Evaluation of intraocular pressure in association with cardiovascular parameters in normocapnic dogs anesthetized with sevoflurane and desflurane

The objective of this study was to determine intraocular pressure (IOP) and cardiac changes in normocapnic dogs maintained under controlled ventilation and anesthetized using sevoflurane or desflurane. Sixteen healthy adult mixed-breed dogs, seven males and nine females, weighing 10-15 kg were used. The dogs were randomly assigned to one of two groups composed of eight animals anesthetized with sevoflurane (SEVO) or desflurane (DESF). In both groups, anesthesia was induced with propofol (10 mg/kg), and neuromuscular blockade was achieved with rocuronium (0.6 mg/kg/h i.v.). No premedication was given. Ventilation was adjusted to maintain end-tidal carbon dioxide partial pressure at 35 mmHg. Anesthesia was maintained with 1.5 minimum alveolar concentration (MAC) of sevoflurane or desflurane. In both groups IOP was measured by applanation tonometry (Tono-Pen) before induction of anesthesia. IOP, mean arterial pressure (MAP), heart rate (HR), cardiac index (CI) and central venous pressure (CVP) were also measured 45 min after the beginning of inhalant anesthesia and then every 20 min for 60 min. A one-way repeated measures anova was used to compare data within the same group and Student's t-test was used to assess differences between groups. P < 0.05 was considered statistically significant. Measurements showed normal IOP values in both groups, even though IOP increased significantly from baseline during the use of desflurane. IOP did not differ between groups. CI in the desflurane group was significantly greater than in the sevoflurane group. Sevoflurane and desflurane have no clinically significant effects on IOP, MAP, HR, CI or VCP in the dog.     

Effects of atropine, isoprenaline, neostigmine and practocol on cardiac arrhythmias induced by potassium in anesthetized dogs

Either atropine, isoprenaline, neostigmine or practolol was given intravenously in therapeutic doses to dogs anesthetized with pentobarbitone sodium. Cardiac arrhythmias were induced by potassium chloride intravenously as a bolus injection in a dose of 0.3 mmol/kg. The standard electrocardiographic lead II was recorded continuously. pH, Po2 and Pco2 were checked from arterial blood samples before and after the injection. The isoprenaline treated dogs showed the smallest amount of arrhythmias and all the dogs survived. More severe arrhythmias were seen in the neostigmine and practolol treated dogs and the most severe occurrences were encountered in the atropine treated dogs.     

Characterization of parasympatholytic chronotropic responses following intravenous administration of atropine to clinically normal dogs.

OBJECTIVE: To determine heart rate (HR) and heart rate variability (HRV) after IV administration of 3 doses of atropine to clinically normal, large-breed adult dogs. ANIMALS: 6 mixed-breed dogs, weighing between 23 and 50 kg. PROCEDURE: Continuous ECG were recorded prior to and following IV administration of saline (0.9% NaCl) solution and 0.02, 0.04, and 0.06 mg of atropine/kg of body weight. Heart rate and HRV within sympathetic and parasympathetic domains were determined, using customized software, and responses to treatments were compared. Each dog received all treatments with > or = 2 days between treatments. RESULTS: HR increased and HRV within the parasympathetic domain decreased after all atropine treatments, compared with pretreatment values. Heart rate was significantly higher after administration of 0.06 mg of atropine/kg than after 0.02 mg/kg but was not different from HR after administration of 0.04 mg/kg. Five of 6 dogs given the 0.04 or 0.06 mg/kg dose attained HR > 135 beats/min, but only 1 of 6 dogs given the 0.02 mg/kg dose attained a HR > 135 beats/min. Heart rate variability within the parasympathetic domain decreased significantly from pretreatment values after all atropine treatments. Atropine doses of 0.04 and 0.06 mg/kg induced significantly lower HRV than did the 0.02 mg/kg dose, but HRV after the higher doses were not different from each other. HRV within the sympathetic domain after any treatment did not change from pretreatment values. CONCLUSIONS AND CLINICAL RELEVANCE: IV administration of 0.04 or 0.06 mg of atropine/kg increased HR and induced complete parasympathetic blockade in clinically normal, large-breed adult dogs.     

