Biomedical subjects
Publications and source records attributed to J C Brearley.
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OBJECTIVE: To compare detomidine hydrochloride and romifidine as premedicants in horses undergoing elective surgery. ANIMALS: 100 client-owned horses. PROCEDURE: After administration of acepromazine (0.03 mg/kg, IV), 50 horses received detomidine hydrochloride (0.02 mg/kg of body weight, IV) and 50 received romifidine (0.1 mg/kg, IV) before induction and maintenance of anesthesia with ketamine hydrochloride (2 mg/kg) and halothane, respectively. Arterial blood pressure and blood gases, ECG, and heart and respiratory rates were recorded. Induction and recovery were timed and graded. RESULTS: Mean (+/- SD) duration of anesthesia for all horses was 104 +/- 28 minutes. Significant differences in induction and recovery times or grades were not detected between groups. Mean arterial blood pressure (MABP) decreased in both groups 30 minutes after induction, compared with values at 10 minutes. From 40 to 70 minutes after induction, MABP was significantly higher in detomidine-treated horses, compared with romifidine-treated horses, although more romifidine-treated horses received dobutamine infusions. In all horses, mean respiratory rate ranged from 9 to 11 breaths/min, PaO2 from 200 to 300 mm Hg, PaCO2 from 59 to 67 mm Hg, arterial pH from 7.33 to 7.29, and heart rate from 30 to 33 beats/min, with no significant differences between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Detomidine and romifidine were both satisfactory premedicants. Romifidine led to more severe hypotension than detomidine, despite administration of dobutamine to more romifidine-treated horses. Both detomidine and romifidine are acceptable alpha2-adrenoceptor agonists for use as premedicants before general anesthesia in horses; however, detomidine may be preferable when maintenance of blood pressure is particularly important.
OBJECTIVE: To assess the suitability of lithium dilution as a method for measuring cardiac output in anesthetized horses, compared with thermodilution and transesophageal Doppler echocardiography. ANIMALS: 6 horses (3 Thoroughbreds, 3 crossbreeds). PROCEDURE: Cardiac output was measured in 6 anesthetized horses as lithium dilution cardiac output (LiDCO), thermodilution cardiac output (TDCO), and transesophageal Doppler echocardiographic cardiac output (DopplerCO). For the LiDCO measurements, lithium chloride was administered i.v., and cardiac output was derived from the arterial lithium dilution curve. Sodium nitroprusside, phenylephrine hydrochloride, and dobutamine hydrochloride were used to alter cardiac output. Experiments were divided into 4 periods. During each period, 3 LiDCO measurements, 3 DopplerCO measurements, and 3 sets of 3 TDCO measurements were obtained. RESULTS: 70 comparisons were made between LiDCO, DopplerCO, and triplicate TDCO measurements over a range of 10 to 43 L/min. The mean (+/- SD) of the differences of LiDCO - TDCO was -0.86 +/- 2.80 L/min; LiDCO = -1.90 + 1.05 TDCO (r = 0.94). The mean of the differences of DopplerCO - TDCO was 1.82 +/- 2.67 L/min; DopplerCO = 2.36 + 0.98 TDCO (r = 0.94). The mean of the differences of LiDCO - DopplerCO was -2.68 +/- 3.01 L/min; LiDCO = -2.53 + 0.99 DopplerCO (r = 0.93). CONCLUSIONS AND CLINICAL RELEVANCE: These results indicate that lithium dilution is a suitable method for measuring cardiac output in horses. As well as being accurate, it avoids the need for pulmonary artery catheterization and is quick and safe to use. Monitoring cardiac output during anesthesia in horses may help reduce the high anesthetic mortality in this species.
