Comparative effects of mu and kappa opiate agonists on the cecocolic motility in the pony.

The electrical and mechanical activity of the large intestine and its response to administration of opiate mu and kappa agonists were assessed from electrodes and inductograph coils chronically implanted on the cecocolic segment in six ponies given a diet of hay and concentrates. Before the drugs were given, migrating complexes propagating from the cecum into the colon occurred at the rate of 1.5 to 16/hour. During this propulsive activity, the cecocolic sphincter opened and closed allowing the outflow of cecal contents and preventing the backflow of colic contents. Each pony was used as its own control and was given fentanyl (0.01 and 0.05 mg/kg of body weight, IV) and U50488H (0.1 and 0.5 mg/kg, IV) at weekly intervals. The mu agonist fentanyl elicited a marked phase of inhibition of the propulsive activity and a closure of the cecocolic sphincter that lasted one to two hours depending on the dose. The kappa agonist U50488H induced an inhibition of the short spiking activity, i.e. of the resting muscle tone. It did not disturb the occurrence of migrating complexes nor that of the openings of the cecocolic sphincter. These kappa compounds may be drugs of choice to alleviate visceral pain in colic stases without inducing delay of transit unlike mu compounds.     

Prokinetic effects of cisapride, naloxone and parasympathetic stimulation at the equine ileo-caeco-colonic junction

The electromyogram of the terminal ileum, the caecum and the proximal right ventral colon was recorded in fasted conscious ponies receiving intravenously equiactive doses of pilocarpine (0.05 mg/kg) and carbachol (0.01 mg/kg) as acetylcholine analogues; cisapride (0.1 mg/kg) and metoclopramide (2 mg/kg) facilitating acetylcholine release from myenteric neurones and naloxone (0.05 mg/kg) as an antagonist of the endogenous inhibitory opioid system. Both cisapride and naloxone induced typical migrating spike bursts in the colon associated with contractions of caecal body and caecal base. Both pilocarpine and carbachol stimulated the terminal ileum but had opposite effects on the activity of the caeco-colonic segment which was decreased by pilocarpine and increased by carbachol. High doses of metoclopramide had weak and unspecific stimulatory motor effects. It is concluded that a true prokinetic effect at the equine ileo-caeco-colonic junction requires a motor profile which includes coordination between contractions sequentially involving the body and the base of the caecum and migrating spike bursts on the proximal colon. Such changes in the motor profile were produced by cisapride and naloxone and to a lesser extent by carbachol.     

Cardiorespiratory and endocrine effects of endogenous opioid antagonism by naloxone in ponies anaesthetised with halothane

Halothane depresses cardiorespiratory function and activates the pituitary-adrenal axis, increasing beta endorphin. In horses, beta endorphin may enhance the anaesthetic-associated cardiorespiratory depression and mortality risk. The authors studied endogenous opioid effects on cardiorespiratory function and pituitary-adrenal activity in halothane-anaesthetised ponies by investigating opioid antagonism by naloxone. Six ponies were anaesthetised three times (crossover design). Anaesthesia was induced with thiopentone and maintained with 1.2 per cent halothane for 2 hours. Immediately after induction, naloxone was administered either intravenously (0.5 mg kg(-1)bolus then 0.25 mg kg(-1)hour(-1)for 2 hours) or intrathecally (0.5 mg) or was replaced by saline as control. Pulse and respiratory rates, arterial blood gases, cardiac output and plasma cortisol and adrenocorticotrophic hormone (ACTH) concentrations were measured. All groups developed cardiorespiratory depression (40 per cent decrease in cardiac output) and plasma cortisol increased. Plasma ACTH concentration was higher in ponies treated with intrathecal naloxone. Endogenous opioids may inhibit ACTH secretion, attenuating the stress response to halothane anaesthesia in equidae.     

Antagonistic effects of alpha-adrenoceptor blocking agents on reticuloruminal hypomotility induced by xylazine in cattle.

