Effects of glucose infusion on the endocrine, metabolic and cardiorespiratory responses to halothane anaesthesia of ponies.

Glucose was infused intravenously into six ponies during halothane anaesthesia, to evaluate its effect on their endocrine response to anaesthesia. The ponies were premedicated with acepromazine, and anaesthesia was induced with thiopentone and maintained with halothane in oxygen for two hours. Glucose was infused to maintain the plasma glucose concentration above 20 mmol/litre. Anaesthesia was associated with hypothermia, a decrease in haematocrit, hypotension, hyperoxaemia, respiratory acidosis and an increase in the plasma concentrations of lactate and arginine vasopressin. The concentration of beta-endorphin in plasma increased transiently after 20 minutes but there were no changes in concentrations of adrenocorticotrophic hormone, dynorphin, cortisol or catecholamines. These data suggest that the glucose infusion attenuated the normal adrenal response of ponies to halothane anaesthesia.     

Cardiorespiratory, endocrine and metabolic changes in ponies undergoing intravenous or inhalation anaesthesia

Six Welsh gelding ponies (weight 246 ± 6 kg) were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) followed by 0.02 mg/kg of detomidine i.v. Anaesthesia was induced with 2 mg/kg of ketamine i.v. Ponies were intubated and lay in left lateral recumbency. On one occasion anaesthesia was maintained for 2 h using 1.2% halothane in oxygen. The same group of ponies were anaesthetized 1 month later using the same induction regime and anaesthesia was maintained with a combination of detomidine, ketamine and guaiphenesin, while the ponies breathed oxygen-enriched air. Electrocardiogram, heart rate, mean arterial blood pressure, cardiac output, respiratory rate, blood gases, temperature, haematocrit, glucose, lactate and cortisol were measured and cardiac index and systemic vascular resistance were calculated in both groups. Beta-endorphin, met-enkephalin, dynorphin, arginine vasopressin (AVP), adrenocorticotrophic hormone (ACTH) and catecholamines were measured in the halothane anaesthesia group only and 11-deoxycortisol during total intravenous anaesthesia (TIVA) only. Cardiorespiratory depression was more marked during halothane anaesthesia. Hyperglycaemia developed in both groups. Lactate and AVP increased during halothane anaesthesia. Cortisol increased during halothane and decreased during TIVA. There were no changes in the other hormones during anaesthesia. Recovery was smooth in both groups. TIVA produced better cardiorespiratory performance and suppressed the endocrine stress response observed during halothane anaesthesia.     

Stress responses in ponies during halothane or isoflurane anaesthesia after induction with thiopentone or xylazine/ketamine

Endocrine and metabolic responses to anaesthesia with three different anaesthetic regimes were examined in six ponies. All animals were anaesthetised with each protocol: acepromazine-thiopentone-isoflurane, xylazine-ketamine- halothane and xylazine-ketamine-isoflurane. Anaesthesia was maintained for 2 h. Pulse rate, respiratory rate, arterial blood pressure, arterial blood gases and pharyngeal and skin temperature were measured and blood was withdrawn for glucose, lactate, cortisol, insulin, liver and muscle enzymes and total protein assay. Measurements were made before anaesthesia, at 20 min intervals during anaesthesia and at 20 mins and 2, 4, 6 and 24 h after anaesthesia. The effects of anaesthesia were similar in all groups. Arterial blood pressure decreased and oxygen tension and plasma cortisol concentration increased in all groups. Arterial carbon dioxide tension increased and respiratory rate and pH decreased in all ponies anaesthetised with isoflurane. There was a tendency for increased glucose and lactate concentrations and decreased insulin concentration and packed cell volume, particularly in the xylazine-ketamine groups. There was no change in pulse rate except for a transient increase at induction with thiopentone. The results were compared with data reported by Taylor (1989), which were collected from the same animals during acepromazine-thiopentone-halothane anaesthesia, and were found to be similar. It was concluded that these commonly used anaesthetic protocols themselves constitute a considerable insult or stressor in horses. However, the stress response to all the regimes investigated was similar and the precise stimulus to this response has yet to be elucidated.     