Use of atropine to reduce mucosal eversion during intestinal resection and anastomosis in the dog

OBJECTIVE: To determine whether atropine altered the degree of mucosal eversion during jejunal resection and anastomosis in the dog. STUDY DESIGN: Part I: Prospective, blinded, randomized, controlled study using a therapeutic dose (0.04 mg/kg systemic) of atropine. Part II: Prospective, unblinded, assigned, controlled study using a pharmacologic (0.04 mg/kg local arterial) dose of atropine. ANIMALS: Part I: Twenty-two young adult female Beagle dogs used during a nonsurvival third-year veterinary student surgical laboratory (small intestinal resection and anastomosis). Part II: Ten young adult female Beagle dogs used immediately after completion of a nonsurvival third-year veterinary student orthopedic surgical laboratory. METHODS: Part I: Dogs were randomly assigned to receive either atropine (0.04 mg/kg), or an equal volume of saline, given intramuscularly (premedication) and again intravenously prior to intestinal resection. Part II: In each dog, atropine (0.04 mg/kg)/saline was alternately given in the proximal/distal jejunum. RESULTS: Part I: There was no clinically or statistically significant difference between systemic atropine and saline solution on the degree of jejunal mucosal eversion after resection. Part II: There was a statistically significant decrease in jejunal mucosal eversion with atropine compared with saline solution when injected into a local jejunal artery. CONCLUSION: Systemic atropine (0.04 mg/kg) does not alter the degree of jejunal mucosal eversion during resection and anastomosis. Jejunal intraarterial atropine (0.04 mg/kg) reduced jejunal mucosal eversion during resection and anastomosis. CLINICAL RELEVANCE: The clinical usefulness and consequences of jejunal arterial atropine administration to reduce mucosal eversion remain to be determined.     

Romifidine, medetomidine or xylazine before propofol-halothane-N2O anesthesia in dogs.

The objective of this paper was to evaluate romifidine as a premedicant in dogs prior to propofol-halothane-N2O anesthesia, and to compare it with the other alpha2-agonists (medetomidine and xylazine). For this, ten healthy dogs were anesthetized. Each dog received 3 preanesthetic protocols: atropine (10 microg/kg BW, IM), and as a sedative, romifidine (ROM; 40 microg/kg BW, IM), xylazine (XYL; 1 microg/kg, IM), or medetomidine (MED; 20 microg/kg BW, IM). Induction of anesthesia was delivered with propofol 15 min later and maintained with halothane and N2O for one hour in all cases. The following variables were registered before preanesthesia, 10 min after the administration of preanesthesia, and at 5-minute intervals during maintenance: PR, RR, rectal temperature (RT), MAP, SAP, and DAP. During maintenance, arterial oxygen saturation (SpO2), end-tidal CO2 (EtCO2) and percentage of halothane necessary for maintaining anesthesia (%HAL) were also recorded. Induction dose of propofol (DOSE), time to extubation (TE), time to sternal recumbency (TSR) and time to standing (TS) were also registered. The statistical analysis was carried out during the anesthetic period. ANOVA for repeat measures revealed no differences between the 3 groups for PR and RR; however, MAP, SAP and DAP were higher in the MED group; SpO2 was lower in MED and EtCO2 was lower in ROM; %HAL was higher in XYL. No statistical differences were observed in DOSE, TE, TSR or TS. Percentage of halothane was lower in romifidine and medetomidine than in xylazine premedicated dogs also anesthetized with propofol. All the cardiorespiratory variables measured were within normal limits. The studied combination of romifidine, atropine, propofol, halothane and N2O appears to be a safe and effective drug combination for inducing and maintaining general anesthesia in healthy dogs.     

Effects of acetylpromazine or morphine on urine production in halothane-anesthetized dogs.

