Analgesic, hemodynamic, and respiratory effects induced by caudal epidural administration of meperidine hydrochloride in mares.

OBJECTIVE: To determine the analgesic, hemodynamic, and respiratory effects induced by caudal epidural administration of meperidine hydrochloride in mares. ANIMALS: 7 healthy mares. PROCEDURE: Each mare received meperidine (5%; 0.8 mg/kg of body weight) or saline (0.9% NaCl) solution via caudal epidural injection on 2 occasions. At least 2 weeks elapsed between treatments. Degree of analgesia in response to noxious electrical, thermal, and skin and muscle prick stimuli was determined before and for 5 hours after treatment. In addition, cardiovascular and respiratory variables were measured and degree of sedation (head position) and ataxia (pelvic limb position) evaluated. RESULTS: Caudal epidural administration of meperidine induced bilateral analgesia extending from the. coccygeal to S1 dermatomes in standing mares; degree of sedation and ataxia was minimal. Mean (+/- SD) onset of analgesia was 12 +/- 4 minutes after meperidine administration, and duration of analgesia ranged from 240 minutes to the entire 300-minute testing period. Heart and respiratory rates, rectal temperature, arterial blood pressures, Hct, PaO2, PaCO2, pHa, total solids and bicarbonate concentrations, and base excess were not significantly different from baseline values after caudal epidural administration of either meperidine or saline solution. CONCLUSIONS AND CLINICAL RELEVANCE: Caudal epidural administration of meperidine induced prolonged perineal analgesia in healthy mares. Degree of sedation and ataxia was minimal, and adverse cardiorespiratory effects were not detected. Meperidine may be a useful agent for induction of caudal epidural analgesia in mares undergoing prolonged diagnostic, obstetric, or surgical procedures in the anal and perineal regions.

Effects of intravenously administered yohimbine on antinociceptive, cardiorespiratory, and postural changes induced by epidural administration of detomidine hydrochloride solution to healthy mares.

OBJECTIVE: To determine effects of i.v. administered yohimbine on perineal analgesia, cardiovascular and respiratory activity, and head and pelvic limb position in healthy mares following epidural administration of detomidine hydrochloride solution. ANIMALS: 8 healthy mares. PROCEDURE: Each mare received detomidine hydrochloride (0.06 mg/kg of body weight), administered in the caudal epidural space, followed 61 minutes later by yohimbine (0.05 mg/kg; test) or sterile saline (0.9% NaCl) solution (control), administered i.v., in a randomized, crossover study design with > or = 2 weeks between treatments. Analgesia was determined by lack of sensory perception to electrical stimulation of perineal dermatomes and needle-prick stimulation of coccygeal to 15th thoracic dermatomes. Arterial pH, PaCO2, PaO2, heart and respiratory rates, rectal temperature, arterial blood pressure, and cardiac output were determined, and mares were observed for sweating and urination. Mean scores obtained for test and control groups were compared. RESULTS: Intravenously administered yohimbine significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, changes in pelvic limb position, and sweating and diuresis; antagonized detomidine-induced decreases in heart rate and cardiac output; but did not affect detomidine-induced decrease in respiratory rate. CONCLUSIONS AND CLINICAL RELEVANCE: Most effects of epidurally administered detomidine, except bradypnea, were antagonized by yohimbine, suggesting that detomidine may influence respiratory rate by mechanisms other than stimulation of alpha2-adrenoceptors, or that yohimbine induces respiratory depressant effects. Yohimbine may be an effective alpha2-adrenoceptor antagonist for all but respiratory depression following epidural administration of detomidine to mares.

Influence of atipamezole on effects of midsacral subarachnoidally administered detomidine in mares.

