Halothane-catecholamine arrhythmias in swine (Sus scrofa)

The arrhythmogenic dose of epinephrine (ADE) was determined in 6 pigs during steady-state anesthesia (1.5% halothane in O2) and steady-state anesthesia plus xylazine (1.1 mg X kg-1 X hr-1; IV infusion) and after either prazosin (alpha 1) or metoprolol (beta 1) adrenergic blockade during halothane-xylazine (H-X) anesthesia. A constant infusion (1, 2, 3, 5, and 10 micrograms X kg-1 X min-1) of freshly mixed epinephrine (100 micrograms X ml-1 in saline solution) was used to determine ADE. The ADE was defined as the total dose of epinephrine which produced 4 or more continuous or intermittent, premature, ventricular contractions within a 15-s period. The mean epinephrine total dose values during 1.5% halothane anesthesia, H-X anesthesia alone, or H-X anesthesia after either prazosin (0.1 mg X kg-1) or metoprolol (0.5 mg X kg-1) adrenergic blockade were 3.60 +/- 0.844, 2.68 +/- 0.402, 11.85 +/- 3.804, and 5.17 +/- 0.587 micrograms X kg-1, respectively. Xylazine administration did not significantly decrease ADE, although mean arterial pressure significantly increased. Prazosin administration significantly increased ADE and was associated with an increased heart rate and a decreased mean arterial pressure. We conclude that alpha 1-blockade with prazosin is more protective to epinephrine-induced arrhythmias in H-X-anesthetized pigs than is beta 1-blockade with metoprolol.     

Inotropic mechanisms of dopexamine hydrochloride in horses.

Mechanisms responsible for the positive inotropic effects of dopexamine were investigated in 8 halothane-anesthetized horses. The hemodynamic effects of increasing infusions of dopexamine (5, 10, 15 micrograms/kg of body weight/min) were determined before and after sequential administration of specific antagonists. Using glycopyrrolate and chlorisondamine, and atenolol and ICI 118,551, muscarinic and nicotinic ganglionic, and beta 1, and beta 2-adrenergic receptor blockade, respectively, was induced. Dopexamine infusions induced increase in heart rate, cardiac output, systolic and mean arterial blood pressure, and maximal rate of left ventricular pressure development (+dP/dtmax). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and +dP/dtmax responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. beta 1-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and +dP/dtmax from baseline values and markedly reduced the response to dopexamine infusion. beta 2-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on +dP/dtmax. These data indicate that baroreflex activity, beta 1- and beta 2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.     

Effects of metoclopramide, clenbuterol and butorphanol on ruminoreticular motility of calves

Rate and amplitude of contractions of the rumen dorsal sac and reticulum of 6 male Holstein calves ages 12 to 20 weeks were monitored with electromyography, strain gauges and an intraruminal pressure catheter. Heart rate and mean arterial pressure were measured with ultrasound. The effects of metoclopramide, a dopamine antagonist, clenbuterol, a beta-2 adrenergic agonist, and butorphanol, a narcotic agonist/antagonist, were observed utilizing dosages bracketing those employed clinically. Metoclopramide significantly decreased the intraruminal pressure peaks associated with cyclical contractions without changing their rate. Clenbuterol had no measurable effect on the ruminoreticulum. Butorphanol totally inhibited ruminoreticular contractions for periods of 6 to greater than 40 min depending on dosage. Only clenbuterol significantly affected cardiovascular function; it increased heart rate and decreased mean arterial pressure. Both metoclopramide and butorphanol produced behavioral changes in the calves.     

Alteration in the arrhythmogenic dose of epinephrine (ADE) following xylazine administration to halothane-anesthetized dogs