The purpose of this study was to compare the haemodynamic effects of equipotent isoflurane and halothane anaesthesia. Six adult horses were investigated on two separate occasions at least 4 weeks apart. On both occasions anaesthesia was induced by ketamine 2.2 mg/kg bwt given 5 min after i.v. administration 100 microg/kg bwt romifidine. Anaesthesia was maintained either by halothane or isoflurane (end-tidal concentrations 0.9-1.0% and 1.3-1.4%, respectively). Horses were ventilated by intermittent positive pressure to maintain PaCO2 between 40-50 mmHg. Haemodynamic variables were measured using catheter-mounted strain gauge transducers in the left and right ventricle, aorta, and right atrium. Cardiac output (CO), velocity time integral (VTI), maximal aortic blood flow velocity (Vmax) and acceleration (dv/dt(max)), left ventricular pre-ejection period (PEP) and ejection time (ET) were measured from aortic blood flow velocity waveforms obtained by transoesophageal Doppler echocardiography. Flow velocity waveforms were recorded from the femoral arteries and veins using low pulse repetition frequency Doppler ultrasound. Time-averaged mean velocity (TAV), velocity of component a (TaVa), velocity of component b (TaVb) and early diastolic deceleration slope (EDDS) were measured. Pulsatility index (PI) and volumetric flow were calculated. Microvascular blood flow was measured in the left and right semimembranosus muscles by laser Doppler flowmetry. Maximal rate of rise of LV pressure (LVdp/dt(max)), CO, Vmax, dv/dt(max), ET, VTI were significantly higher at all time points during isoflurane anaesthesia compared to halothane anaesthesia. Pre-ejection period and diastolic aortic blood pressure were significantly less throughout isoflurane anaesthesia compared to halothane. Isoflurane anaesthesia was associated with significantly lower systemic vascular resistance than halothane anaesthesia. Femoral arterial and venous blood flow were significantly higher and EDDS and PI were significantly lower during isoflurane anaesthesia compared to halothane anaesthesia. In addition during both halothane and isoflurane anaesthesia, femoral arterial flow was higher and EDDS and PI lower in the left (dependent) artery compared to the right (nondependent) artery. This study supports previous work demonstrating improved left ventricular systolic function during isoflurane compared to halothane anaesthesia. This improvement was still evident after premedication with a potent-long acting alpha2-adrenoreceptor agonist, romifidine, and induction of anaesthesia with ketamine. There was also evidence of increased hindlimb blood flow during isoflurane anaesthesia. However, there were differences observed in flow between the left and right hindlimb during maintenance of anaesthesia with each agent, suggesting that there were differences in regional perfusion in anaesthetised horses caused by factors unrelated to agents administered.
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.
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This prospective clinical study compared the physiological effects of two commonly used anaesthetic induction techniques in horses maintained with halothane. One hundred horses admitted for elective surgery were randomly allocated to receive either guaiphenesin (to effect) and thiopentone (5 mg/kg), or detomidine (20 microg/kg) and ketamine (2 mg/kg) for the induction of anaesthesia after acepromazine premedication. Anaesthesia was maintained with halothane in oxygen. There were no significant differences in breed, age, sex, weight, type of surgery and duration of anaesthesia between the groups. Immediately after induction of anaesthesia heart rate was higher after guaiphenesin and thiopentone, and arterial blood pressure was higher after detomidine and ketamine. Thereafter hypotension, often necessitating an infusion of dobutamine, developed in both groups. Arterial blood gases and respiratory rates were similar in the two groups. There were no significant differences between the groups in the subjectively scored quality of induction and recovery, or in recovery time.
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Horses undergoing surgery were randomly assigned to one of three groups to receive phenylbutazone at 4 mg/kg (n = 72), flunixin at 1 mg/kg (n = 68) or carprofen at 0.7 mg/kg (n = 63) by slow intravenous injection at the end of surgery, just before they were disconnected from halothane. Pain was assessed by either of two resident surgical clinicians (who did not know which non-steroidal anti-inflammatory drug had been given) when the horses first stood up, two and four hours later and the next morning. If repeated doses of analgesic drugs were given the time was recorded and taken as an end point for the study. The presence or absence of side effects was also recorded. In the three groups there was no significant difference between the types of surgery performed, the numbers of horses requiring further analgesia or the pain scores at any time. In the horses needing further analgesia there was a significant difference in the time after surgery at which the further analgesia was given between those in the flunixin group, 12.8 +/- 4.3 hours (mean +/- sd) and those in the phenylbutazone group, 8.4 +/- 4.6 hours; the carprofen group had an intermediate interval of 11.7 +/- 6.9 hours. Significantly fewer of the horses that received butorphanol during surgery needed further analgesia than of those that did not receive any opioid.
The effects of the sedatives acepromazine (an alpha-adrenergic antagonist) and xylazine (an alpha 2-adrenergic agonist) on plasma indicators of stress in cows were assessed after intramuscular injection and transport. After blood samples had been taken for baseline values, nine cows were given an intramuscular injection of saline (2.5 ml), acepromazine (0.05 mg/kg in 2.5 ml) or xylazine (0.05 mg/kg in 2.5 ml) on different occasions at least 1 week apart. The animals were then transported for 5 min by truck to a different environment and blood sampled for a further 1-3 h. There was a significant increase in plasma cortisol concentration (3.29 +/- 1.59 x baseline) after the injection of saline and transport. The injection of acepromazine also resulted in a significant increase in cortisol concentration (2.84 +/- 0.84 x baseline). There was no similar increase after injection of xylazine. This suggests that alpha 2-adrenergic receptors are involved in the response of plasma cortisol concentrations to stressors. An hyperglycaemic response occurred after xylazine (1.66 +/- 0.49 x baseline) and saline (1.20 +/- 0.1 x baseline) but not after acepromazine. Both sedatives produced a metabolic alkalosis (1.13 +/- 0.01 x baseline pH after xylazine and 1.034 +/- 0.02 x baseline pH after acepromazine). A greater decrease in haematocrit was seen after both sedatives (0.88 +/- 0.04 x baseline after xylazine, 0.81 +/- 0.08 x baseline after acepromazine) than after the injection of saline (0.97 +/- 0.06 x baseline).
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