The intravenous injection of a standard dose (0.05 mg/kg) of xylazine inhibited reticuloruminal motility in cattle. Pretreatment with adrenoceptor antagonists showing alpha 2-blocking activity, tolazoline (0.5 mg/kg) and yohimbine (0.2 mg/kg), antagonized the xylazine-induced reticuloruminal amotility. Tolazoline was more effective than yohimbine, since an antagonistic effect was not seen at 0.5 mg/kg yohimbine, and yohimbine at 0.2 mg/kg was less effective than tolazoline at 0.5 mg/kg. An adrenoceptor antagonist showing alpha 1-blocking activity, prazosin, did not prevent the inhibition of reticuloruminal motility by xylazine. The xylazine-induced reticuloruminal amotility was also not prevented by either a dopamine receptor antagonist, domperidone, or an opiate receptor antagonist, naloxone. These results suggest that xylazine inhibits bovine reticuloruminal motility through its activation of alpha 2-adrenoceptors, and show that tolazoline can be used as a specific antagonist of xylazine in studies of the alpha-adrenergic influence on reticuloruminal motility in cattle.     

Reversal of Oxymorphone Sedation by Naloxone, Nalmefene, and Butorphanol

The effects of naloxone (0.4 mg and 1.2 mg intravenously [IV]), nalmefene (0.03 mg/kg IV) and butorphanol (0.2 mg/kg IV and 0.4 mg/kg IV) on oxymorphone-induced sedation were studied in six dogs over a 4-hour observation period. The same dogs were observed for 4 hours untreated (unsedated control) and with oxymorphone sedation followed by saline solution (sedated control). The reversal drug or saline placebo was administered IV 20 minutes after oxymorphone (4.5 mg IV). Blinded observers evaluated the dogs for positional and attitudinal responses, heart rate, and respiratory rate. Sedated dogs treated with nalmefene most closely resembled unsedated dogs in all observed variables. Naloxone was most effective when administered at the higher dose. Mild renarcotization occurred in two dogs at hour 2, even after the higher naloxone dose. Residual sedation was observed in all dogs treated with 0.4 mg naloxone. Butorphanol resulted in partial reversal of sedation at both dosage levels. However, the degree of sedation was significantly less than that observed in the saline-treated controls, and it appeared that 0.4 mg/kg butorphanol may be clinically useful for opiate reversal in some situations.     

Electromyoenterography During Normal Gastro-Intestinal Activity, Painful or Non-painful Colic and Morphine Analgesia, in the Horse

The electrical potentials were recorded from the antrum, the duodenum, the ileum and the first part of the colon of ponies under (a) normal resting conditions, (b) during nonpainful colic and (c) after intravenous morphine administration.

The normal pony, at rest, had five contractions of the antrum per minute. On the small intestine, the basal electrical activity decreased from the duodenum (14-15/min) to the ileum (10-11/min). The small bowel also had three types of motility: peristaltic waves, rhythmic segmentations and random contractions. On the colon, bursts of potentials indicating intense motor activity occurred at the rate of 20 to 30 per hour. Morphine given intravenously (IV) greatly increased the frequency of the electrical potentials of the antrum and the longitudinal bands of the colon.

During non-painful colic, hyperactivity of the cranial small intestine was continuous. Spasms of the jejunum occurred every minute and could not be relieved by morphine (IV).

When colic was painful, jejunal spasms announced the crisis of intense abdominal pain. After morphine (IV) the spasms and pain disappeared; the jejunum remained hyperactive, the motility of the colon was increased while the antrum became quiet.

