Anaesthetic and cardiorespiratory effects of propofol at 10% for induction and 1% for maintenance of anaesthesia in horses.

REASONS FOR PERFORMING STUDY: Studies have demonstrated the clinical usefulness of propofol for anaesthesia in horses but the use of a concentrated solution requires further investigation. OBJECTIVES: To determine the anaesthetic and cardiorespiratory responses to a bolus injection of 10% propofol solution in mature horses. METHODS: Three randomised crossover experimental trials were completed. Trial 1: 6 horses were selected randomly to receive 10% propofol (2, 4 or 8 mg/kg bwt i.v.). Trial 2: 6 horses received 1.1 mg/kg bwt i.v. xylazine before being assigned at random to receive one of 5 different doses (1-5 mg/kg bwt) of 10% propofol. Trial 3: 6 horses were sedated with xylazine (0.5 mg/kg bwt, i.v.) and assigned randomly to receive 10% propofol (3, 4 or 5 mg/kg bwt, i.v.); anaesthesia was maintained for 60 min using an infusion of 1% propofol (0.2-0.4 mg/kg bwt/min). Cardiorespiratory data, the quality of anaesthesia, and times for induction, maintenance and recovery from anaesthesia and the number of attempts to stand were recorded. RESULTS: Trial 1 was terminated after 2 horses had received each dose of 10% propofol. The quality of induction, anaesthesia and recovery from anaesthesia was judged to be unsatisfactory. Trial 2: 3 horses administered 1 mg/kg bwt and one administered 2 mg/kg bwt were not considered to be anaesthetised. Horses administered 3-5 mg/kg bwt i.v. propofol were anaesthetised for periods ranging from approximately 10-25 min. The PaO2 was significantly decreased in horses administered 3-5 mg/kg bwt i.v. propofol. Trial 3: The quality of induction and recovery from anaesthesia were judged to be acceptable in all horses. Heart rate and rhythm, and arterial blood pressure were unchanged or decreased slightly during propofol infusion period. CONCLUSIONS: Anaesthesia can be induced with a 10% propofol solution and maintained with a 1% propofol solution in horses administered xylazine as preanaesthetic medication. Hypoventilation and hypoxaemia may occur following administration to mature horses. POTENTIAL RELEVANCE: Adequate preanaesthetic sedation and oxygen supplementation are required in horses anaesthetised with propofol.

Pharmacokinetics of detomidine administered to horses at rest and after maximal exercise.

REASON FOR PERFORMING STUDY: Increased doses of detomidine are required to produce sedation in horses after maximal exercise compared to calm or resting horses. OBJECTIVES: To determine if the pharmacokinetics of detomidine in Thoroughbred horses are different when the drug is given during recuperation from a brief period of maximal exercise compared to administration at rest. METHODS: Six Thoroughbred horses were preconditioned by exercising them on a treadmill. Each horse ran a simulated race at a treadmill speed that caused it to exercise at 120% of its maximal oxygen consumption. One minute after the end of exercise, horses were treated with detomidine. Each horse was treated with the same dose of detomidine on a second occasion a minimum of 14 days later while standing in a stocks. Samples of heparinised blood were obtained at various time points on both occasions. Plasma detomidine concentrations were determined by liquid chromatography-mass spectrometry. The plasma concentration vs. time data were analysed by nonlinear regression analysis. RESULTS: Median back-extrapolated time zero plasma concentration was significantly lower and median plasma half-life and median mean residence time were significantly longer when detomidine was administered after exercise compared to administration at rest. Median volume of distribution was significantly higher after exercise but median plasma clearance was not different between the 2 administrations. CONCLUSIONS AND POTENTIAL RELEVANCE: Detomidine i.v. is more widely distributed when administered to horses immediately after exercise compared to administration at rest resulting in lower peak plasma concentrations and a slower rate of elimination. The dose requirement to produce an equivalent effect may be higher in horses after exercise than in resting horses and less frequent subsequent doses may be required to produce a sustained effect.

Pharmacokinetic and pharmacodynamic evaluation of propofol administered to cats in a novel, aqueous, nano-droplet formulation or as an oil-in-water macroemulsion.