The arrhythmogenic dose of epinephrine (ADE) was determined in six dogs during halothane (1.35%) anesthesia before and after xylazine administration (1.1 mg/kg, i.v. bolus; 1.1 mg/kg/hr, i.v. infusion). The arrhythmogenic dose was determined by constant infusion of freshly mixed epinephrine (100 microgram/ml). The ADE was defined as the total dose of epinephrine which produced four or more intermittent or continuous premature ventricular contractions within a 15-sec period. Total dose was calculated as a function of infusion rate and time to arrhythmia. Following xylazine administration, ADE significantly decreased from 6.28 +/- 0.522 to 4.17 +/- 0.679 micrograms/kg. At the end of i.v. xylazine bolus administration, heart rate significantly decreased (115 +/- 4 to 99 +/- 4.9 b.p.m.), and mean arterial pressure significantly increased (83 +/- 4.0 to 122 +/- 3.4 mm Hg). Heart rate measured immediately prior to epinephrine-induced arrhythmia formation was significantly increased following xylazine administration (177 +/- 8 vs 78 +/- 3 b.p.m.). Mean arterial blood pressure was unchanged. Apparently, xylazine, a mixed alpha agonist, potentiated halothane-induced myocardial sensitization to ventricular arrhythmogenesis and was associated with a significant increase in heart rate, but not blood pressure, during subsequent epinephrine infusions.     

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.     

Side effects of clenbuterol as a repartitioning agent

Clenbuterol, a synthetic beta-adrenergic agonist drug, can be used to increase the ratio of protein to fat in the carcase of meat animals. During the first one to three days of its administration to sheep or calves clenbuterol increased their heart rate, and in sheep it decreased blood pressure. Continued administration had no further effect on heart rate or blood pressure but in sheep dose levels above 1.5 mg/day depressed appetite for up to five days; at all dose levels clenbuterol brought about a long term increase in metabolic rate.     

Cardiovascular and allied actions of xylazine and atropine in the unanaesthetized goat

The cardiovascular effects of xylazine and atropine, separately and in combination, were studied in goats. Methylatropine was used to distinguish between the central and peripheral effects of atropine. Mean arterial blood pressure and heart rate were recorded, and the sedative effect and changes in respiration and salivation noted. Intravenous infusion of xylazine (2.4-80.0 micrograms/kg) decreased mean arterial blood pressure and heart rate in a dose-dependent manner. Single intravenous injections of both atropine sulphate (0.1 mg/kg) and methylatropine bromide (0.05 mg/kg) increased blood pressure and heart rate. After methylatropine, tachycardia lasted twice as long as after atropine. Following atropinization, a potentiated rise in mean arterial blood pressure was present during the infusion of xylazine (80 micrograms/kg). Xylazine-induced bradycardia was reversed by both atropine and methylatropine. The action of atropine is presumed to be primarily peripheral because of the similar effects with methylatropine. Xylazine-induced sedation was dose dependent. At the highest dose the goats were unable to stand for 30-60 min, respiration became irregular with periods of apnoea, and saliva started to drip a few minutes after infusion without increased salivation. Atropine had no visible effect on the sedation, pattern of respiration or saliva dripping effect of xylazine.     

Sevoflurane anaesthesia in chickens during spontaneous and controlled ventilation

A crossover study design was used to investigate the dose-related effects of sevoflurane at end-tidal concentrations of 2.2 to 4.4 per cent on the respiratory rate, blood gases, heart rate, arterial blood pressure and ocular signs of chickens during spontaneous and controlled ventilation. The mean (sd) carbon dioxide partial pressure (PaCO2) increased as the concentration of sevoflurane increased, and was 86 (29) mmHg at an end-tidal concentration of 4.4 per cent during spontaneous ventilation, but was maintained between 29 and 42 mmHg during controlled ventilation. The heart rate increased as the concentration of sevoflurane increased during spontaneous ventilation, but did not change during controlled ventilation. Sevoflurane decreased arterial blood pressure during both spontaneous and controlled ventilation, but a dose-dependent decrease in arterial blood pressure was observed only during controlled ventilation. The mean arterial blood pressure at an end-tidal concentration of 4.4 per cent was significantly higher during spontaneous ventilation than during controlled ventilation. Controlled ventilation prevented the increases in PaCO2 and heart rate that were observed during spontaneous ventilation. The decrease in arterial blood pressure during spontaneous ventilation was less than that during controlled ventilation, possibly owing to the effects of hypercapnia.     

