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.     

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.     

The stress response to anaesthesia in ponies: barbiturate anaesthesia

Information on the equine stress response to anaesthesia and surgery is sparse but offers a promising approach to elucidating the high anaesthetic risk in this species. Previous work has shown that halothane anaesthesia induces substantial metabolic and endocrine changes. This paper reports the effects of barbiturate anaesthesia. Anaesthesia was induced with thiopentone in six ponies and no further agents were given. They stood within 30 mins. On another occasion, these animals, and three further ponies, were anaesthetised with pentobarbitone and anaesthesia was maintained for 2 h. No surgery was performed on either occasion. Plasma concentrations of glucose, lactate, non esterified fatty acids, cortisol, insulin, catecholamines and adrenocorticotrophic hormone were measured at the same time intervals in both groups before, during and after anaesthesia. There were no significant changes in hormones or metabolites during either period of anaesthesia and normotension was maintained. This was in marked contrast to the substantial stress response and hypotension under halothane anaesthesia in the same ponies. These results suggest that barbiturates may induce less of a stress response than halothane in horses. Recovery after 2 h of pentobarbitone anaesthesia was poor, precluding its clinical use. The need for a non-cumulative intravenous agent or a non-hypotensive volatile agent for use in equine anaesthesia is discussed.     

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.     

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.     

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.     

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.     

Midazolam and ketamine induction before halothane anaesthesia in ponies: cardiorespiratory, endocrine and metabolic changes

Six Welsh gelding ponies were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) prior to induction of anaesthesia with midazolam at 0.2 mg/kg and ketamine at 2 mg/kg i.v.. Anaesthesia was maintained for 2 h using 1.2 % halothane concentration in oxygen. Heart rate, electrocardiograph (ECG), arterial blood pressure, respiratory rate, blood gases, temperature, haematocrit, plasma arginine vasopressin (AVP), dynorphin, ß-endorphin, adrenocorticotropic hormone (ACTH), cortisol, dopamine, noradrenaline, adrenaline, glucose and lactate concentrations were measured before and after premedication, immediately after induction, every 20 min during anaesthesia, and at 20 and 120 min after disconnection. Induction was rapid, excitement-free and good muscle relaxation was observed. There were no changes in heart and respiratory rates. Decrease in temperature, hyperoxia and respiratory acidosis developed during anaes-thesia and slight hypotension was observed (minimum value 76 ± 10 mm Hg at 40 mins). No changes were observed in dynorphin, ß-endorphin, ACTH, catecholamines and glucose. Plasma cortisol concentration increased from 220 ± 17 basal to 354 ± 22 nmol/L at 120 min during anaesthesia; plasma AVP concentration increased from 3 ± 1 basal to 346 ± 64 pmol/L at 100 min during anaesthesia and plasma lactate concentration increased from 1.22 ± 0.08 basal to 1.76 ± 0.13 mmol/L at 80 min during anaesthesia. Recovery was rapid and uneventful with ponies taking 46 ± 6 min to stand. When midazolam/ketamine was compared with thiopentone or detomidine/ketamine for induction before halothane anaesthesia using an otherwise similar protocol in the same ponies, it caused slightly more respiratory depression, but less hypotension. Additionally, midazolam reduced the hormonal stress response commonly observed during halothane anaesthesia and appears to have a good potential for use in horses.     

Comparison of two pre-anaesthetic medetomidine doses in isoflurane anaesthetized sheep