OBJECTIVE: To assess the influence of preanesthetic administration of acetylpromazine or morphine and fluids on urine production, arginine vasopressin (AVP; previously known as antidiuretic hormone) concentrations, mean arterial blood pressure (MAP), plasma osmolality (Osm), PCV, and concentration of total solids (TS) during anesthesia and surgery in dogs. ANIMALS: 19 adult dogs. PROCEDURE: Concentration of AVP, indirect MAP, Osm, PCV, and concentration of TS were measured at 5 time points (before administration of acetylpromazine or morphine, after administration of those drugs, after induction of anesthesia, 1 hour after the start of surgery, and 2 hours after the start of surgery). Urine output and end-tidal halothane concentrations were measured 1 and 2 hours after the start of surgery. All dogs were administered lactated Ringer's solution (20 ml/kg of body weight/h, i.v.) during surgery. RESULTS: Compared with values for acetylpromazine, preoperative administration of morphine resulted in significantly lower urine output during the surgical period. Groups did not differ significantly for AVP concentration, Osm, MAP, and end-tidal halothane concentration; however, PCV and concentration of TS decreased over time in both groups and were lower in dogs given acetylpromazine. CONCLUSIONS AND CLINICAL RELEVANCE: Preanesthetic administration of morphine resulted in significantly lower urine output, compared with values after administration of acetylpromazine, which cannot be explained by differences in AVP concentration or MAP When urine output is used as a guide for determining rate for i.v. administration of fluids in the perioperative period, the type of preanesthetic agent used must be considered.     

Cardiovascular effects of dose escalating of norepinephrine in healthy dogs anesthetized with isoflurane

ObjectiveTo evaluate the systemic cardiovascular effects of dose escalating administration of norepinephrine in healthy dogs anesthetized with isoflurane.Study designExperimental study.AnimalsA total of six adult laboratory Beagle dogs, 10.5 (9.2–12.0) kg [median (range)].MethodsEach dog was anesthetized with isoflurane at an end-tidal concentration of 1.7%, mechanically ventilated and administered a continuous rate infusion of rocuronium (0.5 mg kg^–1 hour^–1). Each dog was administered incremental dose rates of norepinephrine (0.05, 0.125, 0.25, 0.5, 1.0 and 2.0 μg kg^–1 minute^–1), and each dose was infused for 15 minutes. Cardiovascular variables were recorded before administration and at the end of each infusion period.ResultsNorepinephrine infusion increased mean arterial pressure (MAP), cardiac output (CO) and oxygen delivery in a dose-dependent manner. Systemic vascular resistance did not significantly change during the experiment. Stroke volume increased at the lower dose rates and heart rate increased at the higher dose rates. Oxygen consumption and lactate concentrations did not significantly change during infusions.ConclusionsIn dogs anesthetized with isoflurane, norepinephrine increased MAP by increasing the CO. CO increased with a change in stroke volume at lower dose rates of norepinephrine. At higher dosage, heart rate also contributed to an increase in CO. Norepinephrine did not cause excessive vasoconstriction that interfered with the CO during this study.Clinical relevanceNorepinephrine can be useful for treating hypotension in dogs anesthetized with isoflurane.     

Effects of intramedullary injection of methiodal and lidocaine on spinal cords of dogs.

A solution of methiodal sodium (20%) and lidocaine HCl (0.20%) was given by intramedullary injection into the lumbar spinal cords of 12 anesthetized dogs (group I). Two control groups of 12 dogs each were subjected to needle placement only or were given 5% dextrose. The results showed that both solutions given by intramedullary injection caused severe spinal cord malacia and cavitation in 2 group I dogs and in 1 group III dog.     

