Effect of acepromazine on the anesthetic requirement of halothane in the dog

Five adult dogs were used to determine whether acepromazine maleate (ACP), administered IM, decreases the maintenance requirement of halothane and to measure any decrease for the ACP dosages of 0.02, 0.04, 0.06, 0.08, 0.10, and 0.20 mg/kg. The value minimal alveolar concentration, a measure of anesthetic potency, was used as the measure of anesthetic requirement of halothane before and after ACP was administered. All dogs were randomly exposed to each dosage of ACP, as well as to control of 0.2 ml of sterile water. At all dosages of ACP, the decrease in the minimal alveolar concentration of halothane was significant (P less than or equal to 0.05) when compared with that of the control. The decreases at the 0.04 and 0.20 mg/kg dosages were significantly (P less than or equal to 0.05) greater than those at the 0.02 and 0.06 mg/kg dosages. Halothane requirements at all other ACP dosages (0.08 and 0.10 mg/kg) were not significantly different from each other or from those at any of the other dosages. The percentage of decrease in anesthetic requirement after ACP was administered varied from 34% to 46%, with a mean decrease of 40%. The largest decrease was recorded at the dosage of 0.04 mg/kg.     

Some physiological and biochemical effects of intravenous fluid administration during halothane anaesthesia in the dog

Six dogs with previously implanted arterial, central venous, pulmonary arterial and left atrial catheters received halothane anaesthesia, and halothane anaesthesia plus administration of a balanced electrolyte solution given over one hour, in a cross-over experiment. Parameters measured included temperature, heart rate (HR), respiratory rate (f), arterial and mixed venous blood-gases and acid-base parameters, mean arterial pressure ( AP ), mean pulmonary artery pressure ( PAP ), mean left atrial pressure ( LAP ), mean central venous pressure ( CVP ), packed cell volume (PCV), total plasma protein (TPP), plasma sodium, potassium and chloride concentrations, and urinary sodium and potassium concentrations.
During halothane anaesthesia there were significant decreases in AP , PCV, TPP, f, and significant increases in arterial and mixed venous oxygen, and glucose concentrations, when compared with conscious control values. When intravenous fluid was administered during anaesthesia, there were significant decreases in temperature, AP , PCV and TPP, with significant increases in PAP , CVP and f, when compared with values during anaesthesia alone. After one hour recovery period from anaesthesia, dogs receiving intravenous fluids had significantly decreased PaO₂ values and significantly increased pH when compared with anaesthesia alone. There was an average urinary excretion of 7 mmol of sodium and 5 mmol of potassium during anaesthesia, and 36 mmol of sodium and 8 mmol potassium during fluid administration.     

Effect of anticholinergic preanesthetic medicaments on the requirements of halothane for anesthesia in the cat

To study the effects of anticholinergics on anesthetic requirements, minimal alveolar concentrations (MAC) for halothane in the cat were measured before and after IM administration of an anticholinergic (atropine sulfate [0.045 mg/kg], glycopyrrolate [0.011 mg/kg], or scopolamine hydrobromide [0.02 mg/kg]) or a physiologic saline control. The study was performed in 8 adult cats, using a randomized-block experimental design. There was no significant difference between the mean MAC obtained before and after administration of any of the test drugs or vs the control values. The mean MAC of halothane in cats was 0.985% atmosphere.     

Butorphanol Does Not Reduce the Minimum Alveolar Concentration of Halothane in Dogs

This study evaluated the effect of butorphanol tartrate, a synthetic opioid agonist-antagonist, on halothane minimum alveolar concentration (MAC) in dogs. Baseline halothane MAC was determined in each of six dogs. Butorphanol was administered and halothane MAC was redeter-mined. Each dog received butorphanol at 0.2, 0.4, and 0.8 mg/kg intravenously at 1 week intervals. Heart rate and arterial blood pressure decreased after butorphanol administration, but returned to baseline by 50 minutes. There was little effect on respiratory parameters. A halothane-sparing effect was not noted with any butorphanol dose.     

