogs were intubated and instrumented for measurement of mean systemic arterial blood pressure and airway concentration of isoflurane and end‐tidal partial pressure of carbon dioxide. The MAC for isoflurane was determined using the tail‐clamp technique. Baseline MAC values were 1.25 (1.15, 1.35)% [median (minimum, maximum)] and 1.25 (1.05, 1.45)% before the saline and adenosine treatments, respectively. After 2 hours of infusion with saline or adenosine, MAC values were not different (p = 0.156) and were 1.25 (0.95, 1.35)% and 1.05 (1.00, 1.25)%, respectively. Two hours following the end of each infusion, the MAC values for saline and adenosine treatment groups differed significantly (p = 0.015), but by no more than the normal variation inherent in this study, and were 1.15 (1.15, 1.35)% and 1.05 (1.05, 1.25)%, respectively. Mean arterial blood pressure was 93 (74, 123) mm Hg for saline treated dogs and 67 (52, 72) mm Hg (p = 0.008) during adenosine infusion. End‐tidal carbon dioxide was not different between the two treatment groups. We conclude that adenosine administered at 0.3 mg kg^–1 minute^–1had no effect on isoflurane MAC in dogs, but decreased mean arterial blood pressure.     

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.     

Validation of several types of noxious stimuli for use in determining the minimum alveolar concentration for inhalation anesthetics in dogs and rabbits

OBJECTIVE: To compare 3 types of noxious stimuli applied to various anatomic areas of anesthetized dogs and rabbits for determination of the minimum alveolar concentration (MAC). ANIMALS: 10 dogs and 10 rabbits. PROCEDURE: Dogs were anesthetized with isoflurane and halothane in a randomized order. Rabbits were anesthetized with isoflurane. The MAC was determined by skin incision on the lateral aspect of the chest; clamping of the tail, paw of the forelimb, and paw of the hind limb; and application of electrical current to the oral mucosa (dogs only), forelimb, and hind limb. The MAC was the end-tidal concentration midway between the value permitting and preventing purposeful movement in response to noxious stimuli. RESULTS: In dogs, mean +/- SEM MAC for isoflurane was 1.27 +/- 0.05% for clamping stimuli, 1.36 +/- 0.04% for oral electrical stimulation, 1.35 +/- 0.04% for electrical stimulation to the limbs, and 1.01 +/- 0.07% for surgical incision. The MAC for halothane was 0.97 +/- 0.03% for tail clamping, 0.96 +/- 0.03% for clamping of the limbs, 1.04 +/- 0.03% for electrical stimulation, and 0.75 +/- 0.06% for surgical incision. In rabbits, MAC for isoflurane was 2.08 +/- 0.02% for clamping stimuli, 2.04 +/- 0.02% for electrical stimulation, and 0.90 +/- 0.02% for surgical incision. The MAC for surgical incision was significantly lower than values for the other methods in both species. CONCLUSIONS AND CLINICAL RELEVANCE: Use of electrical current and clamping techniques resulted in similar MAC values. Surgical incision underestimated MAC values in dogs and rabbits.     

Evaluation of induction characteristics and hypnotic potency of isoflurane and sevoflurane in healthy dogs

OBJECTIVE: To determine induction characteristics and the minimum alveolar concentration (MAC) at which consciousness returned (MACawake) in dogs anesthetized with isoflurane or sevoflurane. ANIMALS: 20 sexually intact male Beagles. PROCEDURES: In experiment 1, 20 dogs were randomly assigned to have anesthesia induced and maintained with isoflurane or sevoflurane. The MAC at which each dog awoke in response to auditory stimulation (MACawake-noise) was determined by decreasing the end-tidal concentration by 0.1 volume (vol %) every 15 minutes and delivering a standard audible stimulus at each concentration until the dog awoke. In experiment 2, 12 dogs received the same anesthetic agent they were administered in experiment 1. After duplicate MAC determination, the end-tidal concentration was continually decreased by 10% every 15 minutes until the dog awoke from anesthesia (MACawake). RESULTS: Mean induction time was significantly greater for isoflurane-anesthetized dogs (212 seconds), compared with the sevoflurane-anesthetized dogs (154 seconds). Mean+/-SD MACawake-noise was 1.1+/-0.1 vol % for isoflurane and 2.0+/-0.2 vol % for sevoflurane. Mean MAC was 1.3+/-0.2 vol % for isoflurane and 2.1+/-0.6 vol % for sevoflurane, and mean MACawake was 1.0+/-0.1 vol % for isoflurane and 1.3+/-0.3 vol % for sevoflurane. CONCLUSIONS AND CLINICAL RELEVANCE: Sevoflurane resulted in a more rapid induction than did isoflurane. The MACawake for dogs was higher than values reported for both agents in humans. Care should be taken to ensure that dogs are at an appropriate anesthetic depth to prevent consciousness, particularly when single-agent inhalant anesthesia is used.     

THE USE OF CZECHOSLOVAK VENTILATOR ELVENT IN ARTIFICIAL VENTILATION DURING HALOTHANE NARCOSIS IN THE DOG

Czechoslovak ventilator ELVENT designed for artificial respiration in human was tested in dogs. SO experimental dogs were divided into 3 groups. The animals were under halothane anaesthesia and myorelaxation with artificial ventilation for 120–180 min. Before, during and after experiments at set intervals heart rate, temperature, ECG and acid-base balance (ABB) from venous and arterial blood values of blood-gases, concentrations of potassium and haemoglobin were determined. The model of ventilation program chosen in the third series appears to be the most acceptable for the clinical use. Ventilator parameters were set as follows: respiratory rate from 15 to 20 breaths per min, respiratory min volume from 1.5 to 3 litres, tidal volume from 0.15 to 03 litres. The duration of inspiration was from 0.8 to 1.2 sec., the duration of expiration was double this. Changes in ABB parameters and the tension of blood gases demonstrated the development of respiratory acidosis, in the majority of cases partly compensated.     