OBJECTIVE: To examine effects of atipamezole on detomidine midsacral subarachnoidally-induced analgesia, cardiovascular and respiratory activity, head ptosis, and position of pelvic limbs in healthy mares. ANIMALS: 10 healthy mares. PROCEDURE: Using a randomized, blinded, crossover study design, mares received detomidine (0.03 mg/kg of body weight, diluted in 3 ml of CSF) midsacral subarachnoidally, followed by atipamezole (0.1 mg/kg [test]) or sterile saline (0.9% NaCl) solution (control), i.v. 61 minutes later and saline solution (3 ml, midsacral subarachnoidally) on a separate occasion, at least 2 weeks later. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle-prick stimulation extending from the coccygeal to T15 dermatomes. Arterial acid-base (pH, standard bicarbonate, and base excess values), gas tensions (PO2, PCO2), PCV, total solids concentration, heart and respiratory rates, rectal temperature, and arterial blood pressure were determined, and mares were observed for sweating and urination. Mean scores of perineal analgesia, head ptosis, position of pelvic limbs, and cardiovascular and respiratory data were compared for the 3-hour test period. RESULTS: Subarachnoidally administered detomidine induced perineal analgesia (mean +/- SD onset, 9.0 +/- 4.6 minutes; duration, 130 +/- 26 minutes), marked head ptosis, moderate changes in pelvic limb position, cardiovascular and respiratory depression, sweating in analgesic zones, and diuresis. Intravenously administered atipamezole significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, pelvic limb position, sweating and diuresis; partially antagonized detomidine-induced bradycardia; and did not effect detomidine-induced bradypnea. CONCLUSIONS AND CLINICAL RELEVANCE: Most effects of midsacral subarachnoidally administered detomidine, except bradycardia and bradypnea, were reversed by atipamezole (0.1 mg/kg, i.v.), indicating that most of the actions of detomidine were mediated via activation of alpha2-adrenergic receptors.

Local and regional anesthesia in ruminants and swine.

This article reviews the use of popular local and regional anesthetic and analgesic techniques for surgical anesthesia and postoperative analgesia in cattle, sheep, goats, and pigs. The emphasis is on proper technique, the use of a 2% lidocaine hydrochloride solution, and the epidural administration of alpha 2-adrenoceptor agonists and opioids for producing intra- and postoperative analgesia in ruminants and swine while preserving consciousness and minimizing side effects.

Comparison of antinociceptive, cardiovascular, and respiratory effects, head ptosis, and position of pelvic limbs in mares after caudal epidural administration of xylazine and detomidine hydrochloride solution.

OBJECTIVE: To examine and compare effects of 2 alpha 2-adrenergic receptor agonists, xylazine and detomidine, administered into the sacrococcygeal epidural space to induce safe and effective perineal analgesia on cardiovascular and respiratory functions, head ptosis, and position of pelvic limbs in healthy mares. ANIMALS: 8 healthy mares. PROCEDURE: Blood samples were drawn and systemic hemodynamics were determined, including cardiac output and pulmonary arterial, systemic arterial, and right atrial pressures. Two-way ANOVA with repeated measures was used to detect significant (P < 0.05) differences between mean scores of perineal analgesia, cardiorespiratory variables, head ptosis, and position of pelvic limbs in mares before and during a 3-hour testing period. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle prick stimulation in dermatomes extending from the coccyx to T15. Avoidance responses to electrical current and needle prick stimulation and behavioral changes (head ptosis, position of pelvic limbs) were quantitatively assessed by use of a scoring system. RESULTS: Epidurally administered xylazine induced perineal analgesia and variable bilateral caudal analgesia extending from the coccyx to S3 dermatome, with minimal cardiovascular and respiratory depression, head ptosis, changes in position of pelvic limbs, and no urination in standing mares. Epidurally administered detomidine induced perineal analgesia, variable bilateral analgesia with dermatomal spread ranging from coccyx to S3 and coccyx to T15, with cardiovascular depression, marked head ptosis, changes in position of pelvic limbs, and diuresis in standing mares. Onset of perineal analgesia after xylazine and detomidine administrations was 13.1 +/- 3.7 and 12.5 +/- 2.7 minutes (mean +/- SD), respectively. The period of perineal analgesia was significantly (P < 0.05) longer in mares after epidural xylazine administration than after epidural detomidine administration (165 to > 180 minutes vs 160 +/- 8 minutes). CONCLUSIONS: Caudal epidurally administered xylazine (0.25 mg/kg of body weight in 8 ml of 0.9% NaCl) offers the most desirable conditions in mares: long-term perineal analgesia (> 2.5 hours), with minimal cardiopulmonary depression, head ptosis, changes in pelvic limb position, and no urination in standing mares during a 3-hour test period.