Cardiovascular effects of halothane in the horse

Cardiovascular effects of venous alveolar concentrations of halothane in oxygen were studied in 8 young, healthy horses under conditions of constant arterial carbon dioxide tension. The alveolar concentration of halothane was expressed as a multiple of the minimal alveolar concentration (MAC) which was known for each animal. Increasing alveolar halothane concentrations to MAC 2.0 resulted in a progressive and significant (P less than 0.05) decline in systemic arterial pressure and left ventricular work. Cardiac output decreased between MAC 1.0 and MAC 2.0 as a result of a significant (P less than 0.05) decrease in stroke volume. Heart rate, total peripheral resistance, pulmonary artery pressure, hematocrit, plasma protein concentration, arterial oxygen tension, and arterial pH remained constant over the same range of anesthetic dosages. Continuation of anesthesia, spontaneous ventilation, and the accompanying rise in arterial carbon dioxide tension and electrical stimulation of the horse's oral mucous membranes produced varying degrees of stimulation of cardiovascular function at MAC 1.5.     

Effect of ether, ethanol and aqueous extracts of ginseng on cardiovascular function in dogs.

Ether, ethanol and aqueous extracts of ginseng were serially prepared from Korean ginseng plants. Each extract in the dose of 40 mg/kg was administered intravenously to ten dogs under light halothane anesthesia while 11 cardiovascular variables were compared during the ensuing two hours. The variable included cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit. Following the administration of the ether extract (40 mg/kg) the heart rate and the central venous pressure decreased significantly. The administration of ethanol extract (40 mg/kg) caused a significant decrease in the heart rate and the mean arterial pressure. After the administration of the aqueous extract (40 mg/kg) the cardiac output, stroke volume and central venous pressure were significantly decreased, while the total peripheral resistance was significantly increased.     

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.     

Cardiovascular effects of halothane anesthesia after diazepam and ketamine administration in beavers (Castor canadensis) during spontaneous or controlled ventilation

Fourteen adult beavers (Castor canadensis) weighing 16.5 +/- 4.14 kg (mean +/- SD) were anesthetized for surgical implantation of radio telemetry devices. Beavers were anesthetized with diazepam (0.1 mg/kg) and ketamine (25 mg/kg) administered IM, which provided smooth anesthetic induction and facilitated tracheal intubation. Anesthesia was maintained with halothane in oxygen via a semiclosed circle anesthetic circuit. Values for heart rate, respiratory rate, esophageal temperature, direct arterial blood pressure, end-tidal halothane concentration, and end-tidal CO2 tension were recorded every 15 minutes during the surgical procedure. Arterial blood samples were collected every 30 minutes to determine pH, PaO2, and PaCO2. Values for plasma bicarbonate, total CO2, and base excess were calculated. Ventilation was spontaneous in 7 beavers and controlled to maintain normocapnia (PaCO2 approx 40 mm of Hg) in 7 others. Vaporizer settings were adjusted to maintain a light surgical plane of anesthesia. Throughout the surgical procedure, all beavers had mean arterial pressure less than 60 mm of Hg and esophageal temperature less than 35 C. Mean values for arterial pH, end-tidal CO2, PaO2, and PaCO2 were significantly (P less than 0.05) different in spontaneously ventilating beavers, compared with those in which ventilation was controlled. Respiratory acidosis during halothane anesthesia was observed in spontaneously ventilating beavers, but not in beavers maintained with controlled ventilation. All beavers recovered unremarkably from anesthesia.     

The cardiovascular sparing effect of fentanyl and atropine, administered to enflurane anesthetized dogs.

Cardiovascular effects of high dose opioid together with low dose inhalant were compared with inhalant alone to determine whether opioid/inhalant techniques were less depressant on the cardiovascular system. The effects of positive pressure ventilation and increasing heart rate to a more physiological level were also studied. Cardiovascular measurements recorded during administration of enflurane at 1.3 minimum alveolar concentration (MAC; 2.89 +/- 0.02%) to spontaneously breathing dogs (time 1) and during controlled ventilation [arterial carbon dioxide tension at 40 +/- 3 mmHg (time 2)] were similar. At time 2, mixed venous oxygen tension and arterial and mixed venous carbon dioxide tensions were significantly decreased, while arterial and mixed venous pH were significantly increased compared to measurements at time 1. After administration of fentanyl to achieve plasma fentanyl concentration of 71.7 +/- 14.4 ng/mL and reduction of enflurane concentration to yield 1.3 MAC multiple (0.99 +/- 0.01%), heart rate significantly decreased, while mean arterial pressure, central venous pressure, stroke index, and systemic vascular resistance index increased compared to measurements taken at times 1 and 2. Pulmonary arterial occlusion pressure was significantly increased compared to measurements taken at time 2. After administration of atropine until heart rate was 93 +/- 5 beats/min (plasma fentanyl concentration 64.5 +/- 13.5 ng/mL) heart rate, mean arterial pressure, cardiac index, oxygen delivery index, and venous admixture increased significantly compared to values obtained at all other times.(ABSTRACT TRUNCATED AT 250 WORDS)     