This study evaluated pharmacokinetic and pharmacologic properties of a novel, non-lipid microemulsion, 1% w/v formulation of propofol to a conventional macroemulsion formulation of propofol (Rapinovet) in cats. The study utilized a two-period crossover design with two treatments and 10 female, intact, purpose bred domestic shorthair cats. Cats were fitted with telemetry transmitters for direct measurement of arterial blood pressure, pulse rate, electrocardiogram (ECG, lead II), and body temperature. At least 7 days separated treatments. Orotracheal intubation was the clinical endpoint utilized to evaluate adequate depth of anesthesia. Blood samples were drawn from jugular vascular access ports before propofol treatment; 3, 5, 15, 25, 35, 45, and 60 min and then 2, 3, 6, 8, 12, 18, and 24 h after administration of propofol into a cephalic vein. Whole blood samples were assayed for propofol concentrations using a gas chromatography/mass spectrometry method validated for feline blood at a limit of quantification of 5 ng/mL. Pulse rate, ECG, heart rhythm, respiratory rate, systolic, diastolic and mean arterial blood pressures, SpO2, and body temperature were monitored continuously during each anesthetic episode. Time to lateral recumbency, orotracheal intubation, and extubation, time to sternal recumbency during recovery, times to adverse events, and doses of propofol required for induction to anesthesia were documented. Cats required 6.96 +/- 0.90 mg propofol/kg from the novel microemulsion formulation of propofol and 7.07 +/- 1.55 mg propofol/kg from Rapinovet to achieve anesthesia adequate to allow orotracheal intubation (P > 0.05). Areas under the dose-normalized propofol concentration by time curves (AUC(0-LOQ)) and maximum propofol concentrations (C(max)) were equal for the novel microemulsion formulation of propofol and Rapinovet (P > 0.05). Effects of anesthesia induction doses on cardiorespiratory values were comparable between treatments, and consistent with known effects of propofol anesthesia. Results provide evidence that the novel microemulsion formulation of propofol and Rapinovet macroemulsion produced comparable pharmacodynamic, physiological, and pharmacokinetic responses in cats. The unique composition of the microemulsion formulation, and the presence of an antimicrobial preservative minimize the potential for bacterial contamination and prolong shelf life.

A new method for determining levels of sedation in dogs: A pilot study with propofol and a novel neuroactive steroid anesthetic.

BACKGROUND: Different levels of consciousness are required in order to perform different medical procedures. Sedation scales established to objectively define various levels of sedation in humans have not been thoroughly characterized in non-human species. Postural changes in rats or dogs are useful as gross measures of sedation but are inadequate for quantitative assessment since graded levels of sedation are difficult to delineate and obscured by movement abnormalities. NEW METHOD: A new canine sedation scoring (CSS) method was developed based on the modified observer's assessment of alertness and sedation score (MOAA/S) used in humans. The method employed a combination of physical, auditory and somatosensory stimuli of increasing intensity. Cardiovascular, respiratory, and a neurophysiological measure of sedation (bispectral index: BIS) data were recorded. Validation studies were performed following intravenous loading and constant rate infusion of propofol or a novel synthetic neuroactive steroid (SGE-746). RESULTS: Four levels of consciousness were identified: 1) Awake, 2) Moderate Sedation (MS), 3) Deep Sedation (DS) and 4) General Anesthesia (GA). Cardiorespiratory measurements obtained after bolus administration of propofol and SGE-746 and at the end of each CRI remained within normal limits. Canine sedation scores correlated with BIS for SGE-746. SGE-746 exhibited a more gradual exposure-response relationship than propofol. Larger increases in the plasma concentration from awake values were required to achieve different levels of sedation with SGE-746 compared to propofol. COMPARISON WITH EXISTING METHODS: No other canine sedation scoring methods are widely accepted. CONCLUSION: A CSS method, based on the human MOAA/S scale defined four levels of consciousness in dogs and provided better resolution of sedation depth than BIS alone.

Antagonism of detomidine sedation in the horse using intravenous tolazoline or atipamezole.