The effects of salbutamol on blood pressure and heart rate in Large White and Pietrain-cross breeds of pig

The effects of the β2-agonist salbutamol, on pig heart rate and blood pressure were evaluated at the expected commercially used concentration of 3 ppm in final feed, and at three times this level. Salbutamol was administered to pigs previously fed on control diet (‘naive’), and in a second study to pigs fed 3 ppm salbutamol for 19 days (‘acclimatized’). Heart rate and blood pressure were measured in conscious 30 kg pigs before (pre-ingestive), during (ingestive) and after ingestion (absorptive) of feed containing 3 or 9 ppm salbutamol. To assess any interaction with ‘stress genotype’ pigs, measurements were performed in Large White and Pietrain-cross breeds. The mean preingestive heart rates for the Large White and Pietrain-cross pigs were 127 and 109 beats/min, respectively. The corresponding figures for mean arterial blood pressure were 121 and 122 mmHg. The act of ingesting control feed caused heart rate to rise by 36–39% and blood pressure to increase by 17–27%. During the absorptive phase for ‘naive’ pigs fed 3 ppm salbutamol in the diet, blood pressure fell 5–11% and heart rate increased 20–24%, reflecting a classical baroreceptor mediated response. At 9 ppm the fall in blood pressure of 5–11% was similar to that at 3 ppm, while the rise in heart rate was larger at 31–38%. The magnitude of the changes at both 3 and 9 ppm was less than that evoked by the act of ingestion, with the exception of the heart rate response in Large Whites at 9 ppm, which was similar. The responses of the two breeds were comparable, indicating that salbutamol is unlikely to exacerbate the cardiovascular responses seen in potentially stress-susceptible pigs. The acute changes elicited by 3 ppm salbutamol during the absorptive phase in ‘naive’ pigs were abolished or substantially less in acclimatized pigs, implying a tachyphylaxis to the agonist's actions. This was confirmed by 9 ppm of salbutamol increasing heart rate of ‘acclimatized’ Large Whites to the same degree as 3 ppm in ‘naive’ counterparts. The desensitization in Pietrain-cross pigs was even more marked with no increase in heart rate produced by 9 ppm salbutamol following acclimatization. These data, combined with the rapid tachyphylaxis of response, indicate that salbutamol at the intended commercial inclusion of 3 ppm will not compromise the cardiovascular stability of the growing pig at rest.     

Effect of azaperone on cardiovascular responsiveness in stress-sensitive pigs

The effect of intramuscular azaperone on the cardiovascular responses to stimulation of the sympathetic nervous system was examined in thiopentone-anaesthetized stress-sensitive pigs. Sympathetic stimulation was achieved with the Valsalva-like manoeuvre, and the intravenous tyramine, isoprenaline and phenylephrine tests. The responses were monitored as the changes in heart rate and blood pressure. Azaperone exerted an alpha adrenergic blocking action and possibly a mild beta adrenergic blocking effect. It also retarded pre-adrenoreceptor activation of heart rate. It is suggested that azaperone has peripheral actions which could contribute towards its prophylactic effect in preventing stress-induced deaths in pigs.     

Cardiopulmonary evaluation of the use of medetomidine hydrochloride in cats.

OBJECTIVE: To evaluate the cardiovascular effects of the alpha2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats. ANIMALS: 7 clinically normal cats. PROCEDURE: Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 microg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration. RESULTS: Heart rate, cardiac index, stroke index, rate-pressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: When administered alone to clinically normal cats, medetomidine (20 microg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central alpha2-adrenergic effect over peripheral vascular effects.     

Reversal of medetomidine-induced cardiovascular and respiratory changes with atipamezole in dogs

The effects of atipamezole, an alpha 2-antagonist, on six medetomidine-sedated laboratory beagles were studied in a randomised complete block design. The dogs were sedated with medetomidine (20, 40 or 80 micrograms/kg intramuscularly) and five- and 10-fold larger doses of atipamezole were administered intramuscularly 30 minutes later. Atipamezole significantly increased the medetomidine-depressed heart rate, respiratory frequency and arterial Po2. The drug also transiently decreased the mean arterial blood pressure but subsequently the blood pressure of the treated group did not differ from that of a group of dogs treated with a placebo.     