Analgesic, hemodynamic, and respiratory effects of caudal epidurally administered xylazine hydrochloride solution in mares.

OBJECTIVE: To examine effects of 0.25 mg of xylazine/kg of body weight diluted to a total volume of 6 ml/450 kg with sterile 0.9% NaCl, administered into the epidural space of the sacrococcygeal joint on perineal analgesia, sedation, ataxia, and respiratory and cardiovascular function in standing mares. DESIGN: Randomized, blinded study, using xylazine (treatment) and 0.9% NaCl (controls). At least 2 weeks elapsed between the treatments. ANIMALS: Eight healthy mares. PROCEDURE: Blood samples were drawn. Systemic hemodynamics were determined, including cardiac output and pulmonary arterial, systemic arterial, and right atrial pressures. Two-way ANOVA with repeated measures was used to detect significant (P < 0.05) differences between mean scores of analgesia, sedation, ataxia, and cardiorespiratory variables before and during a 3-hour testing period. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle prick stimulation extending from coccyx to S3 dermatomes. Sedation was determined by head ptosis. RESULTS: Epidurally administered xylazine induced variable bilateral caudal analgesia extending from coccyx to S3, with minimal sedation, ataxia, and cardiovascular and respiratory depression in standing mares. Analgesia was attained at 15 +/- 6 minutes and lasted for 165 to over 180 minutes. Heart and respiratory rates, systolic, diastolic, and mean arterial blood pressure, PCV, hemoglobin concentration, arterial oxygen content, and oxygen transport were decreased after xylazine, but not 0.9% NaCl, treatment. Cardiac output, stroke volume, mean right atrial pressure, mean pulmonary artery pressure, systemic vascular resistance, pulmonary vascular resistance, arterial and mixed venous pH and gas tensions (PO2 and PCO2), oxygen consumption, blood temperature, and rectal temperature did not change significantly (P < 0.05) after epidural administration of xylazine or 0.9% NaCl. CONCLUSIONS: Caudal epidurally administered xylazine (0.25 mg/kg in 6 ml of 0.9% NaCl) can be given safely to induce prolonged (>2 hours) caudal analgesia with minimal sedation, ataxia, and circulatory and respiratory disturbances in conscious, standing mares.

[Sedation and anesthesia in dogs and cats with cardiovascular diseases. III. Ventilation, respiratory monitoring, treatment for postoperative pain]. / Sedation und Narkose bei Hund und Katze mit Herzkreislaufkrankheit. III. Teil: Ventilation, Uberwaching der Atmung, postoperative Schmerzbehandlung.

The purpose of this study was to review ventilation and postoperative analgesic technics in 137 dogs and 13 cats with congenital or acquired heart disease. The animals were referred to the Department of Veterinary Clinical Sciences at The Ohio State University, U.S.A, for the following surgical interventions: correction of patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch ring anomaly (3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart base tumor (2%), and palliative surgery for ventricular septal defect (VSD, 0.7%). Controlled ventilation was used in all animals during thoracotomy. Anesthesia was maintained over 2.3 +/- 1.3 hours by using either isoflurane, halothane, propofol, or diazepam-ketamine in 64%, 32%, 2%, and 0.7% of animals, respectively. Postoperative analgesia was necessary in 20% of animals and was provided by using different technics over several hours. The technics and respective percentages of animals in which they were used, were: intravenous buprenorphine (3.3%), intercostal nerve blocks (8.7%), epidural morphine (4%), and interpleural regional analgesia (4%).

[Sedation and anesthesia in dogs and cats with cardiovascular diseases. I. Anesthesia plan considering risk assessment, hemodynamic effects of drugs and monitoring]. / Sedation und Narkose bei Hund und Katze mit Herzkreislaufkrankheit. I. Teil: Narkoseplanung nach Risikobeurteilung, hämodynamische Wirkung der Pharmaka, Monitoring.