     

Effects of naloxone in treating hemorrhagic shock in dogs with maintained baroreceptor responsiveness

The efficacy of treating hemorrhagic shock with naloxone in conjunction with fluids, compared with fluid therapy alone, was studied. Previously instrumented dogs were anesthetized with 0.04 mg of fentanyl/kg + 2.2 mg of droperidol/kg and pentobarbital sodium (to effect). Blood was withdrawn from each animal to achieve and maintain a mean arterial blood pressure of 40 to 50 mm of Hg for the first 2 hours of the experiment (t = 0 to 120 minutes). At t = 120 minutes, IV fluid administration was begun (all dogs) and continued for 1 hour (lactated Ringer's solution at a dosage of 70 ml/kg/hr). Hypothermia was corrected. Control dogs were given no other treatment. Dogs in the naloxone plus fluids group were given an IV bolus of naloxone (1 mg/kg) at t = 120 minutes and 1 mg of naloxone/kg/hr in the fluids from t = 120 to t = 180 minutes. Treatment (either naloxone plus fluids or fluids alone) was stopped at t = 180 minutes, and measuring of response was continued for an additional hour (posttherapeutic period). Significant differences were not seen in mean arterial pressures, left ventricular peak systolic pressures, dP/dt max, time constant T (a measure of left ventricular elasticity), and mean pulmonary arterial pressures between the dogs given naloxone and fluid therapy and those given fluid therapy alone. All dogs in both groups survived the procedure.     

Effects of naloxone on endotoxin-induced changes in ponies

The value of naloxone (1 mg/kg of body weight/hr for 4 hrs), a beta-endorphin antagonist, was assessed in the management of endotoxin-induced shock in ponies. Three groups of 5 ponies each were used: controls, ponies given Escherichia coli endotoxin put untreated, and ponies given endotoxin and then treated with naloxone. Endotoxin-induced changes in hemodynamics, blood chemical values, regional blood flow, plasma enzymes, and energy supplies were measured at selected times during the first 6 hours after endotoxin was given. There was no evidence that beta-endorphins released during shock were responsible for the hemodynamic changes, blood flow changes, plasma enzyme changes, or energy deficits, because naloxone, at this dosage level, did not prevent these endotoxin-induced changes.     

Effects of heparin treatment on colonic torsion-associated hemodynamic and plasma eicosanoid changes in anesthetized ponies

Large colon torsion frequently is a fatal condition in horses. The purpose of the study reported here was to determine systemic arterial pressure, plasma eicosanoid concentrations, colonic blood flow, vascular resistance, tissue pH, and morphologic features associated with large colon torsion and detorsion, and to evaluate the effects of sodium heparin (80 IU/kg of body weight, IV) treatment on these values. Values were determined in 20 anesthetized ponies that were randomly assigned into 4 equal groups: control; control/heparin; torsion; torsion/heparin. Torsions were created by a 720 degrees rotation of the cecum and colon around their long axes at the sternal and diaphragmatic flexures. After 1 hour of torsion, the torsion was corrected and the colon was allowed to reperfuse for 1 hour. Heparin was administered 30 minutes into the experiment. Parametric data were analyzed (P less than or equal to 0.05), using split-plot analysis of variance, with differences between means evaluated with a modified Bonferroni t test; histopathologic data were analyzed (P less than or equal to 0.05) with a Kruskal-Wallis one-way analysis of variance by ranks. Heparin prevented colonic detorsion-induced hypotension and increases in vascular resistance and thromboxane concentration, and it significantly increased colonic blood flow for 40 minutes during reperfusion. Heparin did not alter prostacyclin concentration or the histologic appearance of the large colon.     

Analgesia and behavioral responses of dogs given oxymorphone-acepromazine and meperidine-acepromazine after methoxyflurane and halothane anesthesia.