OBJECTIVE: To compare the sedative, anaesthetic-sparing and arterial blood-gas effects of two medetomidine (MED) doses used as pre-anaesthetic medication in sheep undergoing experimental orthopaedic surgery. STUDY DESIGN: Randomized, prospective, controlled experimental trial. ANIMALS: Twenty-four adult, non-pregnant, female sheep of various breeds, weighing 53.9 +/- 7.3 kg (mean +/- SD). METHODS: All animals underwent experimental tibial osteotomy. Group 0 (n = 8) received 0.9% NaCl, group L (low dose) (n = 8) received 5 microg kg(-1) MED and group H (high dose) (n = 8) received 10 microg kg(-1) MED by intramuscular (IM) injection 30 minutes before induction of anaesthesia with intravenous (IV) propofol 1% and maintenance with isoflurane delivered in oxygen. The propofol doses required for induction and endtidal isoflurane concentrations (F(E')ISO) required to maintain anaesthesia were recorded. Heart and respiratory rates and rectal temperature were determined before and 30 minutes after administration of the test substance. The degree of sedation before induction of anaesthesia was assessed using a numerical rating scale. Arterial blood pressure, heart rate, respiratory rate, FE'ISO, end-tidal CO2 (FE'CO2) and inspired O2 (FIO2) concentration were recorded every 10 minutes during anaesthesia. Arterial blood gas values were determined 10 minutes after induction of anaesthesia and every 30 minutes thereafter. Changes over time and differences between groups were examined by analysis of variance (anova) for repeated measures followed by Bonferroni-adjusted t-tests for effects over time. RESULTS: Both MED doses produced mild sedation. The dose of propofol for induction of anaesthesia decreased in a dose-dependent manner: mean (+/-SE) values for group 0 were 4.7 (+/-0.4) mg kg(-1), for group L, 3.2 (+/-0.4) mg kg(-1) and for group H, 2.3 (+/-0.3) mg kg(-1)). The mean (+/-SE) FE'ISO required to maintain anaesthesia was 30% lower in both MED groups [group L: 0.96 (+/-0.07) %; group H: 1.06 (+/-0.09) %] compared with control group values [(1.54 +/- 0.17) %]. Heart rates were constantly higher in the control group with a tendency towards lower arterial blood pressures when compared with the MED groups. Respiratory rates and PaCO2 were similar in all groups while PaO2 increased during anaesthesia with no significant difference between groups. In group H, one animal developed a transient hypoxaemia: PaO2 was 7.4 kPa (55.7 mmHg) 40 minutes after induction of anaesthesia. Arterial pH values and bicarbonate concentrations were higher in the MED groups at all time points. CONCLUSION AND CLINICAL RELEVANCE: Intramuscular MED doses of 5 and 10 microg kg(-1) reduced the propofol and isoflurane requirements for induction and maintenance of anaesthesia respectively. Cardiovascular variables and blood gas measurements remained stable over the course of anaesthesia but hypoxaemia developed in one of 16 sheep receiving MED.     

β-endorphin immunoreactivity during anaesthesia in equidae

Objective To determine the effects of surgery, hypoxia, hypercapnia and flunixin administration on plasma β‐endorphin immunoreactivity (BEI) in anaesthetized horses. Study design Prospective crossover study. Animals Six healthy adult Welsh Mountain ponies and seven healthy adult Thoroughbreds. Methods Ponies were anaesthetized with thiopentone and halothane or with pentobarbitone and the horses with guaiphenesin, thiopentone and halothane. Ponies were anaesthetized for 2 hours and on separate occasions underwent a period of hypoxia, hypercapnia, anaesthesia only, or were given flunixin at induction. The horses were anaesthetized for 2 hours and on separate occasions underwent surgery to relocate one carotid artery subcutaneously or anaesthesia only. Plasma samples were taken pre‐anaesthesia, at 20 minute intervals during, and after anaesthesia for BEI assay using radio‐immunoassay. Analysis of variance of the concentration‐time curve was used for statistical analysis. Results Pre‐anaesthetic β‐endorphin immunoreactivity (BEI) values ranged between 5.7 and 20.4 pmol L^?1. Induction of anaesthesia caused a five to 10 fold increase in mean plasma BEI in all cases except the hypercapnia group. Halothane anaesthesia increased BEI in ponies and horses but there were no significant changes during pentobarbitone anaesthesia. The increase in BEI in the hypoxic group was greater (peak value 136.8 ± 32.2 pmol L^?1) and sustained for a longer period compared with levels in those given halothane alone or in those which became hypercapnic. There was marked individual variation in the flunixin group and changes were not significant. Surgery in the horses resulted in the highest peak values in the study (182.5 ± 153.0 pmol L^?1) but the AUC was not significantly higher than in the same animals without surgery, where the peak value was 102.9 ± 42.1 pmol L^?1. Conclusions Beta‐endorphin appeared to be a sensitive marker of an endocrine stress response but its physiological role during equine anaesthesia is unknown. Clinical relevance Unknown.     

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.     

