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 Pulse rate, arterial blood pressure and gases were measured and sequential samples withdrawn for analysis of plasma cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate.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.     

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.     

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.     

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.     

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.     

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.     

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.     

Does the induction agent affect the course of halothane anaesthesia in horses?

Four hundred and ninety horses were anaesthetised with halothane for clinical surgical or diagnostic procedures following induction with either detomidine/keta-mine, detomidine/thiopentone, xylazine/ketamine or guaiphenesin/thiopentone. Routine clinical monitoring was performed during anaesthesia. All horses developed hypotension (mean arterial pressures below 80 mm Hg) and respiratory depression (significant fall in respiratory rate and arterial carbon dioxide tension above 7 kPa (53 mm Hg)) consistent with the recognised effects of halothane. All anaesthetic procedures incorporating xylazine or detomidine resulted in lower pulse rates (28–35 per min) than after guaiphenesin/thiopentone (36–44 per min) and there was greater respiratory depression after techniques employing thiopentone rather than keta-mine. Development of hypotension was delayed after techniques using the α₂ adrenoceptor agonist agents (xylazine and detomidine), particularly detomidine. Prernedication with acepromazine did not affect any of the physiological variables measured after techniques employing detomidine. Recovery to standing was fastest after xylazine/ketamine (31±1 min) and slowest after detomidine/thiopentone (53±2 min). Recovery quality was best after detomidine/thiopentone and all techniques employing an α₂ adrenoceptor agonist agent resulted in smoother recovery than after guaiphenesin/thiopentone. This study demonstrates that most of the physiological effects of individual induction agents are overridden by the cardiovascular and respiratory depressant effects of halothane. The study also shows that detomidine is an acceptable sedative for use before general anaesthesia with halothane in horses.     

Endocrine response to lactate infusion during pentobarbitone anaesthesia

Lactic acid was infused iv in 6 Welsh ponies during pentobarbitone anaesthesia to investigate whether lactate triggers the pituitary-adrenal response to anaesthesia. Ponies were premedicated with acepromazine and anaesthesia was induced with pentobarbitone iv and maintained with pentobarbitone/oxygen for 2 h. Immediately after induction, 3% L(+) lactic acid infusion was started and adjusted to maintain plasma lactate concentration between 2 and 2.5 mmol/l. Cardiorespiratory function, temperature. PCV, plasma glucose, lactate, βendorphin, ACTH, cortisol and catecholamine concentrations were measured before, during and after anaesthesia. Hypothermia, reduced PCV, slight hypotension (minimum value 84 ± 6 mmHg 20 min after induction of anaesthesia), hyperoxia and marked bradypnoea developed during anaesthesia. No acidaemia occurred. Plasma glucose concentration increased at the end of anaesthesia. There were no changes in plasma ACTH, cortisol and catecholamine concentrations, but plasma & endorphin increased after induction until the end of anaesthesia. There was a correlation between plasma lactate and β-endorphin concentrations (P<0.001, r=0.63), which may suggest that lactate stimulates βendorphin release. Beta-endorphin was apparently secreted independently from ACTH and appears to be a sensitive marker of a stress response.     

Effects of hypertonic saline infusion on the adrenocortical response to thiopental-halothane anesthesia in sheep after premedication with acepromazine

OBJECTIVE: To investigate whether hypertonic saline infusion would prevent hypotension and pituitary-adrenocortical axis activation during halothane anesthesia after acepromazine premedication and thiopental induction in sheep. STUDY DESIGN: Randomized crossover study. ANIMALS: Six Welsh Mountain ewes weighing 40+/-2 kg and aged 2 to 3 years. METHODS: The sheep were studied on two occasions with 2 weeks between anesthetics. After acepromazine premedication, anesthesia was induced with thiopental and maintained for 120 minutes with halothane. During the first 15 minutes of anesthesia, 7.5% saline (4 mL/kg) was infused intravenously (HS group), but no infusion was given in the control (CONT) group. Sequential blood samples were taken for blood gas, cortisol, adenocorticotropic hormone (ACTH), glucose, and lactate assay. RESULTS: Hypotension developed in both treatments; blood pressure decreased to a nadir of 58+/-5 mm Hg in the HS group and to 63+/-4 mm Hg in the CONT group (P>.05). Plasma cortisol increased significantly in both groups, reaching a peak of 420+/-130 nmol/L in HS and 483+/-157 nmol/L in CONT (P>.05). ACTH increased similarly in both groups, reaching 128+/-64 pmol/L in HS and 134+/-55 pmol/L in CONT (P>.05). pH was slightly higher in CONT, but no other differences were detected between the two groups. CONCLUSIONS: Hypertonic saline did not ameliorate the adrenocortical response during anesthesia; this may be a result of its failure to prevent the hypotension.     

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.     

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.     

ACTH stimulation test in the captive cheetah (Acinonyx jubatus)

Serum cortisol response was assessed in 8 captive cheetahs, of varying ages, after the intravenous administration of 500 microg of tetracosactide (Synacthen Depot, Novartis, Kempton Park) while maintained under general anaesthesia. In addition, 8 cheetahs were anaesthetised and given an equal volume of saline in order to establish baseline cortisol concentrations at similar stages of anaesthesia. A significant difference in the median cortisol concentration measured over time was found following ACTH administration in the ACTH group (P < 0.001). There was no difference between the median cortisol concentrations in the ACTH group at time-points 120, 150 and 180 min after ACTH stimulation (P = 0.867). Thus it appears appropriate to collect serum 120 to 180 min after tetracosactide administration to assess maximal stimulation of the adrenal in the cheetah. No statistically significant rise was seen in the anaesthetised control group following the injection of saline (P = 0.238).     