Naloxone reversal of oxymorphone effects in dogs

Oxymorphone was administered IV to dogs 4 times at 20-minute intervals (total dosage, 1 mg/kg of body weight, IV) on 2 separate occasions. Minute ventilation, mixed-expired carbon dioxide concentration, arterial and mixed-venous pH and blood gas tensions, arterial, central venous, pulmonary arterial, and pulmonary wedge pressures, and cardiac output were measured. Physiologic dead space, base deficit, oxygen transport, and vascular resistance were calculated before and at 5 minutes after the first dose of oxymorphone (0.4 mg/kg) and at 15 minutes after the first and the 3 subsequent doses of oxymorphone (0.2 mg/kg). During 1 of the 2 experiments in each dog, naloxone was administered 20 minutes after the last dose of oxymorphone; during the alternate experiment, naloxone was not administered. In 5 dogs, naloxone was administered IV in titrated dosages (0.005 mg/kg) at 1-minute intervals until the dogs were able to maintain sternal recumbency, and in the other 5 dogs, naloxone was administered IM as a single dose (0.04 mg/kg). Naloxone (0.01 mg/kg, IV or 0.04 mg/kg, IM) transiently reversed most of the effects of oxymorphone. Within 20 to 40 minutes after IV naloxone administration and within 40 to 70 minutes after IM naloxone administration, most variables returned to the approximate values measured before naloxone administration. The effects of oxymorphone outlasted the effects of naloxone; cardiovascular and pulmonary depression and sedation recurred in all dogs. Four hours and 20 minutes after the last dose of oxymorphone, alertness, responsiveness, and coordination improved in all dogs after IM administration of naloxone. Cardiac arrhythmia, hypertension, or excitement was not observed after naloxone administration.     

The pharmacological effects of the anesthetic alfaxalone after intramuscular administration to dogs

The pharmacological effects of the anesthetic alfaxalone were evaluated after intramuscular (IM) administration to 6 healthy beagle dogs. The dogs received three IM doses each of alfaxalone at increasing dose rates of 5 mg/kg (IM5), 7.5 mg/kg (IM7.5) and 10 mg/kg (IM10) every other day. Anesthetic effect was subjectively evaluated by using an ordinal scoring system to determine the degree of neuro-depression and the quality of anesthetic induction and recovery from anesthesia. Cardiorespiratory variables were measured using noninvasive methods. Alfaxalone administered IM produced dose-dependent neuro-depression and lateral recumbency (i.e., 36 ± 28 min, 87 ± 26 min and 115 ± 29 min after the IM5, IM7.5 and IM10 treatments, respectively). The endotracheal tube was tolerated in all dogs for 46 ± 20 and 58 ± 21 min after the IM7.5 and IM10 treatments, respectively. It was not possible to place endotracheal tubes in 5 of the 6 dogs after the IM5 treatment. Most cardiorespiratory variables remained within clinically acceptable ranges, but hypoxemia was observed by pulse oximetry for 5 to 10 min in 2 dogs receiving the IM10 treatment. Dose-dependent decreases in rectal temperature, respiratory rate and arterial blood pressure also occurred. The quality of recovery was considered satisfactory in all dogs receiving each treatment; all the dog exhibited transient muscular tremors and staggering gait. In conclusion, IM alfaxalone produced a dose-dependent anesthetic effect with relatively mild cardiorespiratory depression in dogs. However, hypoxemia may occur at higher IM doses of alfaxalone.     