Comparison of morphine and butorphanol as pre-anaesthetic agents in combination with romifidine for field castration in ponies

OBJECTIVE: The aim of this study was to compare two different alpha2 agonist-opioid combinations in ponies undergoing field castration. STUDY DESIGN: Prospective double-blind randomized clinical trial. ANIMAL POPULATION: Fifty-four ponies undergoing field castration. MATERIALS AND METHODS: The ponies were randomly allocated to receive one of three different pre-anaesthetic medications [intravenous (IV) romifidine 100 microg kg(-1) and butorphanol 50 micro kg(-1); romifidine 100 microg kg(-1) and morphine 0.1 mg kg(-1) IV, or romifidine 100 microg kg(-1) and saline IV] before induction of anaesthesia with ketamine 2.2 mg kg(-1) IV. Further doses of romifidine (25 microg kg(-1)) and ketamine (0.5 mg kg(-1)) were given when required to maintain anaesthesia. Quality of sedation, induction of anaesthesia, maintenance of anaesthesia, recovery, and surgical condition were assessed using a visual analogue scale scoring system and compared. The effects of the different drug combinations on heart and respiratory rate were evaluated and the recovery time was recorded. RESULTS: Anaesthesia was considered adequate for surgery in all ponies. No anaesthetic complications were observed. Quality of sedation was significantly better in the butorphanol group compared with the control group (p = 0.0428). Overall quality of anaesthesia was better in the butorphanol group compared with morphine (p = 0.0157) and control (p < 0.05) groups. Quality of induction of anaesthesia and recovery were not significantly different between groups, nor were the surgical conditions, recovery time and the number of repeated anaesthetic doses required during the procedure. Muscle twitches were observed in both the control and morphine groups. Maintenance of anaesthesia was judged to be smoother in the butorphanol group compared with the morphine and control groups (p = 0.006). Heart rate decreased significantly (p < 0.01) in all groups after administration of sedatives but did not differ significantly between groups at any time point. CONCLUSION: The combination of butorphanol and romifidine was found to provide better sedation compared with the other drug combinations. CLINICAL RELEVANCE: The combination of butorphanol and romifidine provided better sedation, but morphine was found to be a suitable alternative to butorphanol. Use of morphine and butorphanol in combination with alpha2 agonists should be further investigated to assess their analgesic effects.     

Pulmonary oedema associated with anaesthesia for colic surgery in a horse

A 506 kg Warmblood horse with colic was anaesthetized for exploratory celiotomy. Anaesthesia was complicated by arterial hypoxaemia which persisted throughout surgery from the induction of anaesthesia. After endotracheal extubation in the recovery box, a degree of airway obstruction probably occurred during a brief delay in naso-tracheal intubation. Signs of pulmonary oedema were seen shortly afterwards. Furosemide and oxygen were given. Arterial hypoxaemia was present [PaO2: 6.5 kPa (49 mmHg)] when FIO2 was an estimated 0.3. The horse recovered and stood after 45 minutes. It was re-anaesthetized 3 days later when arterial blood gas analysis did not reveal hypoxaemia. The horse was killed on this occasion; post-mortem examination revealed the presence of pulmonary oedema, which probably resulted from multiple causes.     

Arterial blood PO2 and PCO2 in horses during early halothane-oxygen anaesthesia

Arterial blood was collected from 25 clinically normal horses immediately before and serially throughout the first hour of halothane oxygen anaesthesia. Blood was analysed for oxygen and carbon dioxide partial pressure (PaO2, PaCO2). Measurements of inspired oxygen concentration during anaesthesia permitted direct correlation with blood gases. Horses were divided arbitrarily into two groups based on their age: two to seven years, n = 15; over seven years, n = 10. Average (+/- sd) PaO2 and PaCO2 was 14.1 +/- 1.5 kPa (106 +/- 11 mmHg) and 5.9 +/- 0.6 kPa (44.4 +/- 4.4 mmHg) respectively in conscious, young horses and 14.0 +/- 0.7 and 5.8 +/- 0.5 kPa (105 +/- 5 and 43.3 +/- 3.8 mmHg) respectively in conscious older horses. Arterial oxygen tension decreased to 9.3 +/- 1.0 and 8.5 +/- 1.4 kPa (69.6 +/- 7.8 and 63.7 +/- 10.4 mmHg) in young and older air breathing horses respectively immediately following intravenous anaesthetic induction, recumbency and orotracheal intubation. At this time, PaCO2 was 6.5 +/- 0.5 and 6.0 +/- 0.7 kPa (48.7 +/- 3.5 and 45.1 +/- 4.9 mmHg) respectively. By 30 mins after the start of halothane in oxygen (6 litres/min) anaesthesia PaO2 increased to a maximum in both study groups. Arterial PCO2 increased steadily during anaesthesia and 60 mins after induction PaCO2 was 10.5 +/- 2.4 kPa (78.5 +/- 17.8 mmHg) in the younger horses and 9.2 +/- 1.6 kPa (68.8 +/- 11.8 mmHg) in the older horses. During inhalation anaesthesia PaO2 tended to be greater at comparable time periods in the younger horses despite a slightly greater degree of hypoventilation.     