The purpose of this study was to review the effects of sedatives and anesthetics in 137 dogs and 13 cats with congenital or acquired heart disease which were referred for diagnostic, therapeutic, and surgical interventions: correction of patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch (ring anomaly, 3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart-base tumors (2%), palliative surgery for ventricular septal defect (VSD, 0.7%), and sick patients with deleterious cardiac arrhythmias (0.7%). The anesthetic plan considered the risks of anesthesia based upon preoperative patient assessment, classification scheme for functional phases of heart failure, and anesthetic drug effects of the cardiovascular system. The effects of sedatives and anesthetic drugs on determinants of cardiac output are described. The most commonly used drugs for premedication, induction, and maintenance of anesthesia were midazolam-oxymorphone (20%), thiopental or etomidate (30%), and isoflurane (64%). Prompt therapy was given to control arrhythmias and provide organ perfusion, pain relief, muscle relaxation and renal diuresis, using lidocaine, dopamine, fentanyl, atracurium, and furosemide in 17.3% 14.7%, 12%, 10%, and 8.7% of animals, respectively. Methods of routine and advanced patient monitoring are described.

[Sedation and anesthesia in dogs and cats with cardiovascular disease. II. Anesthesia planning with respect to pathophysiology, heart arrhythmia]. / Sedation und Narkose bei Hund und Katze mit herzkreislaufkrankheit. II. Teil: Narkoseplanung an Hand der Pathophysiologie, Herzarrhythmien.

The purpose of this study was to review the incidence of cardiac arrhythmias in 137 anesthetized dogs and 13 anesthetized cats with congenital or acquired heart disease that were referred for correction of following procedures: patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch (ring anomaly, 3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart base tumor (2%), and palliative surgery for ventricular septal defect (VSD, 0.7%). The anesthetic plan considered the risks of anesthesia based upon the pathophysiology of cardiac lesions and the anesthetic drug effects on the cardiovascular system. Recommendations are made for dogs with decreased cardiac contractility, cardiac disease with volume overload, cardiac disease with pressure overload, and pericardial tamponade. The percentages of animals and their associated cardiac arrhythmias after premedication and during and after anesthesia were: sinus bradycardia (15.3%), sinus tachycardia (3.3%), atrial flutter (0.7%), atrial fibrillation (0.7%), premature ventricular contraction (14%), and ventricular tachycardia (1.3%). Prompt therapy was given to a percentage of animals in order to control arrhythmia and support cardiovascular system, by using atropine or glycopyrrolate (14%), lidocaine (17.3%), and dopamine (14.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Caudal analgesia induced by epidural or subarachnoid administration of detomidine hydrochloride solution in mares.

Seven adult mares were used to determine the analgesic, CNS, and cardiopulmonary effects of detomidine hydrochloride solution after epidural or subarachnoid administration, using both regimens in random sequence. At least 1 week elapsed between experiments. A 17-gauge Huber point (Tuohy) directional needle was used to place a catheter with stylet into either the epidural space at the first coccygeal interspace or the subarachnoid space at the lumbosacral intervertebral junction. Catheters were advanced so that the tips lay at the caudal sacral (S5 to S4) epidural space or at the midsacral (S3 to S2) subarachnoid space. Position of the catheter was confirmed radiographically. A 1% solution of detomidine HCl was injected into the epidural catheter at a dosage of 60 micrograms/kg of body weight, and was expanded to a 10-ml volume with sterile water to induce selective caudal epidural analgesia (CEA). A dose of 30 micrograms of detomidine HCl/kg expanded to a 3-ml volume with spinal fluid was injected into the subarachnoid catheter to induce caudal subarachnoid analgesia (CSA). Analgesia was determined by lack of sensory perception to electrical stimulation (avoidance threshold > 40 V, 0.5-ms duration) at the perineal dermatomes and no response to superficial and deep muscular pinprick stimulation at the pelvic limb and lumbar and thoracic dermatomes. Maximal CEA and CSA extended from the coccyx to spinal cord segments T15 and T14 at 10 to 25 minutes after epidural and subarachnoid drug administrations in 2 mares. Analgesia at the perineal area lasted longer after epidural than after subarachnoid administration (142.8 +/- 28.8 minutes vs 127.1 +/- 27.7 minutes). All mares remained standing. Both CEA and CSA induced marked sedation, moderate ataxia, minimal cardiopulmonary depression, increased frequency of second-degree atrioventricular heart block, and renal diuresis. All treatments resulted in significantly (P < 0.05) decreased heart rate, respiratory rate, systemic arterial blood pressure, PCV, and plasma total solids concentration. To the contrary, arterial carbon dioxide tension, plasma bicarbonate, and standard base excess concentrations were significantly (P < 0.05) increased. Arterial oxygen tension, pH, and rectal temperature did not change significantly from baseline values. Results indicate that use of detomidine for CEA and CSA in mares probably induces local spinal and CNS effects, marked sedation, moderate ataxia, mild cardiopulmonary depression, and renal diuresis.