Cardiorespiratory effects of a 5HT2 antagonist (R51703) in awake and anesthetized dogs.

To investigate cardiorespiratory effects of an experimental 5-hydroxytryptamine receptor antagonist (R51703) with sedative properties, intramuscular doses of the drug were studied in 6 awake dogs of mixed breed, and in 6 anesthetized beagles. Two doses (0.2 and 0.4 mg/kg) of R51703 and a saline control were studied in the awake dogs using a randomized crossover trial. Subsequently, the higher dose of R51703 was included as a component of halothane anesthesia to determine whether the halothane sparing effect of R51703 produced a beneficial alteration of hemodynamic function. Data were obtained at equipotent halothane/R51703 (H/R) and halothane/saline (H/S) doses equivalent to 1.0, 1.5 and 2.0 MAC. In awake dogs, heart rates tended to be lower in dogs sedated with R51703, significantly so at 30 min for both doses, and at 90 and 120 min for the 0.2 and 0.4 mg/kg doses, respectively (P < 0.05). The cardiac index (CI) was lower at 60 min with both doses compared to the saline control group. Both doses of R51703 reduced mean blood pressure at 30, 90 and 120 min, and diastolic pressure at 30 and 90 min after administration; however, systolic blood pressure (SBP) was not altered. Overall, the cardiovascular alterations were minimal in conscious dogs and there was no evidence of respiratory depression. In the anesthetized dogs, at equipotent MAC, CI tended to be lower with H/R than with H/S, though the difference was not significant. Heart rate and stroke volume index also tended to be lower in the dogs treated with R51703, while systemic vascular resistance tended to be higher: these changes were not significant. Mean and SBP were higher at each MAC multiple in the H/R group. It was concluded that the halothane sparing effect of R51703 did not substantially improve hemodynamic function compared to the use of halothane alone at equipotent doses.     

Haemodynamic effects of ATP in dogs during hypoxia-induced pulmonary hypertension

Pulmonary hypertension may result from an increase in vascular resistance caused by persistent hypoxia. We have investigated the effects of adenosine triphosphate (ATP), administered into the pulmonary artery, on haemodynamic changes occurring in anaesthetized adult dogs subjected to acute hypoxic pulmonary vasoconstriction. Hypoxia alone (ventilation with 10% O2/90% N2) caused significant increases in mean pulmonary arterial blood pressure (PAP), central venous pressure (CVP), and cardiac index (CI) by 71, 102 and 38%, respectively. ATP (0.03-3.0 micromol/kg/min approximately 0.02-1.65 mg/kg/min), when infused under hypoxic conditions, significantly reduced both mean PAP and systemic arterial blood pressure (ABP) in a dose-dependent manner. The maximum decrease in mean PAP amounted to 20%; mean ABP, on the other hand, was decreased by up to 52% (P<0.01). Heart rate, CI, CVP and pulmonary occlusion pressure were not dose-dependently affected by ATP. Our data indicate that while pulmonary arterial administration of ATP in mature dogs during hypoxic pulmonary hypertension causes dilation in the pulmonary vascular bed, it is even more effective in dilating the systemic vasculature. This result suggests a need for further evaluation and warrants cautious use of ATP in the treatment of hypoxic pulmonary hypertension in adult dogs.     

Romifidine, medetomidine or xylazine before propofol-halothane-N2O anesthesia in dogs.