REASONS FOR PERFORMING STUDY: The ability to shorten the duration of sedation would potentially improve safety and utility of detomidine. OBJECTIVES: To determine the effects of tolazoline and atipamezole after detomidine sedation. HYPOTHESIS: Administration of tolazoline or atipamezole would not affect detomidine sedation. METHODS: In a randomised, placebo-controlled, double-blind, descriptive study, detomidine (0.02 mg/kg bwt i.v.) was administered to 6 mature horses on 4 separate occasions. Twenty-five mins later, each horse received one of 4 treatments: Group 1 saline (0.9% i.v.) as a placebo control; Group 2 atipamezole (0.05 mg/kg bwt i.v.); Group 3 atipamezole (0.1 mg/kg bwt i.v.); and Group 4 tolazoline (4.0 mg/kg bwt i.v.). Sedation, muscle relaxation and ataxia were scored by 3 independent observers at 9 time points. Horses were led through an obstacle course at 7 time points. Course completion time was recorded and the ability of the horse to traverse the course was scored by 3 independent observers. Horses were videotaped before, during and after each trip through the obstacle course. RESULTS: Atipamezole and tolazoline administration incompletely antagonised the effects of detomidine, but the time course to recovery was shortened. CONCLUSIONS AND POTENTIAL RELEVANCE: Single bolus administration of atipamezole or tolazoline produced partial reversal of detomidine sedation and may be useful for minimising detomidine sedation.

Coronary artery pressure development and wave transmission characteristics in the horse.

Measurements of the pressure waveform development and the wave transmission characteristics in the left extramural coronary arteries of the horse have been carried out. Near the ostium the left coronary pressure waveforms are seen to be virtually identical to the corresponding aortic root waveforms; however, the present of low frequency, relatively large amplitude pressure oscillations (on the order of 5 to 10 Hz) gradually become the dominant diastolic feature as one proceeds distally from the left ostium, and these eventually completely mask the incisura. In a limited number of experiments, these oscillations have been simultaneously observed on both centerline velocity and phasic flow signals. These are felt to be primarily due to wave reflection phenomena, but may represent a combined effect of wave reflections and the natural oscillatory motion of the heart mass. Peak systolic pressures were found to remain relatively unchanged as one proceeds distally; however, the end-diastolic pressures were found to decrease steadily, thus giving rise to an increasing pulse pressure and a gradually decreasing mean pressure. Wave speeds in the coronary arteries were found to range between 4 and 11 m.s-1, and the data obtained indicate the wave speed to be highly dependent on both local intralumenal pressure and spatial location.

Hot film coronary artery velocity measurements in horses.

Coronary velocity measurements have been carried out in anaesthetized, open-chest horses using a constant-temperature, hot-film anemometer system. L-shaped needle probes inserted by direct vessel puncture have been used to measure velocity profiles in the left common, left anterior descending (LAD), and left circumflex coronary arteries. The flow conditions were characterized by peak Reynolds numbers from approximately 200 to 1500 and values of the unsteadiness parameter from 3 to 10. These measurements indicate that in the left common coronary artery the profile is in general skewed towards the outer wall as would be expected for fully viscous flow in a curved tube. In the left anterior descending and left circumflex coronary arteries just distal to the bifurcation, the skewing was found in general to be away from the flow divider. However, in regions of the LAD and left circumflex 5-6 diameters downstream of the bifurcation, the peak systolic and diastolic profiles were indicative of a more fully developed, Poiseuille type flow with only slight skewing observed. The results of this study indicate that the flow in the coronary system, though in general laminar and disturbance free, is extremely varied in character and may exhibit large amplitude, low frequency flow oscillations. Furthermore, for these vessels which all lie on the surface of the myocardium, large systolic flows were observed to be present, even though the major portion of the volume flow was reserved for the diastolic period.

Oxygenation, oxygen delivery and anaesthesia in the horse.

Horses are the most difficult of the common companion animals to anaesthetise. Hypoxaemia or inadequate oxygen delivery to peripheral tissues during anaesthesia would seem a potential cause of increased mortality, but no direct link has been established. A number of methods of increasing oxygenation and oxygen delivery have been reported, with varying results and potential applicability. The purpose of this article is to review the literature with regard to oxygenation, oxygen delivery and methods to improve each and to make recommendations for clinical application.

Joint pressure influences synovial tissue blood flow as determined by colored microspheres.

We measured regional blood flow in synovial tissue of the antebrachiocarpal, midcarpal, and metacarpophalangeal joints of six normal adult anesthetized horses by using 15-microns-diameter polystyrene colored microspheres. The midcarpal fibrous capsule and synovial membrane blood flows (SMBF) were compared, and the effect of increased intra-articular pressure (30 and 60 mmHg) on midcarpal SMBF was investigated. Dorsal, medial palmar, and lateral palmar midcarpal SMBF measured 108 +/- 36, 61 +/- 12, and 50 +/- 11 microliters.min-1.g-1, respectively. Antebrachiocarpal, dorsal, and palmar metacarpophalangeal SMBF measured 103 +/- 8, 17 +/- 3, and 26 +/- 5 microliters.min-1.g-1, respectively. Midcarpal fibrous joint capsule blood flow was significantly lower than that of the synovial membrane. An increase in midcarpal intra-articular pressure to 30 or 60 mmHg resulted in an 84% decrease in SMBF. Colored microspheres provided a useful technique to determine sequential SMBF. Increased intra-articular pressure significantly altered SMBF, suggesting a role of the regional circulation in the pathogenesis of joint disease.