This study was designed to test analgesia, duration, and cardiovascular changes induced by meperidine (MEP) and oxymorphone (OXY) following methoxyflurane (MOF) and halothane (HAL) anesthesia. Eight healthy dogs were given atropine and acepromazine, and anesthesia was induced with thiamylal and maintained with 1.5 minimal alveolar concentration of MOF or HAL for 1 hour during controlled ventilation. Eight treatments were given with each anesthetic: 3 with MEP (0.5, 1.0, and 2.0 mg/kg, IV), 3 with oxymorphone (OXY; 0.05, 0.1, and 0.2 mg/kg, IV), and 2 placebos with sterile water. Test drugs were given at the end of anesthesia when early signs of recovery were evident. Minimal threshold stimulus/response nociception was assessed by use of an inflatable soft plastic colonic balloon. Blood pressures and pulse rate were measured with a noninvasive monitor. Meperidine and OXY were found to be effective analgesics and could be reversed with naloxone. Intravenous administration of 2.0 mg of MEP/kg provided analgesia for 36 +/- 6 minutes and 39 +/- 15 minutes after MOF and HAL, respectively. In contrast, OXY was effective at all 3 doses with effects of IV administration of 0.2 mg of OXY/kg lasting 154 +/- 13 minutes and 152 +/- 12 minutes, after MOF and HAL, respectively. Analgesia could not be demonstrated after anesthesia for acepromazine, MOF, or HAL. Blood pressure was not changed by either anesthetic nor was it influenced by MEP or OXY. Pulse rate was significantly depressed by the higher doses of OXY following HAL, but was not changed by MEP following either anesthetic.(ABSTRACT TRUNCATED AT 250 WORDS)     

Infusion of a combination of propofol and medetomidine for long-term anesthesia in ponies

OBJECTIVE: To determine the minimal infusion rate of propofol in combination with medetomidine for long-term anesthesia in ponies and the effects of atipamezole on recovery. ANIMALS: 12 ponies. PROCEDURE: Ponies were sedated with medetomidine (7 microg/kg of body weight, IV). Ten minutes later, anesthesia was induced with propofol (2 mg/kg, IV). Anesthesia was maintained for 4 hours, using an infusion of medetomidine (3.5 microg/kg per hour, IV) and propofol at a rate sufficient to prevent ponies from moving after electrical stimulation. Arterial blood pressures and blood gas analysis, heart rates, and respiratory rates were monitored. For recovery, 6 ponies were given atipamezole (60 microg/kg, IV). Induction and recovery were scored. RESULTS: Minimal propofol infusion rates ranged from 0.06 to 0.1 mg/kg per min. Mean arterial blood pressure was stable (range, 74 to 86 mm Hg), and heart rate (34 to 51 beats/min) had minimal variations. Variable breathing patterns were observed. Mean PaO2 (range, 116 to 146 mm Hg) and mean PaCO2 (range, 48 to 51 mm Hg) did not change significantly with time, but hypoxemia was evident in some ponies (minimal PaO2, 47 mm Hg). Recovery was fast and uneventful with and without atipamezole (completed in 20.2 and 20.9 minutes, respectively). CONCLUSIONS AND CLINICAL RELEVANCE: Infusion of a combination of medetomidine and propofol was suitable for prolonged anesthesia in ponies. Recovery was rapid and uneventful. A combination of propofol and medetomidine may prove suitable for long-term anesthesia in horses. Monitoring of blood gases is essential because of potential hypoxemia.     

Actions of the novel gastrointestinal pro kinetic agent cisapride on equine bowel motility

The effect of cisapride was evaluated on the normal fasting bowel motility of four ponies with chronically implanted electromechanical transducers. Cisapride was infused over 60-min periods at 0.05 mg/kg (n = 4), 0.1 mg/kg (n = 5) and 0.25 mg/kg (n = 5). It produced marked and prolonged increases in electrical and mechanical activity at all sites examined. In the stomach there was increased total contraction activity with increased contraction amplitude and a slight reduction in rate. In the small intestine there was an increase in irregular (phase II) activity with an increase in number and amplitude of contractions and a decrease in the number of regular (phase III) activity fronts. There was a decrease in the number of phase III fronts that spread distally from the jejunum to the ileum. The phase II activity was coordinated temporally with prolonged activity in the stomach. Cisapride increased electrical and contractile activity in the left dorsal colon with increased contraction amplitude and an increase in electrical activity in the small colon. In the stomach and small intestine cisapride produced dose-dependent increases in activity but in the left dorsal and small colon the intermediate dose (0.1 mg/kg) produced the largest and most consistent responses. Side-effects observed were increased bowel sounds and frequency of defaecation, a slight increase in heart rate and transient signs of discomfort at the highest (0.25 mg/kg) dose rate.     