Pulsus alternans during halothane anesthesia in a dog.

An adult dog with pyloric obstruction was anesthetized with thiamylal and halothane for surgical revision. When an ECG was attached, the QRS-complex rate was noted to differ dramatically from the peripheral pulse rate. A dorsal pedal arterial catheter was introduced, and direct arterial pressure measurements revealed a blood pressure waveform that alternated in amplitude. Blood pressure and ECG traces were recorded, and the condition was diagnosed as pulsus alternans. The inhalation anesthetic was changed to isoflurane, and the condition was resolved.

The pharmacology of local anesthetics.

Understanding of the pharmacology of local anesthesia is important for selection of a local anesthetic for use in equine standing surgery. In general, the action potential is inhibited by local anesthetics by preventing the influx of sodium ions across the axonal membrane. The physicochemical properties of each local anesthetic determine the onset of action, potency, and duration of action. Procaine, chlorprocaine, lidocaine, and mepivacaine are the local anesthetics still used clinically in horses; lidocaine is the most widely used. The future of equine local anesthesia may see the introduction of longer acting, more potent drugs currently used clinically in humans and dogs as well as drugs not classified as local anesthetics--alpha-2 agonists and opioids--for use in epidural anesthesia.

Caudal epidural analgesia induced by xylazine administration in cows.

Xylazine (0.05 mg/kg of body weight diluted to a 5-ml volume, using 0.9% NaCl) or 5 ml of 0.9% NaCl was administered epidurally into the first caudal intervertebral space (Co1-Co2) in 8 cows (mean +/- SD body weight, 583 +/- 150 kg). Cows were observed for responses to deep needle pricking of the caudal dermatomes (S3 to Co), sedation, and ataxia. Heart rate, respiratory rate, body temperature, rate of ruminal contractions, coccygeal arterial blood pressure, pHa, blood gas tension (PaO2, PaCO2), base excess, total solids concentration, and PCV were determined before and after xylazine administration. Epidurally administered xylazine induced sedation and selective (S3 to Co) analgesia for at least 2 hours. Mild ataxia of hind limbs was observed in 6 cows, but all cows remained standing. Heart rate, respiratory rate, rate of ruminal contractions, arterial blood pressure, PaO2, PCV, and total solids concentration were significantly (P less than 0.05) decreased, and PaCO2, base excess, and bicarbonate concentration were significantly (P less than 0.05) increased after xylazine administration. Epidurally administered 0.9% NaCl did not alter sensory perception to needle pricking and did not affect any of the physiologic variables determined. Although epidural administration of xylazine induced analgesia and sedation in healthy cows, it should be avoided for epidural analgesia in cattle with heart disease, lung disease, and/or gastrointestinal disease because of its potent cardiopulmonary and ruminal depressant effects.

Influence of tolazoline on caudal epidural administration of xylazine in cattle.