Metabolic and hormonal changes associated with arthroscopic surgery in the horse

The effect of general anaesthesia and arthroscopic surgery on blood glucose and lactate, plasma non-esterified fatty acids, insulin, beta-endorphin and cortisol was investigated in seven horses. Animals were premedicated with xylazine and anaesthesia was induced with guaifenesin and sodium thiamylal and maintained with halothane vaporised in oxygen. Blood samples were collected in the pre-, intra- and post operative period. Induction of anaesthesia was associated with a transient hyperglycaemia and a significant rise in plasma insulin levels. Plasma insulin values fell during surgery but showed a significant increase post operatively. Surgery stimulated a small but significant rise in plasma beta-endorphin and cortisol values but these had returned to baseline values in the early post operative period. No changes in blood lactate were recorded.     

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.     

Adrenocorticotropic hormone and cortisol in calves after corticotropin-releasing hormone.

The aim for this study was to analyze responsiveness of the hypothalamo-pituitary-adrenocortical axis to exogenous bovine corticotropin-releasing hormone (bCRH) in calves. Two dose-response studies were carried out, using either bCRH alone (dose rates of 0, .01, .03, and .1 microg bCRH/kg live weight) or in combination with arginine-vasopressin (bCRH:AVP, 0:0, .1:.05, .5:.25, and 1:.5 microg kg live weight). The bCRH was administered i.v. to calves (n = 5 to 7 per dose) housed individually or in groups. Serial blood samples were obtained from before to 300 min after injection and analyzed for plasma ACTH and cortisol concentrations. The lowest bCRH dose that produced a response in all calves was .1 microg/kg. In the experiment using bCRH with AVP, increasing the bCRH dose from .1 to 1 microg/kg resulted in an increase in peak ACTH concentration (321 vs. 2,003 pg/mL) but did not significantly affect the peak cortisol concentration (37 vs. 40 ng/mL). The time to reach the peak cortisol concentration increased with the dose of bCRH with AVP (from 38 to 111 min). The ACTH and cortisol concentrations determined at any time between 20 and 90 min after bCRH injection were correlated to the integrated responses calculated as areas under the ACTH and the cortisol curves (r between .61 and .99, P<.05). In comparison with results from studies in humans, pigs, and sheep, our data showed that the pituitary of calves seems less sensitive to CRH than that of other mammals, despite a greater capacity to produce ACTH. Moreover, the calf's adrenals seem to have a lower capacity to produce cortisol than adrenals of other mammals. As in other species, it seems that AVP enhances the release of ACTH and cortisol. For CRH challenge to be used in calves, we suggest injecting at least .1 microg of bCRH/kg live weight either with or without AVP and taking several blood samples before injection and between 20 and 90 min after injection.     

Combined xylazine and ketamine as an analgesic regimen in sheep

OBJECTIVE: To determine whether low dose xylazine with ketamine reduces the concentrations of cortisol and prolactin in sheep postoperatively and to characterise the effects of the drugs on behaviour during recovery. DESIGN: Analysis of variance was used to compare the effects of anaesthesia, surgery and combined ketamine/xylazine treatment on the plasma cortisol and prolactin concentrations and on behavioural variables in pregnant ewes subjected to abdominal surgery. PROCEDURE: Twelve ewes were randomly assigned to receive either ketamine/xylazine or placebo in association with anaesthesia and surgery. Both groups of ewes underwent anaesthesia alone followed a week later by anaesthesia with laparotomy and hysterotomy. Plasma cortisol and prolactin concentrations were assayed during these procedures and for 5 days afterwards. Behavioural observations were made remotely during recovery from anaesthesia and anaesthesia plus surgery. RESULTS: The concentrations of cortisol in the plasma of pregnant ewes undergoing surgery were increased by preoperative handling and the onset of thiopentone/halothane anaesthesia, with a further increase during surgery (P = 0.033). Cortisol concentrations decreased over the first four postoperative hours (P = 0.029) and were normal by 24 h. The drug treatment did not affect the immediate responses of ewes to anaesthesia or surgery, although treated ewes had lower cortisol concentrations than saline-treated controls over the first five postoperative days (P = 0.018). Prolactin concentrations increased in response to anaesthesia (P = 0.047), but were not affected by surgery or the drug treatment. Drug-treated ewes had prolonged sleeping time after surgery (P = 0.002), but they took no longer to stand than saline-treated controls and required fewer attempts to stand successfully (P = 0.025). CONCLUSION: At the doses used, ketamine and xylazine did not mitigate the immediate endocrine consequences of surgery but the behavioural data provide a basis for further investigations that may lead to improvements in analgesic treatments.     

Some metabolic and hormonal changes associated with general anaesthesia and surgery in the horse

Three different anaesthetic techniques were studied in normal, healthy Thoroughbred or Thoroughbred type horses. These were (a) acepromazine, thiopentone and suxamethonium; (b) acepromazine, glyceryl guaiacolate and a 'half-dose' of thiopentone; and (c) xylazine and ketamine. Anaesthesia was maintained with halothane vaporized in oxygen and nitrous oxide. All horses underwent either laryngeal or body surface surgery. Heart rate, packed cell volume, blood glucose and lactate, plasma non-esterified fatty acids, insulin and cortisol were measured before, during and after surgery. The greatest metabolic and hormonal changes occurred immediately after anaesthetic induction and were different in each group. The combination of acepromazine, glyceryl guaiacolate and a 'half-dose' of thiopentone was associated with the least change in the physiological and metabolic variables measured.     

Hepatic effects of halothane, isoflurane or sevoflurane anaesthesia in dogs

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