Effects of butorphanol, flunixin, levorphanol, morphine, and xylazine in ponies

The analgesic and behavioral effects of butorphanol (0.22 mg/kg), flunixin (2.2 mg/kg), levorphanol (0.033 mg/kg), morphine (0.66 mg/kg), and xylazine (2.2 mg/kg), given IM were observed in 8 ponies. These ponies were instrumented to measure response objectively to painful superficial and visceral stimuli. Effects on the cardiopulmonary system and rectal temperature also were evaluated in 6 of these ponies. Observations were conducted before drug injection (base-line values) and after injection at 30, 60, 120, 180, and 240 minutes. Xylazine provided the highest pain threshold for the first 60 minutes and a sedative effect for 105 minutes. The effects for superficial pain and visceral pain persisted 3 hours and 4 hours, respectively. Morphine produced good analgesia for superficial pain (30 minutes), whereas butorphanol provided good effect for visceral pain (4 hours). A slight degree of analgesia for visceral pain was obtained after morphine (1 hour) and levorphanol (4 hours); flunixin did not induce analgesia. Butorphanol, levorphanol, and morphine stimulated motor activity. Behavioral effects did not occur after flunixin was given. Xylazine decreased systolic, diastolic, and mean blood pressures. Marked increases in these pressures, heart rate, and respiratory rate were observed after morphine was given. Changes of central venous pressure, rectal temperature, and blood gas values remained within base-line limits after both drugs were given. Butorphanol increased heart rates for 1 hour; flunixin and levorphanol did not alter any of the above values.     

Lincomycin-induced severe colitis in ponies: association with Clostridium cadaveris.

Four groups of two ponies, free of fecal Salmonella and Clostridium cadaveris, were treated as follows: Group A, control group; B, single nasogastrically administered dose of lincomycin (25 mg/kg) followed 48 h later by 3 L of C. cadaveris (10(9) organisms/mL); C, the same dose of lincomycin as group B; D, the same dose of C. cadaveris as group B on each of three occasions at 12 h intervals. Groups A and D remained healthy, but groups B and C developed severe colitis 48-56 h (B) or 72 h (C) after administration of lincomycin. Three ponies were euthanized and one in group B died. Clostridium cadaveris was isolated at about 10(6)/mL of colonic contents from these ponies, but one pony in group B also yielded Salmonella typhimurium from the colon. Subsequent challenge of group A ponies (3 L of C. cadaveris 10(9)/mL, three times at 12 h intervals) did not produce colitis. Nasogastric administration of lincomycin (25 mg/kg) to group A and D ponies, 20 days after administration of C. cadaveris, resulted in severe colitis in all ponies within 48-72 h. Salmonella agona was isolated from the colonic contents of one pony and C. cadaveris (10(6)/mL) from all four ponies. Clostridium cadaveris was not isolated from the colonic content of 45 healthy horses examined immediately after death. These studies confirm the potential for lincomycin to induce severe enterocolitis in ponies and implicate C. cadaveris further as a cause of "idiopathic colitis" in ponies.     

Evaluations of buparvaquone as a treatment for equine babesiosis (Babesia equi)

We evaluated the efficacy of buparvaquone in eliminating Babesia equi of European origin in carrier horses and in experimentally infected splenectomized ponies. When administered at the rate of 2.5 mg/kg of body weight, IM, 4 times at 96-hour intervals, buparvaquone was effective in eliminating B equi carrier infection in 1 horse. Such results could not be repeated at the same dosage or at 3.5 or 5 mg/kg, IM. Buparvaquone given at the rate of 4 to 6 mg/kg IV and/or IM was therapeutically effective in 4 of 5 acute B equi infections in splenectomized ponies. The treated ponies became carriers.     