Parenteral use of medroxyprogesterone acetate as an antifertility agent in the bitch

10 kg unbred Beagle and mongrel bitches were used in each of 4 experiments (exp). 6 alpha-methyl-17 alpha-acetoxyprogesterone (MAP or medroxyprogesterone acetate) was prepared as a sterile aqueous suspension (50 mg/ml) and was used in exps 1, 2 and 3. Tritiated MAP was used in exp 4. In exp 1, 7 bitches were given 500 mg and 7 were given 50 mg subcutaneously (sc). 6 controls were used. In exp 2, 50, 100 or 250 mg were given sc, intramuscular (im) or intraperitoneal (ip) to 4 dogs at each dose level and route of administration. In exp 3, 12.5 or 25 mg was given either sc or im in 4 groups of 8 bitches each. In exp 4, a single 50 mg mixture of MAP and tritiated MAP was given to each of 3 dogs: 1 sc, 1 im, and 1 ip. Results of exp 1 showed those on 500 mg had first posttreatment estrus an average of 504 days (range of 247-730) after injection. Those on 50 mg averaged 329 days (range of 205-429). Breeding resulted in 6 live pups/litter for the controls 5.2 for those on 50 mg, and 4 for those on 500 mg. In exp 2, results showed prolonged cycling in those injected sc (295 days to estrus), while those injected im reached estrous in 225 days and those injected ip in 148 days. In exp 3, 3 on 25 mg sc had a 6 month estrous delay while 4 did when injected im. 3 of 16 given 12.5 mg sc and im had a 6 month delay in cycling. Exp 4 showed ip treated dogs had estrus 148 days after treatment, 225 days for im, and 295 days for sc. Ip treated dogs whelped 5 pups; im 7 pups; and sc, 5 pups. 7 months lapsed before nearly all of the 50 mg sc administered dose was excreted. An additional 2.5 months lapsed before estrus occurred in this dog.     

cis-Atracurium in dogs with and without porto-systemic shunts

OBJECTIVE: To evaluate the non-depolarizing neuromuscular blocking drug cis-atracurium in dogs with porto-systemic shunts, and to compare it in clinically normal animals. ANIMALS: Thirteen dogs of mixed breed and sex, aged between 3 and 31 months old, weighing 2.2-25.5 kg, with ASA physical status II-IV, and undergoing surgical attenuation of porto-systemic shunt. A control group of 11 bitches of mixed breed, between 8 and 60 months old, and weighing 4.5-41.0 kg, all ASA physical status I, undergoing routine ovarohysterectomy were also studied. MATERIALS AND METHODS: Pre-anaesthetic medication was an opioid analgesic, given either alone or in combination with acepromazine. Following induction of general anaesthesia with intravenous (IV) propofol and oro-tracheal intubation, anaesthesia was maintained using isoflurane in either oxygen or oxygen and nitrous oxide. Ventilation was controlled. The train of four (TOF) technique was used to monitor neuromuscular blockade. An initial dose of 0.1 mg kg(-1)cis-atracurium was given IV and additional doses of 0.03 mg kg(-1)cis-atracurium were administered when at least one twitch of the TOF was present. RESULTS: Except for one dog that was killed during surgery because its anomaly was inoperable, all animals recovered satisfactorily from anaesthesia and surgery. In dogs with porto-systemic shunt, onset of neuromuscular blockade was 3.1 +/- 1.1 minutes (mean +/- SD) and in control dogs was 3.4 +/- 0.7 minutes (not significantly different). Neuromuscular blockade lasted 34 +/- 13 minutes in dogs with porto-systemic shunt and 29 +/- 17 minutes in control dogs (not significantly different). CONCLUSIONS: The presence of porto-systemic shunt did not affect the rate of onset or duration of action of cis-atracurium. CLINICAL RELEVANCE: cis-Atracurium may have a use in veterinary anaesthesia for producing neuromuscular blockade in dogs with hepatic insufficiency, including those with porto-systemic shunt.     