Adrenocortical and metabolic responses to dobutamine infusion during halothane anaesthesia in ponies

The study investigated whether hypotension in halothane-anaesthetised ponies is the stimulus inducing an endocrine stress response by assessing the effect of maintenance of normotension with a dobutamine infusion. Groups of six ponies were studied. After premedication with acepromazine (0.04 mg/kg) anaesthesia was induced with thiopentone (10 mg/kg) and maintained for 120 min with halothane (group AN). Dobutamine was infused to effect (1.1–4.4 μg/kg/min) to maintain arterial pressure at pre anaesthetic levels. The conscious group (CON) were prepared as for AN and then received only dobutamine infusion 1.0 μg/kg/min for 120 min. Arterial blood pressure, pH, oxygen and carbon dioxide tension, pulse rate, haematocrit, and plasma cortisol, glucose and lactate concentrations were measured before, at 20 min intervals during anaesthesia, and 20 and 120 min after anaesthesia ceased. Blood pressure remained close to control in both groups. The AN group became hypercapnic and acidotic, pulse rate and haematocrit increased, cortisol increased more than twofold and plasma glucose and lactate did not change. All values remained at control in the CON group except for small increases in haematocrit and decreases in pulse rate. Maintenance of normotension during halothane anaesthesia did not blunt the adrenocortical response to anaesthesia nor did the same dose of dobutamine alone increase plasma cortisol. Hypotension appears not to be the sole stimulus to equine adrenocortical activity during halothane anaesthesia.     

Endocrine and metabolic responses to plasma volume expansion during halothane anaesthesia in ponies

The study was designed to contribute to identification of the stimulus to adrenocortical activity during halothane anaesthesia in equidae . Two groups of six ponies were premedicated with acepromazine before induction of anaesthesia with thiopentone and maintenance for 120 min with halothane in oxygen. In group H Haemaccel® modified gelatine plasma replacer was infused (48 ± 13 mL/kg) to maintain mean arterial blood pressure (MABP) close to preanaesthetic values. In group DH, blood pressure was maintained close to preanaesthetic levels with a lower dose of Haemaccel® (10 mL/kg) combined with an infusion of dobutamine. Measurements were made before anaesthesia, at 20 min intervals during anaesthesia and 20 and 120 min after anaesthesia. MABP and blood gases, pulse and respiratory rates were measured, and blood was withdrawn for assay of cortisol, adrenocorticotrophic hormone (ACTH), glucose and lactate. Ponies in both groups became hyperoxic, hypercapnic and developed a respiratory acidosis; pulse rate increased in both groups but this was more marked in group H. Haematocrit decreased by 50% in H and by 20% in DH. Cortisol and ACTH did not change significantly during anaesthesia in either group and the area under the time curve ( AUC _(0–140)) was lower in the DH group. Plasma glucose and lactate remained stable. After the H treatment all ponies had a watery nasal discharge and one pony died from endotoxaemia. This investigation demonstrated that the adrenocortical response to halothane anaesthesia in ponies can be ameliorated by manipulation of ABP using plasma expansion with or without inotrope infusion; however, low dose Haemaccel® with dobutamine was safer and more practical. It is suggested that, although hypotension is not the sole stimulus to adrenocortical activity during halothane anaesthesia, it may contribute, probably through an effect on tissue perfusion.     