Effects of isoproterenol infusion on the hindlimb metabolism of growing wether lambs

The effect of a mixed beta 1/beta 2-adrenergic agonist, isoproterenol, on hindlimb metabolism was studied in growing wether lambs using arteriovenous difference and blood flow rate techniques. Isoproterenol (48 micrograms kg-1 d-1), or saline, was infused into a jugular vein of five wether lambs (30 to 35 kg) for five days and samples taken on the fifth day of treatment. Infusion of isoproterenol significantly increased blood flow, oxygen uptake and tyrosine uptake across the hindlimb. Hindlimb non-esterified fatty acid uptake was increased but not significantly (P = 0.11) and arterial growth hormone concentration was not altered by isoproterenol infusion. Results suggest that beta-adrenergic agonists promote lean tissue deposition by increased muscle blood flow rate and amino acid uptake.     

New perspectives in cardiopulmonary therapeutics: receptor-selective adrenergic drugs

Recent advances in basic biomedical research have led to the development of clinically useful drugs known as "second generation" adrenergic receptor stimulants (agonists) and blockers (antagonists). Adrenergic receptors are now differentiated into 4 distinct subtypes: alpha 1, alpha 2, beta 1, and beta 2. The new drugs are more receptor-selective and tissue-specific than older ones and, hence, have increased potential for directed therapeutic action, with relatively less side effects on nontargeted organs. The beta 2-selective agonist terbutaline, eg, causes bronchodilation with less beta 1-cardiac excitation than does the beta 1-beta 2 nonselective agonist isoproterenol. Compared with the latter, the beta 1-selective agonist dobutamine increases myocardial contractile force and cardiac output with less beta 2-mediated vasodilation and hypotension. The beta 1-selective antagonist metoprolol has advantage over the beta 1-beta 2 nonselective blocker propranolol for controlling beta 1-cardiac excitation in patients with compromised pulmonary function. Prazosin, an alpha 1-selective blocking agent, evokes peripheral vasodilation with less reflex tachycardia than does the nonselective alpha 1-alpha 2 blocker phentolamine, probably because the former spares the prejunctional alpha 2-receptors that subserve autoinhibition of norepinephrine release from the sympathetic neuron. The contemporary practice of internal medicine will no doubt include an understanding of the pharmacologic properties associated with the various adrenergic receptor subtypes.     

Cardiovascular and respiratory effects of thiopental administration in hypovolemic dogs

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.     

Cardiorespiratory and anesthetic effects of clinical and supraclinical doses of alfaxalone in dogs

ObjectiveTo determine the cardiorespiratory and anesthetic effects of 2, 6, and 20 mg kg⁻¹ IV alfaxalone in hydroxypropyl beta cyclodextrin (Alfaxan) in dogs.Study designBlinded four-way crossover randomized by dose.AnimalsEight healthy adult purpose-bred mixed breed dogs (four male, four female) weighing between 12 and 28 kg.MethodsFour (0, 2, 6, 20 mg kg⁻¹) IV treatments of alfaxalone were administered to each dog with a 3-hour washout period between doses. Measurements of heart rate, aortic systolic, mean, and diastolic blood pressures, pulmonary arterial and right atrial mean pressures, cardiac output, respiratory rate, tidal and minute volumes, and arterial blood pH, blood gases (PaO₂, PaCO₂) were performed prior to and at predetermined intervals after drug administration. Systemic vascular resistance and rate pressure product were calculated. The quality of induction, maintenance, and recovery from anesthesia were categorically scored as was the response to noxious stimulation.ResultsThe administration of alfaxalone resulted in dose-dependent changes in cardiovascular and respiratory parameters. Decreases in arterial blood pressure and increases in heart rate occurred at higher doses with most variables returning to baseline in 15–30 minutes. Respiratory rate, minute volume, and PaO₂ decreased and apnea was the most common side effect. The duration of anesthesia increased with dose, and induction, maintenance, and recovery were judged to be good to excellent with all doses studied.Conclusions and clinical relevanceAlfaxalone produced good to excellent short-term anesthesia in unpremedicated dogs. Cardiorespiratory effects were minimal at lower doses. Anesthesia was judged to be good to excellent and associated with unresponsiveness to noxious stimulation for the majority of anesthesia. Hypoventilation and apnea were the most prominent and dose-dependent effects.     