Hypoxaemia during anaesthesia in seven horses with colic

Anaesthetic records of horses with colic anaesthetised between June 1987 and May 1989 were reviewed. pH and blood gas analyses were performed during 157 operations from which the horses were allowed to recover. A PaO₂ of 8.0 kPa or less was measured during anaesthesia in seven of these horses. The horses were of different breeds, ages and sexes. Anaesthesia was induced with xylazine, guaifenesin and ketamine in four horses and with xylazine, guaifenesin and thiobarbiturate in three horses. Anaesthesia was maintained with inhalation anaesthetic agent and oxygen: isoflurane in five horses, halothane in one horse, and initially halothane but later isoflurane in one horse. Systolic arterial pressures during anaesthesia ranged from 80 to 150 mmHg, diastolic arterial pressures were between 60 and 128 mmHg, and heart rates were between 28 and 44 beats /min. Controlled ventilation was initiated at the start of anaesthesia. PaCO₂ exceeded 6.7 kPa in three horses but was subsequently decreased by adjustment of the ventilator. PaO₂ of 8.0 kPa or less was measured during early anaesthesia, with one exception, and persisted for the duration of anaesthesia. The horses' inspired air was supplemented with oxygen during recovery from anaesthesia, at which time measurement of blood gases in three horses revealed no increase in PaO₂. Recovery from anaesthesia was uneventful. The surgical problems involved primarily the large intestine in five horses and the small intestine in two horses. Six horses were discharged from the hospital alive; one horse was reanaesthetised later the same day and destroyed without regaining consciousness. We concluded that none of the objective values recorded during the pre-anaesthetic evaluation could have been used to predict the complication of intraoperative hypoxaemia. We observed that once hypoxaemia developed it persisted for the duration of anaesthesia and even into the recovery period when the horses were in lateral recumbency and regaining consciousness. We assume that the altered metabolism from anaesthetic agents and hypothermia combined with adequate peripheral perfusion contributed to the lack of adverse consequences in six of the horses. The contribution of hypoxaemia to the deteriorating condition of the seventh horse is speculative.     

The cardiopulmonary effects of clenbuterol when administered to dorsally recumbent halothane-anaesthetised ponies - failure to increase arterial oxygenation

Clenbuterol (0·8 μg kg ⁻¹ intravenously) was investigated in ponies (small horses) anaesthetised with acepromazine, detomidine and thiopentone, then halothane in oxygen alone (hyperoxic group) or with nitrous oxide (hypoxic group). Following instrumentation, ponies were placed in dorsal recumbency for 60 minutes, clenbuterol (both groups) or a saline control (hyperoxic group) given, and cardiopulmonary parameters monitored for a further 60 minutes. In the hyperoxic group, clenbuterol administration resulted in a transitory (<five minutes) 15 per cent fall in arterial blood pressure and 78 per cent rise in intramuscular blood flow. Heart rate increased from a mean of 42 (SD 4) to 54 (12) beats per minute, the rise being significant for 15 minutes. Cardiac index increased from 2·1 (0·7) to 3·-9 (0·7) litres m⁻² and remained significantly elevated for the remainder of the measurement period. Cardiovascular changes in the hypoxic group were similar. 30 minutes after clenbuterol administration, PaO₂ had changed non-significantly from 32·.3 (19·2) to 33·.4 (17) kPa in the hyperoxic group and from 7·9 (1·8) to 8·.6 (1·3) kPa in the hypoxic group. The study concludes that under these experimental conditions, clenbuterol does not cause significant improvement in arterial oxygenation, but its cardiovascular effects are minimal or advantageous.     