Pressure-volume relationships in equine midcarpal joint.

The effects of joint angle, fluid infusion, history-dependence, and time dependence on the pressure-volume (PV) relationships of normal equine midcarpal joints were determined. Horses (n = 24 and 48 midcarpal joints) were anesthetized and placed in dorsal recumbency, and the four midcarpal joint pouches were cannulated for intra-articular pressure (IAP) measurements and recording. Fluid (synovial fluid or saline) was infused or withdrawn through the dorsal joint capsule. The PV curves were sigmoid and best described by IAP = A x e(B x volume) - C, where B is the fractional change in pressure per unit change of volume, and A and C are constants. Compartmentation was not observed. Elastance was greater at sub- than supra-atmospheric pressures, at 90 degrees than 135 degrees angles, and with saline than synovial fluid. Hysteresis was greater at 90 degrees than 135 degrees angle, and with synovial fluid than saline. Elastance progressively increased with sequential distention at high IAPs. IAP relaxation was a positive logarithmic relationship of IAP. These findings suggest an important role of synovial fluid in articular PV relationships and emphasize the role of joint angle, prior distention cycles, and decay of IAP with time in future studies investigating these phenomena.

Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion.

We theorized that furosemide-induced weight reduction would reduce the contribution of anaerobic metabolism to energy expenditure of horses during intense exertion. The effects of furosemide on accumulated O2 deficit and plasma lactate concentration of horses during high-intensity exercise were examined in a three-way balance randomized crossover study. Nine horses completed each of three trials: 1) a control (C) trial, 2) a furosemide-unloaded (FU) trial in which the horse received furosemide 4 h before running, and 3) a furosemide weight-loaded (FL) trial during which the horse received furosemide and carried weight equal to the weight lost after furosemide administration. Horses ran for 2 min at approximately 120% maximal O2 consumption. Furosemide (FU) increased O2 consumption (ml.2 min-1.kg-1) compared with C (268 +/- 9 and 257 +/- 9, P < 0.05), whereas FL was not different from C (252 +/- 8). Accumulated O2 deficit (ml O2 equivalents/kg) was significantly (P < 0.05) lower during FU (81.2 +/- 12.5), but not during FL (96.9 +/- 12.4), than during C (91.4 +/- 11.5). Rate of increase in blood lactate concentration (mmol.2 min-1.kg-1) after FU (0.058 +/- 0.001), but not after FL (0.061 +/- 0.001), was significantly (P < 0.05) lower than after C (0.061 +/- 0.001). Furosemide decreased the accumulated O2 deficit and rate of increase in blood lactate concentration of horses during brief high-intensity exertion. The reduction in accumulated O2 deficit in FU-treated horses was attributable to an increase in the mass-specific rate of O2 consumption during the high-intensity exercise test.

Effect of phenylbutazone on the haemodynamic, acid-base and eicosanoid responses of horses to sustained submaximal exertion.

The systemic haemodynamic and acid-base effects of the administration of phenylbutazone (4.4 mg kg-1 intravenously) to standing and running horses were investigated. Phenylbutazone, or a placebo, was administered to each of six mares either 15 minutes before, or after 30 minutes of a 60-minute submaximal exercise test which elicited heart rates approximately 55 per cent of maximal, and to the same horses at rest. The variables examined included the cardiac output, heart rate, systemic and pulmonary arterial pressures, right atrial and right ventricular pressures, and arterial and mixed venous blood gases and pH. Serum sodium, potassium and chloride concentrations, and plasma thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and prostaglandin E2 (PGE2) concentrations were measured in separate studies using similar protocols in the same horses. Running produced increases in heart rate, cardiac output, mean arterial and right ventricular pressure, and decreases in total peripheral resistance. The acid:base responses to exertion were characterised by respiratory alkalosis. Exertion did not significantly influence plasma 6-keto-PGF1 alpha or PGE2 concentrations but plasma thromboxane B2 concentrations were increased significantly by 60 minutes of exertion in the untreated horses. This exercise-induced increase in plasma thromboxane B2 concentration was inhibited by the previous administration of phenylbutazone, but phenylbutazone did not produce detectable changes in systemic haemodynamic or acid-base variables in either standing or running horses.