The objective of this paper was to evaluate romifidine as a premedicant in dogs prior to propofol-halothane-N2O anesthesia, and to compare it with the other alpha2-agonists (medetomidine and xylazine). For this, ten healthy dogs were anesthetized. Each dog received 3 preanesthetic protocols: atropine (10 microg/kg BW, IM), and as a sedative, romifidine (ROM; 40 microg/kg BW, IM), xylazine (XYL; 1 microg/kg, IM), or medetomidine (MED; 20 microg/kg BW, IM). Induction of anesthesia was delivered with propofol 15 min later and maintained with halothane and N2O for one hour in all cases. The following variables were registered before preanesthesia, 10 min after the administration of preanesthesia, and at 5-minute intervals during maintenance: PR, RR, rectal temperature (RT), MAP, SAP, and DAP. During maintenance, arterial oxygen saturation (SpO2), end-tidal CO2 (EtCO2) and percentage of halothane necessary for maintaining anesthesia (%HAL) were also recorded. Induction dose of propofol (DOSE), time to extubation (TE), time to sternal recumbency (TSR) and time to standing (TS) were also registered. The statistical analysis was carried out during the anesthetic period. ANOVA for repeat measures revealed no differences between the 3 groups for PR and RR; however, MAP, SAP and DAP were higher in the MED group; SpO2 was lower in MED and EtCO2 was lower in ROM; %HAL was higher in XYL. No statistical differences were observed in DOSE, TE, TSR or TS. Percentage of halothane was lower in romifidine and medetomidine than in xylazine premedicated dogs also anesthetized with propofol. All the cardiorespiratory variables measured were within normal limits. The studied combination of romifidine, atropine, propofol, halothane and N2O appears to be a safe and effective drug combination for inducing and maintaining general anesthesia in healthy dogs.     

Isoflurane sparing action of epidurally administered xylazine hydrochloride in anesthetized dogs

OBJECTIVE: To evaluate the influence of epidural administration of xylazine hydrochloride on the minimum alveolar concentration of isoflurane (MAC(ISAO)) and cardiopulmonary system in anesthetized dogs. ANIMALS: 6 clinically normal dogs. PROCEDURE: Dogs were anesthetized with isoflurane in oxygen after randomly being assigned to receive 1 of the following 4 treatments: epidural administration of saline (0.9% NaCl) solution or xylazine at a dose of 0.1, 0.2, or 0.4 mg x kg(-1). Experiments were performed on 5 occasions with at least a 1-week interval between experiments; each dog received all 4 treatments. Following instrumentation, the concentration of isoflurane was maintained constant for 15 minutes at the MAC(ISO) that had been determined for each dog, and data on heart rate, arterial blood pressure, respiratory rate, tidal volume, minute volume, arterial partial pressure of oxygen, arterial partial pressure of carbon dioxide, and arterial pH were collected. The epidural treatment was administered, and 30 minutes later, data were again collected. From this point on, determination of the MAC(ISO) following epidural treatment (ie, MAC(ISO+EPI)) was initiated. Cardiopulmonary data were collected before each electrical supramaximal stimulus during MAC(ISO+EPI) determinations. RESULTS: The mean (+/-SD) MAC(ISO) was 1.29 +/- 0.04%. The epidural administration of xylazine at doses of 0.1, 0.2, and 0.4 mg x kg(-1) decreased the MAC(ISO), respectively, by 8.4 +/- 2.4%, 21.7 +/- 4.9%, and 33.4 +/- 2.64%. Cardiopulmonary effects were limited. CONCLUSIONS AND CLINICAL RELEVANCE: Epidural administration of xylazine decreases the MAC(ISO) in a dose-dependent manner and is associated with few cardiopulmonary effects in anesthetized dogs.     

Effects of butorphanol and carprofen on the minimal alveolar concentration of isoflurane in dogs

OBJECTIVE: To evaluate the effects of butorphanol and carprofen, alone and in combination, on the minimal alveolar concentration (MAC) of isoflurane in dogs. DESIGN: Randomized complete-block crossover study. ANIMALS: 6 healthy adult dogs. PROCEDURE: Minimal alveolar concentration of isoflurane was determined following administration of carprofen alone, butorphanol alone, carprofen and butorphanol, and neither drug (control). Anesthesia was induced with isoflurane in oxygen, and MAC was determined by use of a tail clamp method. Three hours prior to induction of anesthesia, dogs were fed a small amount of canned food without any drugs (control) or with carprofen (2.2 mg/kg of body weight [1 mg/lb]). Following initial determination of MAC, butorphanol (0.4 mg/kg [0.18 mg/lb], i.v.) was administered, and MAC was determined again. Heart rate, respiratory rate, indirect arterial blood pressure, endtidal partial pressure of CO2, and saturation of hemoglobin with oxygen were recorded at the time MAC was determined. RESULTS: Mean +/- SD MAC of isoflurane following administration of butorphanol alone (1.03 +/- 0.22%) or carprofen and butorphanol (0.90 +/- 0.21%) were significantly less than the control MAC (1.28 +/- 0.14%), but MAC after administration of carprofen alone (1.20 +/- 0.13%) was not significantly different from the control value. The effects of carprofen and butorphanol on the MAC of isoflurane were additive. There were not any significant differences among treatments in regard to cardiorespiratory data. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that administration of butorphanol alone or in combination with carprofen significantly reduces the MAC of isoflurane in dogs; however, the effects of butorphanol and carprofen are additive, not synergistic.     