Effect of Buscopan compositum on the motility of the duodenum, cecum and left ventral colon in healthy conscious horses

Seven adult, healthy, conscious warmblood horses were used in a crossover study. They were fed twice a day on 1 kg hay/100 kg BW and 0.5 kg concentrates with unlimited access to water. One hour after feeding, the contractive motility of the descending duodenum, cecal body and left ventral colon were measured using a 5 MHz transcutaneus ultrasonographic transducer. Each horse was treated with 0.9% NaCl (5 ml/100 kg BW; i.v.), and with Buscopan compositum (BC) at its therapeutic dosage (25 mg/kg BW; metamizol-sodium, 0.2 mg/kg BW; N-butylscopolammonium bromide, i.v.) in a control and an experimental trial respectively. The contractive motility was counted in a 3-min period immediately and 5, 15, 30, 45, 60, 120, 180 and 240 min after application in both trials. There was an immediate, rapid and significant (p < 0.05) reduction of duodenal, cecal and left ventral colon contractions after BC administration. Cecal and left ventral colon contractions rapidly restored their normal contractions after 30 min, while duodenal contractions returned to the normal rate after 120 min of BC administration. It was concluded that Buscopan compositum at its therapeutic dosage has an immediate, potent, short-lived reductive effect on cecum and left ventral colon contractions but a minor, longer effect on the duodenal contractions. Therefore, it is recommended for treatment of spasmodic colic as well as spasms resulting from acute simple impaction in horses but it is not recommended for repeated short-interval administration.     

Evidence for the involvement of alpha 2-adrenoceptors in the emetic action of xylazine in cats

Intramuscular injection of xylazine induced dose-dependent vomiting in cats (ED50 = 0.277 mg/kg); administration of standard dose of xylazine (2 mg/kg, 2 times the 100% emetic dose) induced vomiting in 100% of the cats studied. The xylazine-induced vomiting was antagonized by adrenoceptor antagonists possessing alpha 2-blocking activity, which were yohimbine, tolazoline, and phentolamine. Of these antagonists, yohimbine was the most effective; the maximal antagonistic effect was seen at 1 mg of yohimbine/kg, a dose at which the other drugs had little or no effect. At the doses studied, prazosin and phenoxybenzamine, adrenoceptor antagonists with alpha 1-blocking activity, did not prevent vomiting induced by xylazine. Beta-Adrenoceptor (propranolol), dopamine receptor (domperidone and chlorpromazine), a cholinoceptor (atropine), an opiate receptor (naloxone), and a histamine-receptor (diphenhydramine) antagonists, at the doses studied, did not prevent xylazine-induced vomiting. Pretreatment with 6-hydroxydopamine failed to prevent xylazine-induced vomiting. These results indicated that xylazine-induced vomiting in cats is mediated by alpha 2-adrenoceptors and suggested that the alpha 2-adrenoceptors mediating the vomiting attributable to xylazine may not be presynaptic alpha 2-receptors located on noradrenergic nerve terminals.     

Effects of xylazine and/or butorphanol or neostigmine on myoelectric activity of the cecum and right ventral colon in female ponies

Effects of xylazine HCl (0.5 mg/kg of body weight, IV) and/or butorphanol tartrate (0.04 mg/kg, IV) or neostigmine methylsulfate (0.022 mg/kg, IV) on myoelectric activity of the cecum and right ventral colon were studied in 4 conscious female ponies. Eight bipolar Ag/AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and right ventral colon (2 electrodes). Recordings began 30 minutes before and continued for 90 minutes after drug administration. Each drug or drug combination was studied on 2 occasions in each pony. Two major patterns of coordinated spike bursts were identified. A series of coordinated spike bursts began at the cecal base and was conducted to the cecal apex (pattern I). A series of coordinated spike bursts began at the cecal apex, traversed the cecum, cecocolic orifice, and right ventral colon and was termed a progressive pattern (pattern II). Xylazine administration caused a significant decrease in patterns I and II for 20 minutes (P less than 0.05). Butorphanol tartrate administration caused a significant decrease in the progressive pattern for 10 minutes (P less than 0.05) without affecting the orally directed pattern. Administration of the combination of xylazine/butorphanol significantly decreased the frequency of pattern I for 40 minutes (P less than 0.05) and pattern II for 30 minutes (P less than 0.05). Neostigmine administration caused a significant increase in the frequency of pattern II for 30 minutes (P less than 0.05) without affecting pattern I (P greater than 0.05). Changes in conduction velocity of pattern I or II or the duration of spiking activity were not significantly different because of any treatment.     