Effect of sustained release isosorbide dinitrate (EV151) in dogs with experimentally-induced mitral insufficiency

To investigate the hemodynamic effects on seven anesthetized dogs with experimentally-induced mitral insufficiency, isosorbide dinitrate (ISDN) in sustained release form (EV151) was administered at different dosages (0, 2, 8 and 16 mg/kg). The drug administration resulted in altered pulmonary arterial wedge pressure (preload), and cardiac output and total systemic resistance (afterload). Arterial pressure increased in the control group and in animals receiving 2 mg/kg, but decreased in animals 1-2 hr after receiving 8 and 16 mg/kg dosages. Cardiac output increased in animals receiving 2, 8 and 16 mg/kg dosages, with concomitant decreases in total systemic resistance. ISDN caused mild vasodilation at 2 mg/kg and severe vasodilation at 8 and 16 mg/kg. Future experiments on non-anesthetized dogs may be of benefit.     

Use of ephedrine and dopamine in dogs for the management of hypotension in routine clinical cases under isoflurane anesthesia

OBJECTIVE: To determine the cardiovascular responses of ephedrine and dopamine for the management of presurgical hypotension in anesthetized dogs. STUDY DESIGN: Prospective, randomized, clinical trial. ANIMALS: Twelve healthy client-owned dogs admitted for orthopedic surgery; six per group METHODS: Prior to surgery, 58 anesthetized dogs were monitored for hypotension [mean arterial pressure (MAP) <60 mmHg] that was not associated with bradycardia or excessive anesthetic depth. Ephedrine (0.2 mg kg(-1), IV) or dopamine (5 microg kg(-1) minute(-1), IV) was randomly assigned for treatment in 12 hypotensive dogs. Ten minutes after the first treatment (Tx(1)-10), ephedrine was repeated or the dopamine infusion rate was doubled. Cardiovascular assessments taken at baseline, Tx(1)-10, and 10 minutes following treatment adjustment (Tx(2)-10) were compared for differences within and between treatments (p < 0.05). RESULTS: Ephedrine increased cardiac index (CI), stroke volume index (SVI), oxygen delivery index (DO(2)I), and decreased total peripheral resistance (TPR) by Tx(1)-10, while MAP increased transiently (<5 minutes). The second ephedrine bolus produced no further improvement. Dopamine failed to produce significant changes at 5 microg kg(-1) minute(-1), while 10 microg kg(-1) minute(-1) increased MAP, CI, SVI significantly from baseline, and DO(2)I compared with Tx(1)-10. The improvement in CI, SVI, and DO(2)I was not significantly different between treatments at Tx(2)-10. CONCLUSIONS AND CLINICAL RELEVANCE: In anesthetized hypotensive dogs, ephedrine and dopamine improved cardiac output and oxygen delivery. However, the pressure-elevating effect of ephedrine is transient, while an infusion of dopamine at 10 microg kg(-1) minute(-1) improved MAP significantly by additionally maintaining TPR.     

Effect of administering dexmedetomidine with or without atropine on cardiac troponin I level in isoflurane-anesthetized dogs

We aimed to determine whether dexmedetomidine administration with or without atropine increases cardiac troponin I (cTnI) level in healthy dogs. We hypothesized that 10 µg/kg dexmedetomidine + atropine increases the cTnI level, whereas 5 µg/kg dexmedetomidine + atropine does not. Eighteen healthy, pet dogs that underwent an orthopedic surgery or ovariohysterectomy were included in this study. The dogs were randomly assigned to atropine (0.02 mg/kg)–dexmedetomidine (10 µg/kg), saline–dexmedetomidine (10 µg/kg), and atropine (0.02 mg/kg)–dexmedetomidine (5 µg/kg) groups. Each dog was premedicated with atropine or saline intramuscularly (IM). After 10 min, they were IM injected with dexmedetomidine (10 or 5 µg/kg)–morphine (0.5 mg/kg)–midazolam (0.2 mg/kg). Following this, anesthesia was induced after 10 min with propofol and maintained with isoflurane in 100% oxygen. The median plasma cTnI level at 6, 12 and 24 hr after premedication was significantly higher than that at baseline. The cTnI level in the atropine–dexmedetomidine (10 µg/kg) group was significantly higher than that in the saline–dexmedetomidine (10 µg/kg) and atropine–dexmedetomidine (5 µg/kg) groups at 6 and 12 hr after premedication. The cTnI level returned to normal within 72 hr after premedication in all groups. The administration of atropine in combination with 10 µg/kg dexmedetomidine increased the cTnI level, indicating subclinical myocardial damage.     