Porcine regional brain and myocardial blood flows during halothane-O2 and halothane-nitrous oxide anesthesia: comparisons with equipotent isoflurane anesthesia

Regional distribution of brain and myocardial blood flow were examined in 9 instrumented isocapnic normothermic swine, using 15-microns diameter radionuclide-labeled microspheres injected into the left atrium. Minimal alveolar concentration (MAC) of halothane required to prevent gross purposeful movement in response to a noxious stimulus in 50% of the pigs was found to be 0.70%. Measurements were made on each animal during nonanesthetized state (control), 1.0 and 1.5 MAC halothane anesthesia, and the equivalent of 1.0 and 1.5 MAC halothane anesthesia, using 50% N2O. The order of anesthetized steps was randomized for each pig. Recovery periods of 60 minutes were interposed between the anesthetic treatments. During halothane + 50% N2O anesthesia, heart rate, cardiac output, mean aortic pressure, and rate-pressure product were higher than comparable levels of halothane-O2 anesthesia. Halothane caused dose-dependent vasodilatation in all regions of the brain. Cerebral, cerebellar, and brain-stem blood flows at 1.5 MAC halothane were 135%, 135%, and 115% of respective control values. Substitution of 50% N2O to maintain same MAC dose markedly exaggerated the increment in porcine cerebral and brainstem blood flows, especially at 1.0 MAC when perfusions in these regions were 204% and 128% of respective control values. At 1.5 MAC anesthesia produced by halothane + 50% N2O, the cerebral, cerebellar, and brain stem perfusions were 153%, 146%, and 129% of control values. Transmural myocardial blood flow decreased from control value with both levels of halothane anesthesia, but with equivalent MAC anesthesia produced by halothane + 50% N2O, myocardial perfusion remained near awake values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of electroencephalogram activity and auditory evoked responses during isoflurane and halothane anaesthesia in the rat

Objectives To compare the second differential index (SDI) calculated from the auditory evoked potential (AEP) and electroencephalogram (EEG) parameters: median frequency (MF), spectral edge frequency (SEF) and burst suppression rate (BSR) determined at four equivalent minimum alveolar concentrations (MAC) of isoflurane or halothane. Animals Twelve male Wistar rats weighing 418 g (SD ± 18.4 g). Methods Auditory evoked potentials and EEG responses were recorded in animals implanted with electrodes at established anaesthetic concentrations. Depth of anaesthesia was assessed using the strength of the pedal withdrawal reflex (PWR), and data were analysed using repeated measures anova and paired t‐tests. Results The SEF tended to decrease with increasing depth of halothane anaesthesia (F = 4.198, p = 0.05), but not with isoflurane. The MF and SDI were significantly higher during halothane than with isoflurane (F = 5.82, p = 0.036 and F = 5.263, p = 0.045, respectively) at equivalent depths of anaesthesia, and EEG burst suppression occurred at deeper planes of isoflurane but not halothane anaesthesia. Conclusions The study demonstrated that EEG and AEP characteristics recorded at MAC equivalent concentrations were suppressed to a greater degree by isoflurane than by halothane. These findings have strong implications for research projects where EEG recordings are collected, and also cast more general doubts upon the value of such parameters for evaluating depth of isoflurane anaesthesia in rats.     

Effects of sevoflurane, isoflurane and halotane anaesthesia on fluorescein angiographic phases of dogs: a comparative study

A fluorescein angiography method was developed to compare the onset and the total duration of the fluorangiographic phases between three anaesthetic protocols in six healthy mixed-breed dogs. The animals were anaesthetized three times. Each dog received, as pre-anaesthetic protocol, atropine (10 micrograms/kg intramuscularly), and as a sedative, romifidine (80 micrograms/kg intravenously). Fifteen minutes later, induction of anaesthesia was delivered with propofol (1 mg/kg intravenously) and maintained either with sevoflurane (SEVO group), isoflurane (ISO group) or halothane (HAL group) for 30 min in all cases. Some angiographic, cardiovascular and respiratory variables were registered during the procedure. Recovery times were also registered. Angiographic variables recorded were: onset of the arterial phase (TA), onset of the arteriovenous phase (TAV), onset of the venous phase (TV), complete arterial phase duration (I1), complete arteriovenous phase duration (I2) and I1 plus I2 (I3). Mean heart rate, mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, respiratory rate, tidal volume, arterial oxygen saturation and end-tidal CO2 during SEVO and ISO anaesthesia, were similar in dogs. Minute ventilation and rectal temperature were higher in dogs with SEVO than ISO. HAL produced higher arterial pressures and a lower arterial oxygen saturation than ISO and SEVO. Mean respiratory rate, rectal temperature and minute ventilation were higher in HAL. Pulse rate, end-tidal CO2 and tidal volume were similar in the dogs of the three groups. No differences in recovery times were found. The fluorescein angiographic times were within the normal range. There were no significant differences between protocols in I1, I2 or I3. HAL produced a significant increase of all temporal variables (TA, TAV and TV) when compared with ISO; TA was higher in HAL than SEVO-treated dogs. All protocols appear to be safe and effective for inducing and maintaining general anaesthesia in healthy dogs for performing fluorescein angiography.