Eight adult female cattle (6 Holstein, 1 Jersey, 1 Brown Swiss) were used to determine the antagonistic effects of tolazoline, and alpha 2-adrenoceptor antagonist, on xylazine-induced (via caudal epidural administration) depression of CNS, respiratory, and cardiovascular activity and rumen motility. A 2% solution of xylazine HCl was injected into the epidural space at the first coccygeal interspace, using a dosage of 0.05 mg/kg of body weight, diluted to a 5-ml volume with sterile water, and administered at a rate of approximately 1 ml/30 s. Eight minutes after xylazine injection, either tolazoline (0.3 mg/kg) or saline solution (4 ml) was administered IV. All 8 cattle were treated, using both regimens in a random sequence; at least 1 week elapsed between treatments. Epidurally administered xylazine induced caudal analgesia (S3 to coccyx), as evaluated by no response to superficial and deep muscular pinprick, and induced sedation, cardiopulmonary depression, and inhibition of rumen motility, but all cattle remained standing. Tolazoline effectively reversed xylazine-induced rumen hypomotility, and partially antagonized xylazine-induced cardiopulmonary depression without affecting sedation and desirable local (S3 to coccyx) analgesic effects.

Comparative study of continuous lumbar segmental epidural and subarachnoid analgesia in Holstein cows.

Eight adult Holstein cows were used to compare the effects of lumbar segmental epidural analgesia (SEA) and lumbar segmental subarachnoid analgesia (SSA). A modified 17-gauge Huber point (Tuohy) needle was used to place a catheter with stylet into either the epidural space at the thoracolumbar (T13-L1) intervertebral space or the subarachnoid space at the lumbosacral intervertebral junction. The catheters were advanced so that their tips lay at the anterior lumbar (L1-L2) epidural space or at the thoracolumbar (T13-L1) subarachnoid space. The position of the catheter was confirmed radiographically. A 5% solution of procaine HCl was used at mean doses of 300 mg (6 ml) to induce SEA and 84.4 +/- 12.9 mg (1.7 +/- 0.3 ml) to induce SSA. Onset of analgesia to superficial and deep muscular pinprick stimulation was significantly (P less than 0.05) faster in cows with SSA than in those with SEA (10.4 +/- 2.3 minutes vs 15.9 +/- 3.8 minutes). Maximal thoracolumbar analgesia extended from spinal cord segments T12 to L4 on one or both sides of the vertebral column during SEA and from T10 to L3 on one or both sides during SSA. Duration of analgesia lasted significantly (P less than 0.05) longer in cows with SEA than in those with SSA (76.2 +/- 16.2 minutes vs 53.7 +/- 14.3 minutes). The advantages and disadvantages of the SEA catheter technique are discussed.

Plasma lidocaine concentrations in conscious horses after cervicothoracic (stellate) ganglion block with 1% lidocaine HCl solution.

Arterial and/or central venous plasma concentrations of lidocaine were determined in 12 nonmedicated adult horses (422 +/- 59 kg of body weight, mean +/- SD) after injecting a 1% lidocaine HCl solution into the cervicothoracic ganglion (CTG). A mean dosage of 2.9 +/- 0.5 mg of lidocaine/kg of body weight was used to induce unilateral CTG blockade in 8 horses and 4.8 +/- 0.8 mg was used to induce bilateral CTG blockade in 4 horses. Blood samples were collected before and at 5, 15, 30, 45, 60, 75, 90, 105, and 120 minutes after injection. The plasma lidocaine concentrations were determined by use of gas chromatography (sensitivity less than 0.01 microgram/ml). Cervicothoracic sympathetic blockade was characterized by Horner's syndrome and by profuse sweating over the face, neck, and thoracic limbs. Mean maximal venous concentrations of lidocaine were 0.86 +/- 0.33 microgram/ml at 26.3 +/- 6.9 minutes after unilateral CTG blockade, and 1.14 +/- 0.25 micrograms/ml at 31.2 +/- 18.9 minutes after bilateral CTG blockade. The mean venous and arterial concentrations of lidocaine were not significantly different at 45 and 120 minutes after injection. Venous concentrations of lidocaine were consistently higher than were concentrations in simultaneously collected arterial blood samples in 2 horses in which the right CTG and brachial plexus were temporarily anesthetized after repeated administration of 100 ml of lidocaine into the right CTG.(ABSTRACT TRUNCATED AT 250 WORDS)