Effects of atropine on xylazine-pentobarbital anesthesia in dogs: preliminary study

The influence of atropine on anesthesia induced by xylazine-pentobarbital administration was studied in 5 dogs. The combination of xylazine (2.2 mg/kg of body weight, IM) and pentobarbital (14.0 mg/kg, IV) caused anesthesia with the duration of absence of the pedal reflex, duration of anesthesia, and the time from return of consciousness to ambulation to be 107.4, 123.4, and 59.2 minutes, respectively. Bradycardia and short-term respiratory depression were observed. An IM injection of atropine sulfate (0.045 mg/kg) did not significantly change the durations of absence of the pedal reflex and of anesthesia, the time from return of consciousness to ambulation, or the pattern of respiration in the anesthetized dogs. The PaO2 increased gradually in both groups; however, atropine caused a marked tachycardia and increased the PaCO2. Fifteen minutes after pentobarbital injection, administration of atropine sulfate caused a slight but significant (P less than 0.01) decrease in arterial pH. Although atropine sulfate antagonized xylazine bradycardia, the data indicated that it may have caused increased respiratory depression in dogs anesthetized with xylazine and pentobarbital.     

Epinephrine-induced ventricular arrhythmias in dogs anesthetized with halothane: potentiation by thiamylal and thiopental

Epinephrine-induced ventricular arrhythmias were studied in 8 dogs anesthetized at weekly intervals with halothane (1.09% end-tidal concentration) preceded by thiamylal or thiopental (20 mg/kg of body weight). Lead II, bundle of His and high right atrial electrograms, and femoral artery and airway pressures were recorded. Epinephrine was infused in logarithmically spaced increasing rates (initial rate = 0.25 micrograms/kg/min) for a maximum of 2.5 minutes. The maximal (greater than or equal to 4 ventricular premature depolarizations within 15 s of each other) and minimal (all other ventricular or junctional rhythms) arrhythmogenic doses were calculated (infusion rate X time to arrhythmia). The mean (+/- SD) minimal arrhythmogenic dosages for the thiamylal-halothane, thiopental-halothane, and halothane-only groups were 1.84 +/- 0.66, 1.83 +/- 0.64, and 3.69 +/- 1.32 micrograms/kg, respectively; the mean (+/- SD) maximal arrhythmogenic dosages were 2.32 +/- 0.77, 3.37 +/- 1.30, and 8.86 +/- 4.40 micrograms/kg, respectively, with no change after 4 hours of anesthesia. During infusion of the maximal arrhythmogenic dosages, the mean infusion of the maximal arrhythmogenic dosages, the mean percentage increase in serum K+ for thiamylal-halothane, thiopental-halothane, and halothane-only groups was 33 +/- 14%, 31 +/- 13%, and 38 +/- 18%, respectively.     

Evaluation of the efficacy and safety for use of two sedation and analgesia protocols to facilitate assisted ventilation of healthy dogs