An investigation of the second heart sound in the normal horse.

The second heart sound was evaluated in conscious, normal horses using intracardiac and external sound detection devices and echocardiography. The second heart sound (S2) in the normal horse is single or split by a narrow interval, not usually detected by external phonocardiographic evaluation. Splitting of S2 was classified as normal (aortic [A2] preceding pulmonic [P2] components) in 66.7 per cent and reversed (P2 preceding A2) in 33.3 per cent of the horses studied. Normal splitting appears to result from lower impedance of the pulmonary vasculature delaying the onset of P2. Reverse splitting appears to result from a delay in A2 resulting from prolongation of PEP and LVET. There does not appear to be variation in splitting of S2 due to respiration based on the cases in which this was measured.

Haematological, serum electrolyte and blood gas effects of small volume hypertonic saline in experimentally induced haemorrhagic shock.

The effects of treatment with small volume hypertonic (2400 mOsm/litre) and isotonic (300 mOsm/litre) saline on serum electrolyte and biochemical concentrations, haemograms and blood gases were evaluated in 12 horses using a haemorrhagic shock model. Intravascular catheters were placed surgically for sample collection prior to anaesthesia. Controlled haemorrhage was initiated and continued until mean systemic pressure reached 50 to 60 mmHg. Hypertonic or isotonic saline (2 litres) was administered by intravenous infusion and data collected for 2 h. Following haemorrhage, packed cell volume (PCV), haemoglobin, blood glucose concentrations and erythrocyte numbers increased whereas plasma total protein and albumin concentrations decreased. Infusion of hypertonic saline resulted in a further decrease in total protein and albumin concentrations. Glucose concentrations and other haematological variables were unaffected. Isotonic saline administration did not affect electrolyte, total protein or albumin concentrations. Concentrations of sodium and chloride were unaffected by hypotension but increased significantly following hypertonic saline treatment, exceeding normal values during the immediate post treatment period. Serum osmolality increased concurrently. No significant changes in arterial and venous blood gas values were observed with haemorrhage or isotonic saline treatment. A transient decrease in arterial and venous blood pH and a sustained decrease in venous bicarbonate and base excess concentrations occurred following hypertonic saline administration. No significant increases in any serum biochemical concentrations occurred during hypotension or following infusion of either isotonic or hypertonic saline. These results demonstrate that small volume hypertonic saline can be administered safely to horses without producing extreme changes in electrolyte concentrations, blood gases or haematological parameters.

Haemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shock.

A comparison of the haemodynamic benefits of small volume hypertonic saline (2,400 mOsm/litre) versus isotonic saline (300 mOsm/litre) was conducted in 12 adult horses using a haemorrhagic shock model. The horses were anaesthetised and intravascular catheters placed for the measurement of haemodynamic data. Mean systemic arterial pressure was then reduced to 50 to 60 mmHg by controlled haemorrhage and maintained at that level for 40 mins. Cardiac output, stroke volume, mean systemic arterial pressure, plasma volume and urine production decreased significantly following blood loss. Hypertonic or isotonic saline was administered randomly by intravenous infusion and haemodynamic data recorded for a 2 h period. Treatment with hypertonic saline produced rapid elevations in cardiac output, stroke volume, mean systemic and pulmonary arterial pressures, cardiac contractility and urine output, and was accompanied by expansion of the plasma volume. The changes in cardiac output and stroke volume were maintained for the duration of the recording period, whereas increases in mean systemic arterial pressure were not as remarkable. Infusion of isotonic saline caused only transient increases in cardiac output and mean systemic and pulmonary arterial pressure, and cardiac output; urine output and plasma volume did not change. This study indicates that hypertonic saline produces haemodynamic improvements in experimentally induced haemorrhagic shock in horses.

Cardiovascular effects of thoracic compression in horses subjected to euthanasia.