Intrathecal morphine overdose in a dog

CASE DESCRIPTION: A healthy 6-year-old 28.5-kg (62.7-lb) spayed female Boxer undergoing surgical repair of a ruptured cranial cruciate ligament was inadvertently administered an overdose of morphine (1.3 mg/kg [0.59 mg/lb]) via subarachnoid injection. CLINICAL FINDINGS: 50 minutes after administration of the overdose, mild multifocal myoclonic contractions became apparent at the level of the tail; the contractions migrated cranially and progressively increased in intensity and frequency during completion of the surgery. TREATMENT AND OUTCOME: The myoclonic contractions were refractory to treatment with midazolam, naloxone, phenobarbital, and pentobarbital; only atracurium (0.1 mg/kg [0.045 mg/lb], IV) was effective in controlling the movements. The dog developed hypertension, dysphoria, hyperthermia, and hypercapnia. The dog remained anesthetized and ventilated mechanically; treatments included continuous rate IV infusions of propofol (1 mg/kg/h [0.45 mg/lb/h]), diazepam (0.25 mg/kg/h [0.11 mg/lb/h]), atracurium (0.1 to 0.3 mg/kg/h [0.045 to 0.14 mg/lb/h]), and naloxone (0.02 mg/kg/h [0.009 mg/lb/h]). Twenty-two hours after the overdose, the myoclonus was no longer present, and the dog was able to ventilate without mechanical assistance. The dog remained sedated until 60 hours after the overdose, at which time its mentation improved, including recognition of caregivers and response to voice commands. No neurologic abnormalities were detectable at discharge (approx 68 hours after the overdose) or at a recheck evaluation 1 week later. CLINICAL RELEVANCE: Although intrathecal administration of an overdose of morphine can be associated with major and potentially fatal complications, it is possible that affected dogs can completely recover with immediate treatment and extensive supportive care.     

Antagonism of xylazine-pentobarbital anesthesia by yohimbine in ponies

Effects of yohimbine on xylazine-pentobarbital anesthesia were evaluated in ponies. Five minutes after the IV injection of xylazine (1.1 mg/kg of body weight), pentobarbital sodium (12.7 mg/kg, IV) and additional xylazine (2.2 mg/kg, IM) were given and produced anesthesia in 12 ponies for 64.0 +/- 16.4 minutes (mean +/- SD) as well as immobilization for 89.8 +/- 34.2 minutes. Eleven ponies were given yohimbine (0.1 mg/kg, IV) 50 minutes after pentobarbital dosing. In these 11 ponies, durations of anesthesia and immobilization were shorter, 52.0 +/- 1.4 and 65.5 +/- 14.8 minutes, respectively. The xylazine-pentobarbital combination caused bradycardia that was reversed by yohimbine injection. Xylazine-pentobarbital produced a small, but steady, decrease of mean arterial blood pressure, which was compounded by yohimbine administration and was evident for approximately 2 minutes. Within a minute after yohimbine injection, the ponies' respiratory rate decreased and the length of inspiration and expiration and thoracic breathing increased. This lasted approximately 2 to 3 minutes and was followed by an increase in respiratory rate. The anesthesia also produced a decrease in PaO2 that gradually returned to base line in 12 control ponies, but was more pronounced in 11 ponies given yohimbine. The PaCO2, although remaining moderately high in control ponies, returned to base line after yohimbine injection. An increased pHa was seen 60 minutes after induction of anesthesia and was especially noticeable after yohimbine administration. Decreases in the number of WBC, hemoglobin content, PCV, plasma protein and serum aspartate transaminase resulting from xylazine-pentobarbital were reversed by yohimbine. Conversely, serum glucose values and creatine kinase activities were increased by xylazine-pentobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)