OBJECTIVE: To determine the effectiveness and safety of 2 sedative-analgesic protocols to facilitate assisted ventilation in healthy dogs. ANIMALS: 12 healthy dogs. PROCEDURES: Dogs were randomly assigned to 2 groups. Mean dosages for protocol 1 were diazepam (0.5 mg/kg/h [n = 3 dogs]) or midazolam (0.5 mg/kg/h [3]), morphine (0.6 mg/kg/h [6]), and medetomidine (1.0 microg/kg/h [6]). Mean dosages for protocol 2 were diazepam (0.5 mg/kg/h [n = 3]) or midazolam (0.5 mg/kg/h [3]), fentanyl (18 microg/kg/h [6]), and propofol (2.5 mg/kg/h [6]). Each dog received the drugs for 24 consecutive hours. All dogs were mechanically ventilated with adjustments in minute volume to maintain normocapnia and normoxemia. Cardiorespiratory variables were recorded. A numeric comfort score was assigned hourly to assess efficacy. Mouth care, position change, and physiotherapy were performed every 6 hours. Urine output was measured every 4 hours. RESULTS: Use of both protocols maintained dogs within optimal comfort ranges > 85% of the time. The first dog in each group was excluded from the study. Significant decreases in heart rate, oxygen consumption, and oxygen extraction ratio were evident for protocol 1. Cardiac index values in ventilated dogs were lower than values reported for healthy unsedated dogs. Oxygen delivery, lactate concentration, and arterial base excess remained within reference ranges for both protocols. CONCLUSIONS AND CLINICAL RELEVANCE: Use of both protocols was effective for facilitating mechanical ventilation. A reduction in cardiac index was detected for both protocols as a result of bradycardia. However, oxygen delivery and global tissue perfusion were not negatively affected.     

Anesthesia of captive African wild dogs (Lycaon pictus) using a medetomidine-ketamine-atropine combination.

Seven captive male African wild dogs (Lycaon pictus) weighing 25-32 kg each, were anesthetized by i.m. injection via hand syringe with a combination of 1.5 mg/kg ketamine, 40 microg/kg medetomidine, and 0.05 mg/kg atropine. Following endotracheal intubation, each animal was connected to a bain closed-circuit system that delivered 1.5% isoflurane and 2 L/min oxygen. Atipamezole (0.1 mg/kg i.v.; 0.1 mg/kg i.m.) was given at the end of each procedure (60 min following injection of medetomidine/ketamine/atropine). Time to sternal recumbency was 5-8 min. Times to standing after atipamezole administration were 8-20 min. This anesthetic regimen was repeated on three separate occasions (September 2000, February 2002, and October 2002) on all males to perform electroejaculation procedures. Each procedure was <80 min from injection to standing. Dogs showed excellent muscle relaxation during the procedures. Arterial blood samples were collected at 10-min intervals for blood gases in one procedure (September 2000). Separate venous samples were taken from each dog during each procedure for hematology and biochemistry. These values were within the normal range for this species. Arterial hemoglobin oxygen saturation (SpO2) and heart rate (HR) were monitored continuously in addition to other anesthesia monitoring procedures (body temperature, respiratory rate [RR], capillary refill time, blink response, pupil position, deep pain perception reflex). All dogs maintained relatively stable SpO2 profiles during monitoring, with a mean (+/-SD) SpO2 of 92% +/-5.4%. All other physiological variables (HR, RR, body temperature, blood pressure) were within normal limits. Following each procedure, normal behavior was noted in all dogs. All the dogs were reunited into the pack at completion of their anesthetic procedures. An injectable medetomidine-ketamine-atropine combination with maintenance by gaseous isoflurane and oxygen provides an inexpensive, reliable anesthetic for captive African wild dogs.     

Cardiopulmonary, anesthetic, and postanesthetic effects of intravenous infusions of propofol in greyhounds and non-greyhounds.

The cardiopulmonary, anesthetic, and postanesthetic effects of an IV infusion of the hypnotic agent propofol were assessed in 6 Greyhounds and 7 non-Greyhounds. After IM injection of acetylpromazine and atropine, a bolus injection of propofol sufficient to allow endotracheal intubation (mean +/- SEM = 4.0 +/- 0.3 mg/kg of body weight in Greyhounds; 3.2 +/- 0.1 mg/kg in non-Greyhounds) was administered, followed by continuous infusion at a rate of 0.4 mg/kg/min for 60 minutes, during which time dogs breathed 100% oxygen. In 23% of all dogs (3 of 13), apnea developed after initial bolus administration of propofol. Arterial blood pressure was well maintained in all dogs, but heart and respiratory rates were decreased significantly (P less than 0.05) during the infusion in Greyhounds. In Greyhounds, mild respiratory acidosis developed after 45 minutes, whereas arterial carbon dioxide tension was increased at all times after propofol administration in non-Greyhounds. In all dogs, PCV and total plasma proteins were unaffected by propofol. Rectal temperature decreased during treatment. Muscle tremors were observed in approximately 50% of dogs (in 3 of 6 Greyhounds and 3 of 7 non-Greyhounds) during and after infusion of propofol. Non-Greyhounds lifted their heads, assumed sternal recumbency, and stood 10 +/- 1, 15 +/- 3, and 28 +/- 5 minutes, respectively, after the end of the infusion; in Greyhounds, the corresponding times were 36 +/- 4, 43 +/- 6, and 63 +/- 7 minutes.     