Six horses scheduled for euthanasia were instrumented for the measurement of blood flow by thermodilution, pulmonary arterial, right atrial and arterial blood pressures and collection of arterial blood for pH and blood gas analysis. The horses were anaesthetised with intravenous (iv) thiamylal sodium (10 mg/kg) and placed in right lateral recumbency. After euthanasia with an overdose of pentobarbitone sodium (100 mg/kg, iv) and loss of the electrocardiogram and arterial pulse pressure, thoracic compression at rates of 40, 60 and 80 compressions/min was instituted. Thoracic compression was accomplished by an investigator who delivered a blow to the chest wall with his knee while dropping from a standing or crouching position. Compression rates of 40, 60 and 80/min produced blood flows of 5.65 +/- 0.5, 6.33 +/- 1.11 and 8.28 +/- 2.16 litres/min, respectively. Compression rates of 80/min produced significantly (P < 0.05) greater blood flows and mean arterial blood pressures than did slower rates. The blood flows produced by 80 thoracic compressions/min were approximately 50% of those reported for deeply anaesthetised horses and while not sufficient to sustain life might be used to prolong life in order to facilitate distribution of resuscitative drugs to vital tissues.

Sequelae of myelography in the horse.

The records of 131 horses undergoing general anaesthesia and positive contrast cervical myelography with metrizamide were examined to determine the effect of the procedure on the 'patient'. Three per cent of minimally ataxic and moderately ataxic horses had serious complications after myelography. Thirty-two per cent of severely ataxic horses died or were destroyed after general anaesthesia and myelography. Although general anaesthesia and myelography are essential components of a complete neurological evaluation of a horse, they impose a significant risk.

Pharmacology of furosemide in the horse: a review.

Furosemide, a diuretic, is frequently administered to horses for the prophylaxis of exercise-induced pulmonary hemorrhage and the treatment of a number of clinical conditions, including acute renal failure and congestive heart failure. Furosemide increases the rate of urinary sodium, chloride, and hydrogen ion excretion. Plasma potassium concentration decreases after furosemide administration but urinary potassium excretion in horses is minimally affected. Renal blood flow increases after furosemide administration. Systemically, furosemide increases venous compliance and decreases right atrial pressure, pulmonary artery pressure, pulmonary artery wedge pressure, and pulmonary blood volume. The systemic hemodynamic effects of furosemide are only manifest in the presence of a functional kidney, but can occur in the absence of diuresis, emphasizing the importance of the renal-dependent extra-renal effects of furosemide. The renal and systemic hemodynamic effects of furosemide are modified by prior administration of nonsteroidal anti-inflammatory drugs. Furosemide administration attenuates exercise-induced increases in right atrial, aortic, and pulmonary artery pressures in ponies. Furosemide prevents exercise and allergen-induced bronchoconstriction in humans and decreases total pulmonary resistance in ponies with recurrent obstructive airway disease. These pharmacologic effects are frequently used to rationalize its questionable efficacy in the prevention of exercise-induced pulmonary hemorrhage. Neither the effect of furosemide on athletic performance nor its efficacy in the prevention of exercise-induced pulmonary hemorrhage has been convincingly demonstrated.

Selected aspects of the clinical pharmacology of visceral analgesics and gut motility modifying drugs in the horse.

Comparison of the visceral analgesic effects of xylazine, morphine, butorphanol, pentazocine, meperidine, dipyrone, and flunixin in a cecal distention model of colic pain indicated that xylazine produces the most relief from abdominal discomfort. Repeated administration of xylazine may reduce visceral pain so effectively that the seriousness of abdominal disease is obscured. Xylazine decreased propulsive motility in the jejunum and pelvic flexure of healthy ponies. Morphine and butorphanol also gave relief from visceral pain in the cecal distention model. Morphine may inhibit colonic, and butophanol jejunal, motility. Whether xylazine or opiate mediated decreases in gut motility cause clinically important slowing of ingesta transit is controversial and requires further investigation. The development of behavioral changes (i.e., apprehension and pawing) in horses given opiate therapy may limit the use of these drugs. Combinations of xylazine and morphine or butorphanol produce excellent, safe, visceral analgesia and sedation without untoward behavioral effects. Although flunixin fails to demonstrate good visceral analgesic effects in the cecal distention model, this drug produces analgesia in some cases of colic by blocking prostaglandin mediated induction of pain. Improvement of propulsive gut motility in patients with ileus may follow administration of neostigmine (which is particularly effective when the large bowel is hypomotile), naloxone (which experimentally stimulates propulsive colonic motility), and metoclopramide (which stimulates stomach and proximal small intestinal motility).

Hemodynamic effects of atropine, dobutamine, nitroprusside, phenylephrine, and propranolol in conscious horses.

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.