Effects of Fosinopril on Renal Function,Baroreflex Response and Noradrenaline Pressor Response in Conscious Normotensive Dogs

The blood pressure, renal function, baroreflex response of heart rate and noradrenaline (norepinephrine) pressor response were determined in conscious, normotensive, sodium-replete dogs that had received fosinopril. Oral administration of fosinopril at a dose of 1 mg/kg per day for 5 days decreased the systolic arterial pressure from 147.1±3 to 131.8±4.3 mmHg (p<0.05) and the mean arterial pressure from 99.7±3.9 to 87.5±2.8 mmHg (p<0.05), while heart rate was unchanged. A study of the noradrenaline pressor response showed a tendency to alleviate the increased MAP by fosinopril treatment, although this was not significant. There were no significant changes in the sensitivity of the baroreflex response in HR, although the setpoint was reduced. After 7 days of fosinopril treatment, the glomerular filtration rate had increased by 18.5% (p<0.05). The effective renal plasma flow tended to increase, leaving the filtration fraction unchanged. The renal vascular resistance was reduced by 11.3% (p<0.05). Fosinopril caused a significant 41.5% increase in urinary excretion of Na⁺ (p<0.05), along with an elevation of urinary excretion of K⁺ and Cl^–. It is concluded that fosinopril can lower the blood pressure, reduce the noradrenaline pressor response and lower the cardiac baroreflex setpoint to noradrenaline. Oral administration of fosinopril for 7 days affects both the renal haemodynamics and electrolyte excretions in conscious, normotensive, sodium-replete dogs.     

Renal actions of the alpha2-adrenoceptor agonist, xylazine, in the anaesthetised rat

AIMS: The aims of the present study were to characterise the renal effects of the alpha2-adrenergic agonist, xylazine, in the rat and to test the role of changes in glomerular filtration rate, glucosuria, and arginine vasopressin (AVP) in its mechanism of action. METHODS: Male Wistar rats were anaesthetised with pentobarbitone sodium (50 mg/kg), and polyethylene cannulae were surgically placed for blood pressure measurement and for blood and urine collection. Rats were given xylazine and other alpha2 agonists by bolus intravenous dose, and the effects of the drugs were monitored in the presence and absence of the selective alpha2 antagonist, yohimbine, the alpha1, alpha2B antagonist, prazosin, and the V2-receptor antagonist, d(CH2)5 [D-Ile2,Ile4,Ala-NH29]AVP. RESULTS: Xylazine at 2.5 mg/kg caused a significant and prolonged dose-dependent increase in urine flow rate and sodium excretion but had only short-lasting effects on blood pressure, heart rate, and glomerular filtration rate. Prazosin had no effect on the measured responses. Although plasma glucose concentration and glucose excretion rate were increased by xylazine, the magnitudes of these increases were insufficient to account for the diuresis observed. Xylazine, and 2 other alpha2 agonists, clonidine and oxymetazoline, increased urine flow and/or sodium excretion despite the presence of d(CH2)5 [D-Ile2,Ile4,Ala-NH29]AVP. CONCLUSIONS: Xylazine causes a diuretic and natriuretic alpha2A-adrenergic response in the rat that is independent of changes in glomerular filtration rate, the development of glucosuria, or AVP action on the distal nephron of the kidney. CLINICAL RELEVANCE: The adverse effects of xylazine on salt and water balance need to be considered and possibly compensated for by fluid replacement or post-surgical administration of alpha2-receptor antagonists.     

Alpha 2 agonists and antagonists.

The alpha 2 agonists can produce reliable dose-dependent sedation and analgesia in most species. Nevertheless, they can also produce significant physiological adverse side effects depending on dose, rate, route of administration, and the concurrent use of other CNS depressants. For this reason, it may be best to use a low dose of an alpha 2 agonist as a preanesthetic agent. The alpha 2 agonists are best suited for young, healthy, exercise-tolerant patients. The combining of low doses of alpha 2, opioid, and benzodiazepine agonists results in a synergistic CNS depressant response while minimizing the undesirable side effects of these three classes of drugs. Each group of drugs has specific antagonists available for their reversal, thus allowing veterinarians to reverse one or more of the agonists depending on the desired response. This may represent a significant advantage to the use of low-dose alpha 2 agonists in combination with opioids and benzodiazepines.     

Cardiopulmonary effects of etomidate in hypovolemic dogs.

Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered IV to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.