Serum salicylate concentrations and endoscopic evaluation of the gastric mucosa in dogs after oral administration of aspirin-containing products

The serum salicylate concentration produced by oral administration of plain aspirin and several aspirin-containing products given at 8-hour intervals for 7 treatments was measured in 36 laboratory-conditioned adult dogs. The dogs were randomly allotted to 6 groups of 6 dogs each: group 1 was given plain aspirin at a dosage of 25 mg/kg of body weight: group 2 was given plain aspirin at a dosage of 10 mg/kg; group 3 was given buffered aspirin at a dosage of 25 mg/kg; group 4 was given enteric-coated aspirin at a dosage of 25 mg/kg; group 5 was given buffered aspirin at a dosage of 25 mg/kg; and, group 6 was given a placebo. Serum salicylate concentration was measured at 2-hour intervals for the first 8 hours, and then at 8-hour intervals for the next 40 hours. Following the last dosing, serum salicylate concentration was measured at 2-hour intervals until 56 hours; the final 2 samples were measured at 64 and 72 hours. The effect of aspirin on the gastric mucosa was studied in 12 dogs, 3 each randomly selected from groups 1, 3, 4, and 5. The gastric mucosa of each dog was examined with a fiberoptic gastroscope 3 days before the beginning of treatment; lesions were not seen. The drugs were administered as described and the gastric mucosa of each dog was reexamined at 72 hours. Administration of the aspirin-containing products at 8-hour intervals resulted in sustained therapeutic serum salicylate concentrations (greater than 5 mg/dl) in all dogs, except those of group 2. The greatest fluctuation in serum salicylate concentration was found in dogs of group 4. Gastric lesions were seen only in the 3 dogs of group 1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Butorphanol Tartrate for Partial Reversal of Oxymorphone-Induced Postoperative Respiratory Depression in the Dog

A randomized, blinded, crossover study was designed to evaluate the respiratory, cardiovascular, and behavioral effects of butorphanol given postoperatively to oxymorphone-premedicated and surgically stimulated dogs. Nine healthy adult dogs were premedicated intramuscularly with atropine (0.04 mg/kg), acepromazine (0.10 mg/kg), and oxymorphone (0.2 mg/kg). Anesthesia was induced with thiamylal (12 mg/kg) and maintained with halothane in oxygen. According to the protocol of a concurrent study, all dogs had percutaneous endoscopic gastrostomy (PEG) feeding tubes placed during the first anesthetic episode and removed during the second anesthetic episode. All dogs received postoperatively either butorphanol tartrate (0.2 mg/kg) or an isovol-umetric dose of saline placebo, both given intravenously. Respiratory rate (RR), tidal volume (TV), minute ventilation (MV), end-tidal CO₂ concentration (ET_CO2). heart rate (HR), and indirect diastolic (DP), systolic (SP) and mean arterial (MAP) blood pressures were measured at times 0, 2, 5, 10, 20, 40, 80, and 120 minutes after injection. The time from injection of the test drug until extubation was recorded. RR, MV, HR, and DP were significantly ( P < .05) increased, while ET_co2 was significantly decreased, for a minimum of 30 minutes in butorphanol-treated dogs compared with saline controls. TV, SP, and MAP were transiently (≤15 minutes) increased in butorphanol-treated dogs compared with saline controls. There was no significant difference between the times to extubation in the butorphanol-treated dogs versus the saline control dogs.