Effects of hypoxia on endocrine and metabolic responses to anaesthesia in ponies

Some metabolic and endocrine effects of hypoxaemia were studied during halothane anaesthesia in six ponies. Each was anaesthetised twice; on one occasion a 20-minute period of hypoxaemia (arterial oxygen tension between 4.4 and 5.8 [mean 5.3] kPa) was imposed during 120 minutes of anaesthesia. On the second occasion arterial oxygen tension was maintained above 17 kPa throughout. Routine cardiovascular monitoring was performed and blood samples were taken to measure haematocrit, cortisol, insulin, glucose and lactate. Anaesthesia was associated with hypotension in both groups (mean ABP < 70 mmHg) but pulse rate changed little from control. Hypercapnia (PaCO2 > 7.0 kPa) developed in the normoxic group and acidosis was more severe than in the hypoxic group. Haematocrit changed little but was higher in the hypoxic group after the hypoxic period (0.39[0.06] vs 0.32[0.06] litre litre(-1)). Plasma cortisol increased significantly during anaesthesia in both groups (maximum values: hypoxic group 418[96], normoxic group 492[102] nmol litre(-1)) and there was no significant difference between them. Glucose concentration increased in the hypoxic group and was significantly higher than in the normoxic group during the hypoxic period (8.8[1.5] vs 6.4[1.5] mmol litre(-1)). Insulin decreased in both groups but this was significant only in the normoxic group (from 34[19] to a nadir of 12[9] iu ml(-1)) and the groups were not significantly different. Lacticacidaemia developed in both groups but was more severe in the hypoxic group (maximum values 2.3[0.6] and 1.3[0.5] mmol litre(-1)). It was concluded that 20 minutes of hypoxia during halothane anaesthesia in ponies did not markedly alter the stress response already induced by anaesthesia.     

Doxapram infusion during halothane anaesthesia in ponies

Doxapram, 0.05 mg/kg bodyweight/min, was infused during the second hour of 2 h halothane anaesthesia in six ponies. Two of the ponies were anaesthetised on a second occasion as controls and given 5 per cent dextrose in place of the doxapram. Respiratory depression typical of halothane anaesthesia in ponies developed in the first hour of anaesthesia and continued during the second hour in the control animals. During doxapram infusion arterial carbon dioxide tension decreased and pH increased. Arterial blood pressure increased but there was no change in pulse rate, the electrocardiogram or arterial oxygen tension. Anaesthesia lightened during doxapram infusion necessitating an increase in the vapouriser setting in order to prevent arousal. Recovery from anaesthesia appeared unaffected by the doxapram infusion.     

Cardiopulmonary effects of romifidine and detomidine used as premedicants for ketamine/halothane anaesthesia in ponies

The cardiopulmonary effects of romifidine at 80 microg/kg (R80) or 120 pg/kg (R120), and detomidine at 20 pg/kg (D20) when used as premedicants for ketamine/halothane anaesthesia were investigated in six ponies. Using a blinded crossover design, acepromazine (0-04 mg/kg) was administered followed by the alpha-2 agonist. Anaesthesia was induced with ketamine at 2.2 mg/kg and maintained with halothane (expired concentration 1.0 per cent) in oxygen for three hours. During anaesthesia, arterial blood pressure, cardiac index, PaO2 and PmvO2 decreased, and systemic vascular resistance and PaCO2 increased. The cardiac indices for R80, R120 and D20 were, respectively, 39, 39 and 32 ml/kg/minute at 30 minutes and 29, 29 and 26 ml/kg/minute at 180 minutes. The alpha-2 agonists had similar cardiovascular effects, but PaO2 was significantly lower with R120. The quality of anaesthesia was similar in all three groups.     

The effect of guaiphenesin on romifidine/ketamine anaesthesia in ponies

The purpose of this study was to investigate the effect of a single dose (50 mg/kg) of guaiphenesin on recumbency time, surgical conditions and the ‘quality’ of anaesthesia in ponies anaesthetised for castration. Sixteen ponies were sedated with romifidine 100 μg/kg and anaesthetised with ketamine (2.2 mg/kg). Ponies allocated to Group A received no treatment and those in Group B were given 50 mg/kg of a 15% guaiphenesin solution. Guaiphenesin was given as a rapid iv injection immediately after induction of anaesthesia. All ponies were subsequently castrated. The mean (± se) time of recumbency in Group A was 20.9 ± 1.37 min and in Group B 27.2 ± 2.1 min to (P<0.05). Subjective assessment scores for the quality of surgical conditions and anaesthesia itself were significantly greater (indicating better conditions) in ponies receiving guaiphenesin, although there was no difference between groups in the quality of recovery.     