Effects of plasma expansion on the pituitary-adrenocortical response to halothane anaesthesia in sheep

The study aimed to investigate the stimulus to adrenocortical activity that is induced by halothane anaesthesia. Groups of 7 sheep were anaesthetised with thiopentone and halothane (TH) or acepromazine, thiopentone and halothane (ATH). During 120 min of anaesthesia hypotension was prevented (mean arterial blood pressure kept at pre-anaesthetic level) by infusion of a modified gelatine plasma replacer given to effect (0.34–1.1 litres with TH and 1.1–3.1 litres with ATH). Pulse rate, arterial blood pressure and gases were measured and sequential samples withdrawn for analysis of plasma cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate. Heart rate increased in the ATH but not the TH group. All sheep were well oxygenated but developed hypercapnia and respiratory acidosis. In both groups, cortisol increased more than 2-fold 20 min after the end of anaesthesia but there were no significant changes in ACTH. AVP was measured in the TH group only and increased 3-fold at the end of anaesthesia. Glucose and lactate remained stable except for lactate in the TH group which decreased during anaesthesia. These data indicate that hypotension is a major component of the stimulus inducing adrenocortical activity during halothane anaesthesia. However, maintenance of normotension did not entirely depress the response; halothane itself or decreased perfusion may also contribute.     

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.     

Intravenous anaesthesia using detomidine, ketamine and guaiphenesin for laparotomy in pregnant pony mares

Objective To characterize intravenous anaesthesia with detomidine, ketamine and guaiphenesin in pregnant ponies. Animals Twelve pony mares, at 260–320 days gestation undergoing abdominal surgery to implant fetal and maternal vascular catheters. Materials and methods Pre‐anaesthetic medication with intravenous (IV) acepromazine (30 µg kg^?1), butorphanol (20 µg kg^?1) and detomidine (10 µg kg^?1) preceded induction of anaesthesia with detomidine (10 µg kg^?1) and ketamine (2 mg kg^?1) IV Maternal arterial blood pressure was measured directly throughout anaesthesia and arterial blood samples were taken at 20‐minute intervals for measurement of blood gases and plasma concentrations of cortisol, glucose and lactate. Anaesthesia was maintained with an IV infusion of detomidine (0.04 mg mL^?1), ketamine (4 mg mL^?1) and guaiphenesin (100 mg mL^?1) (DKG) for 140 minutes. Oxygen was supplied by intermittent positive pressure ventilation (IPPV) adjusted to maintain PaCO₂ between 5.0 and 6.0 kPa (38 and 45 mm Hg), while PaO₂ was kept close to 20.0 kPa (150 mm Hg) by adding nitrous oxide. Simultaneous fetal and maternal blood samples were withdrawn at 90 minutes. Recovery quality was assessed. Results DKG was infused at 0.67 ± 0.17 mL kg^?1 hour^?1 for 1 hour then reduced, reaching 0.28 ± 0.14 mL kg^?1 hour^?1 at 140 minutes. Arterial blood gas values and pH remained within intended limits. During anaesthesia there was no change in heart rate, but arterial blood pressure decreased by 10%. Plasma glucose and lactate increased (10‐fold and 2‐fold, respectively) and cortisol decreased by 50% during anaesthesia. Fetal umbilical venous pH, PO₂ and PCO₂ were 7.34 ± 0.06, 5.8 ± 0.9 kPa (44 ± 7 mm Hg) and 6.7 ± 0.8 kPa (50 ± 6 mm Hg); and fetal arterial pH, PO₂ and PCO₂ were 7.29 ± 0.06, 4.0 ± 0.7 kPa (30 ± 5 mm Hg) and 7.8 ± 1.7 kPa (59 ± 13 mm Hg), respectively. Surgical conditions were good but four ponies required a single additional dose of ketamine. Ponies took 60 ± 28 minutes to stand and recovery was good. Conclusions and clinical relevance Anaesthesia produced with DKG was smooth while cardiovascular function in mare and fetus was well preserved. This indicates that DKG infusion is suitable for maintenance of anaesthesia in pregnant equidae.