Cardiovascular and respiratory effects of propofol administration in hypovolemic dogs.

Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.     

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.     

Blood pressure response to phenylephrine infusion in halothane-anesthetized dogs given acetylpromazine maleate

To quantitate acetylpromazine-induced alpha-adrenergic receptor blockade, phenylephrine was infused into dogs. The amount of phenylephrine necessary to increase the mean arterial blood pressure (MAP) 50% above base line, with or without the prior administration of acetylpromazine, served to quantify the degree of acetylpromazine-induced alpha-adrenergic receptor blockade. Seven dogs were anesthetized with thiopental, maintained on halothane in oxygen, and mechanically ventilated. All infusions were made through a catheter in the cephalic vein. Continuous recordings were made of MAP and a lead II ECG. After induction of anesthesia, instrumentation, and stabilization of heart rate, MAP, and ventilation, 6 group I dogs were infused with phenylephrine until a 50% increase in MAP was recorded (phenylephrine control). On subsequent research days, each dog was anesthetized, instrumented as described, and given (IV) 1 of 3 dosages of acetylpromazine in the following order--0.05, 0.125, and 0.25 mg/kg. The dose of phenylephrine necessary to increase MAP 50% in the presence of acetylpromazine was recorded. Five group II dogs were studied as in group I, but each dog was given (IM) atropine (0.04 mg/kg) before anesthetization. Two dosages of acetylpromazine were studied in the following order--0.05 and 0.25 mg/kg. Group I dogs, when compared with their phenylephrine controls, were given significantly more phenylephrine to raise MAP 50% at each dose of acetylpromazine studied. The same trend was observed in group II dogs, but at smaller doses of phenylephrine, probably as a result of the positive chronotropic effect of atropine on the heart.     

Pre-anesthetic meperidine: associated vomiting and gastroesophageal reflux during the subsequent anesthetic in dogs

OBJECTIVE: To determine the effect of meperidine administered prior to anesthesia on the incidence of vomiting before, and gastroesophageal reflux (GER) and regurgitation during, the subsequent period of anesthesia in dogs. STUDY DESIGN: Randomized, controlled trial. ANIMALS: A total of 60 healthy dogs, 4.3 +/- 2.3 years old, and weighing 35.5 +/- 13.1 kg. METHODS: Dogs were admitted to the study if they were healthy, had no history of vomiting, and were scheduled to undergo elective orthopedic surgery. The anesthetic protocol used was standardized to include thiopental and isoflurane in oxygen. Dogs were randomly selected to receive one of the following pre-medications: morphine (0.66 mg kg(-1) IM) with acepromazine (0.044 mg kg(-1) IM), meperidine (8.8 mg kg(-1) IM) with acepromazine (0.044 mg kg(-1) IM) or meperidine alone (8.8 mg kg(-1) IM). A sensor-tipped catheter was placed to measure esophageal pH during anesthesia. Gastro-esophageal reflux was judged to have occurred if there was a decrease in esophageal pH below four or an increase above 7.5. RESULTS: No dogs vomited after the administration of meperidine, but 50% of dogs vomited after the administration of morphine. When compared with morphine, treatment with meperidine alone or combined with acepromazine before anesthesia was associated with a 55% and 27% reduction in absolute risk of developing GER, respectively. Dogs receiving meperidine alone were significantly less sedate than other dogs in the study, and required more thiopental to induce anesthesia. Arterial blood pressure and heart rate were not significantly different between groups at the start of the measurement period. Cutaneous erythema and swelling were evident in four dogs receiving meperidine. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of meperidine to healthy dogs prior to anesthesia was not associated with vomiting and tended to reduce the occurrence of GER, but produced less sedation when compared with morphine. Meperidine is not a useful addition to the anesthetic protocol if prevention of GER is desired.