Midazolam/ketamine induction and isoflurane maintenance of anaesthesia in a 2-month-old, hand-raised African buffalo (Syncerus caffer)

The use of a midazolam/ketamine combination for induction of anaesthesia in a 2-month-old, hand-raised buffalo calf (Syncerus caffer) is described to allow endotracheal intubation for the maintenance of anaesthesia with isoflurane and oxygen. Intraoperative complications were hypotension and hypothermia. For postoperative analgesia meloxicam and butorphanol was administered intramuscularly.     

Comparison of respiratory function during TIVA (romifidine,ketamine, midazolam) and isoflurane anaesthesia in spontaneously breathing ponies Part I: blood gas analysis and cardiorespiratory variables

ObjectiveTo compare pulmonary function and gas exchange in ponies during maintenance of anaesthesia with isoflurane or by a total intravenous anaesthesia (TIVA) technique.Study designExperimental, cross–over study.AnimalsSix healthy ponies weighing mean 286 (range 233–388) ± SD 61 kg, age 13 (9-16) ± 3 years.MethodsThe ponies were anaesthetized twice, a minimum of two weeks apart. Following sedation with romifidine [80 μg kg^?1 intravenously (IV)], anaesthesia was induced IV with midazolam (0.06 mg kg^?1) and ketamine (2.5 mg kg^?1), then maintained either with inhaled isoflurane (Fe’Iso = 1.1 vol%) (T-ISO) or an IV infusion of romifidine (120 μg kg^?1 hour^?1), midazolam (0.09 mg kg^?1 hour^?1 IV) and ketamine (3.3 mg kg^?1 hour^?1) (T-TIVA). Ponies were placed in lateral recumbency. Breathing was spontaneous and Fi’O₂ 60%. After an instrumentation/stabilisation period of 30 minutes, arterial and mixed venous blood samples were taken simultaneously every 10 minutes for 60 minutes and analysed immediately. Oxygen extraction ratio (O₂ER) and venous admixture were calculated. Tidal volume (TV), minute volume (MV), respiratory rate (f_R), packed cell volume (PCV), arterial blood pressure and heart rate (HR) were measured and recorded. Data were analysed with mixed model anova (a = 0.05). Treatments were compared overall and at two selected time points (T30 and T60) using Bonferroni correction.ResultsArterial and mixed venous partial pressures of O₂ and CO₂, and TV were significantly lower and MV and f_R were higher in T-TIVA compared to T-ISO. Venous admixture did not differ between treatments. O₂ER was significantly higher in T-TIVA. Mean arterial pressure was higher and HR was lower in T-TIVA compared to T-ISO.Conclusions and clinical relevanceWhilst arterial CO₂ was within an acceptable range during both protocols, the impairment of oxygenation was more pronounced with the T-TIVA evidenced by lower arterial and venous oxygen partial pressures.     

Investigation of the EEG effects of intravenous lidocaine during halothane anaesthesia in ponies

OBJECTIVE: To record the electroencephalographic changes during castration in ponies anaesthetized with halothane and given intravenous (IV) lidocaine by infusion. The hypothesis tested was that in ponies, IV lidocaine is antinociceptive and would therefore obtund EEG changes during castration. ANIMALS: Ten Welsh mountain ponies referred to the Department of Clinical Veterinary Medicine, Cambridge for castration under general anaesthesia. MATERIALS AND METHODS: Following pre-anaesthetic medication with intramuscular acepromazine (0.02 mg kg(-1)) anaesthesia was induced with IV guaiphenesin (60 mg kg(-1)) and thiopental (9 mg kg(-1)) and maintained with halothane at an end-tidal concentration (FE'HAL) of 1.2%. A constant rate infusion of IV lidocaine (100 microg kg(-1) minute(-1)) was administered throughout anaesthesia. The electroencephalogram (EEG) was recorded continuously using subcutaneous needle electrodes. All animals were castrated using a closed technique. The raw EEG signal was analysed after completion of each investigation, and the mean values of EEG variables (median frequency, spectral edge frequency, total amplitude) recorded during a baseline period (before surgery began) and the removal of each testicle were compared using anova for repeated measures. RESULTS: Spectral edge frequency (SEF) 95% decreased during removal of the second testicle compared with baseline recordings. No other significant EEG changes during castration were measured. CONCLUSIONS: Lidocaine obtunded the EEG changes identified during castration in a previous control study, providing indirect evidence that lidocaine administered peri-operatively was antinociceptive and contributed to anaesthesia during castration. CLINICAL RELEVANCE: The antinociceptive effect of lidocaine combined with its minimal cardiovascular effects indicate a potential use for systemic lidocaine in clinical anaesthetic techniques.     

Endocrine and metabolic responses to halothane and pentobarbitone anaesthesia in sheep

Some metabolic and endocrine responses to anaesthesia in sheep were studied. Adult sheep were anaesthetised with thiopentone and halothane (n=9), acepromazine, thiopentone and halothane (n=8) and pentobarbitone (n=10) on separate occasions. Routine cardiovascular monitoring was carried out and blood samples were taken for assay of cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate. Halothane anaesthesia induced hypotension, hypercapnia and respiratory acidosis. Sheep anaesthetised with pentobarbitone were also hypercapnic and acidotic but did not develop hypotension. Plasma cortisol, ACTH and AVP (mean maximum values: cortisol: 83 ng/ml, ACTH 278 ng/ml, AVP 135 pg/ml), increased during halothane anaesthesia but did not change significantly from control values during pentobarbitone anaesthesia (mean maximum values: cortisol: 30 ng/ml, ACTH 71 ng/ml, AVP 7.8 pg/ml). Glucose tended to increase during both halothane and pentobarbitone anaesthesia but lactate decreased. It is not clear what facet of halothane anaesthesia evokes the stress response but it may be associated with cardiovascular depression.     

Cardiorespiratory and endocrine effects of endogenous opioid antagonism by naloxone in ponies anaesthetised with halothane

Halothane depresses cardiorespiratory function and activates the pituitary-adrenal axis, increasing beta endorphin. In horses, beta endorphin may enhance the anaesthetic-associated cardiorespiratory depression and mortality risk. The authors studied endogenous opioid effects on cardiorespiratory function and pituitary-adrenal activity in halothane-anaesthetised ponies by investigating opioid antagonism by naloxone. Six ponies were anaesthetised three times (crossover design). Anaesthesia was induced with thiopentone and maintained with 1.2 per cent halothane for 2 hours. Immediately after induction, naloxone was administered either intravenously (0.5 mg kg(-1)bolus then 0.25 mg kg(-1)hour(-1)for 2 hours) or intrathecally (0.5 mg) or was replaced by saline as control. Pulse and respiratory rates, arterial blood gases, cardiac output and plasma cortisol and adrenocorticotrophic hormone (ACTH) concentrations were measured. All groups developed cardiorespiratory depression (40 per cent decrease in cardiac output) and plasma cortisol increased. Plasma ACTH concentration was higher in ponies treated with intrathecal naloxone. Endogenous opioids may inhibit ACTH secretion, attenuating the stress response to halothane anaesthesia in equidae.     

Stress responses during total intravenous anaesthesia in ponies with detomidine - guaiphenesin - ketamine

Six ponies were anaesthetised for two hours with intermittent injections of a combination of guaiphenesin (72 mg/kg/hr), ketamine (1.4 mg/kg/hr) and detomidine (0.015 mg/kg/hr) after premedication with detomidine 0.01 mg/kg and induction of anaesthesia with guaiphenesin 50 mg/kg and ketamine 2 mg/kg. Induction of anaesthesia was smooth, the ponies were easily intubated and after intubation breathed 100% oxygen spontaneously. During anaesthesia mean pulse rate ranged between 31–44 beats per minute and mean respiratory rate between 12–23 breaths per minute. Mean arterial blood pressure remained between 110–130 mm Hg, mean arterial carbon dioxide tension between 6.1–6.9 kPa and pH between 737–7.42. Arterial oxygen tension was over 23 kPa throughout anaesthesia. Plasma glucose increased to more than 25 mmol per litre during anaesthesia; there was no change in lactate or ACTH concentration and plasma cortisol concentration decreased. Recovery was rapid and smooth. A guaiphenesin, ketamine and detomidine combination appeared to offer potential as a total intravenous technique for maintenance of anaesthesia in horses.     

Desflurane anaesthesia in the horse: minimum alveolar concentration following induction of anaesthesia with xylazine and ketamine

The minimum alveolar concentration (MAC) of desflurane was measured in 6 ponies (aged 1 or 2 years) following induction of anaesthesia with iv xylazine (1.1 mgkg bwt) followed by ketamine (2.2 mgkg bwt). The stimulus utilised was electrical; pulses of 50 volts, 10 dsec duration delivered at 5 Hz, applied for 60 s across needles inserted 1 cm apart into the buccal mucosa (n = 2) and/or the coronary band (n = 6). Stimulation was not commenced until at least 1 h following anaesthetic induction, and the time of the final MAC measurement ranged from 2.5–3.5 h. The mean (± sd) MAC of desflurane under these circumstances was 7.0% (± 0.85) with a range from 5.8%-8.3%. One pony behaved aberrantly following a positive response to the stimulus and the MAC measurement was repeated 10 weeks later. At the end of the anaesthetic period xylazine (0.2 mgkg bwt) was administered iv. Mean time to standing was 13.3 (± 2.9) min, range 9–17 min, and the quality of recovery was excellent.     

The pharmacokinetics of ketamine after a continuous infusion under halothane anaesthesia in horses

The pharmacodynamics and pharmacokinetics of ketamine, when administered by infusion as an adjunct to halothane anaesthesia in horses, were investigated in 5 equine patients presented for routine castration. Anaesthesia was induced with detomidine, 20 μg/kg, followed by ketamine, 2.2 mg/kg bwt, the trachea intubated and the horses allowed to breathe halothane in oxygen. Five minutes later, a constant rate infusion of ketamine, 40 μg/kg min, was commenced and the halothane vaporiser concentration adjusted to maintain a light plane of anaesthesia. The mean infusion duration was 62 min (range 40–103). The ketamine was switched off approximately 15 min before the halothane. Plasma ketamine and norketamine levels, determined by high performance liquid chromatography, ranged from 0.74–2.04 μg/ml and 0.15–0.75 μg/ml, respectively, during the infusion period. The harmonic mean elimination half-life of ketamine was 46.1 min, mean volume of distribution at steady state (Vdss) was 1365 (271) ml/kg, mean body clearance (Cl) was 32.3 (9.1) ml/min.kg, and average mean residence time for the infusion (MRTinf) was 105.9 (20.4) min, respectively. Following termination of halothane, mean times to sternal recumbency and standing were 21.1 (6.9) and 41.6 (17.0) min, respectively. Surgical conditions were considered highly satisfactory, and physiological parameters were well preserved in most animals.     

Biochemical and haematological changes following prolonged halothane anaesthesia in horses

Six healthy horses were anaesthetised with halothane (1·2 times the horse minimal alveolar concentration) in oxygen for more than 12 hours. Serum bilirubin, aspartate aminotransferase, alkaline phosphatase and L-iditol dehydrogenase values were significantly (P<0·05) increased for up to nine days after anaesthesia. These changes suggest au anaesthesia related liver dysfunction. Creatine kinase increased to an average of more than 1400 iu litre⁻¹ 24 hours after anaesthesia and this change is indicative of muscle cell disruption. Renal-associated biochemical results, (that is serum creatinine and inorganic phosphate concentrations) were significantly increased transiently and are indicative of reduced renal function during and immediately after anaesthesia. Plasma concentrations of eicosanoids (6-keto-PGF_1a, PGF_2a, pge and thromboxane) following anaesthesia were not different from preanaesthetic values. The magnitude of liver and muscle cell related increases in serum enzyme activities resulting from prolonged halothane anaesthesia was in excess of that previously reported for anaesthesia of shorter duration.