Cardiopulmonary, blood and peritoneal fluid alterations associated with abdominal insufflation of carbon dioxide in standing horses.

REASONS FOR PERFORMING STUDY: Abdominal insufflation is performed routinely during laparoscopy in horses to improve visualisation and facilitate instrument and visceral manipulations during surgery. It has been shown that high-pressure pneumoperitoneum with carbon dioxide (CO2) has deleterious cardiopulmonary effects in dorsally recumbent, mechanically ventilated, halothane-anaesthetised horses. There is no information on the effects of CO2 pneumoperitoneum on cardiopulmonary function and haematology, plasma chemistry and peritoneal fluid (PF) variables in standing sedated horses during laparoscopic surgery. OBJECTIVES: To determine the effects of high pressure CO2 pneumoperitoneum in standing sedated horses on cardiopulmonary function, blood gas, haematology, plasma chemistry and PF variables. METHODS: Six healthy, mature horses were sedated with an i.v. bolus of detomidine (0.02 mg/kg bwt) and butorphanol (0.02 mg/kg bwt) and instrumented to determine the changes in cardiopulmonary function, haematology, serum chemistry and PF values during and after pneumoperitoneum with CO2 to 15 mmHg pressure for standing laparoscopy. Each horse was assigned at random to either a standing left flank exploratory laparoscopy (LFL) with CO2 pneumoperitoneum or sham procedure (SLFL) without insufflation, and instrumented for measurement of cardiopulmonary variables. Each horse underwent a second procedure in crossover fashion one month later so that all 6 horses had both an LFL and SLFL performed. Cardiopulmonary variables and blood gas analyses were obtained 5 mins after sedation and every 15 mins during 60 mins baseline (BL), insufflation (15 mmHg) and desufflation. Haematology, serum chemistry analysis and PF analysis were performed at BL, insufflation and desufflation, and 24 h after the conclusion of each procedure. RESULTS: Significant decreases in heart rate, cardiac output and cardiac index and significant increases in mean right atrial pressure, systemic vascular resistance and pulmonary vascular resistance were recorded immediately after and during sedation in both groups of horses. Pneumoperitoneum with CO2 at 15 mmHg had no significant effect on cardiopulmonary function during surgery. There were no significant differences in blood gas, haematology or plasma chemistry values within or between groups at any time interval during the study. There was a significant increase in the PF total nucleated cell count 24 h following LFL compared to baseline values for LFL or SLFL at 24 h. There were no differences in PF protein concentrations within or between groups at any time interval. CONCLUSIONS: Pneumoperitoneum with CO2 during standing laparoscopy in healthy horses does not cause adverse alterations in cardiopulmonary, haematology or plasma chemistry variables, but does induce a mild inflammatory response within the peritoneal cavity. POTENTIAL RELEVANCE: High pressure (15 mmHg) pneumoperitoneum in standing sedated mature horses for laparoscopic surgery can be performed safely without any short-term or cumulative adverse effects on haemodynamic or cardiopulmonary function.

Safety and efficacy of preoperative administration of meloxicam, compared with that of ketoprofen and butorphanol in dogs undergoing abdominal surgery.

OBJECTIVE: To compare the safety and efficacy of preoperative administration of meloxicam with that of ketoprofen and butorphanol in dogs undergoing abdominal surgery. ANIMALS: 36 dogs undergoing laparotomy, splenectomy, or cystotomy. PROCEDURE: Dogs were randomly assigned to 1 of 3 groups. In the first part of the study, dogs were given a single dose of meloxicam, ketoprofen, or a placebo, and buccal mucosal bleeding times were measured. In the second part of the study, dogs were given meloxicam, ketoprofen, or butorphanol prior to surgery. Dogs in the butorphanol group received a second dose immediately after surgery. Pain scores (1 to 10) were assigned hourly for 20 hours after surgery and used to determine an overall efficacy score for each dog. Dogs with a pain score > or =3 were given oxymorphone for pain. Dogs were euthanatized 8 days after surgery, and gross and histologic examinations of the liver, kidneys, and gastrointestinal tract were conducted. RESULTS: Overall efficacy was rated as good or excellent in 9 of the 12 dogs that received meloxicam, compared with 9 of the 12 dogs that received ketoprofen and only 1 of the 12 dogs that received butorphanol. No clinically important hematologic, biochemical, or pathologic abnormalities were detected. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that preoperative administration of meloxicam is a safe and effective method of controlling postoperative pain for 20 hours in dogs undergoing abdominal surgery; the analgesic effects of meloxicam were comparable to those of ketoprofen and superior to those of butorphanol.

End tidal halothane concentration and postoperative analgesia requirements in dogs: a comparison between intravenous oxymorphone and epidural bupivacaine alone and in combination with oxymorphone.

The purpose of this study was to compare the effects of epidural bupivacaine (BUP) and oxymorphone/bupivacaine (O/B) and intravenous (i.v.) oxymorphone (IVO) on halothane requirements during hind end surgery and postoperative analgesia in 24 dogs. Dogs were randomly assigned to treatment groups: O/B--oxymorphone (0.1 mg/kg) in 0.75% bupivacaine (1 mg/kg for a total volume of 0.2 ml/kg); BUP--0.5% bupivacaine (1 mg/kg for a total volume of 0.2 ml/kg) with i.v. oxymorphone (0.05 mg/kg) postoperatively; and IVO--oxymorphone (0.05 mg/kg) pre- and postoperatively. Heart rate (HR), respiratory rate, arterial blood pressure, end-tidal carbon dioxide and halothane, and arterial blood gases were recorded prior to treatment and every 15 minutes thereafter. Once surgery had begun, end-tidal halothane concentrations were decreased as low as possible while still maintaining a stable anesthetic plane. Data were analyzed using ANOVA with P < 0.05 considered significant. End-tidal halothane requirements did not differ significantly among treatments. Respiratory depression was increased and HR was decreased in the O/B and IVO groups. Postoperative analgesic requirements were significantly less in dogs receiving O/B.

Evaluation of the arrhythmogenicity of a low dose of acepromazine: comparison with xylazine.

Alteration in the arrhythmogenic dose of epinephrine (ADE) was determined in 6 healthy dogs under halothane anesthesia following the administration of xylazine at 1.1 mg/kg i.v. and acepromazine at 0.025 mg/kg i.v. The order of treatment was randomly assigned with each dog receiving both treatments and testing was carried out on 2 separate occasions with at least a 1 wk interval. The ADE determinations were made prior to drug administration during halothane anesthesia (CNTL) and then 20 min and 4 h following drug treatment. Epinephrine was infused for 3 min at increasing dose rates (2.5, 5.0, 10.0 micrograms/kg/min) until the arrhythmia criterion (4 or more intermittent or continuous premature ventricular contractions) was reached within the 3 min of infusion or the 1 min following cessation. The interinfusion interval was 20 min. There was a significant difference (P = 0.0001) in the ADE determined following acepromazine administration at 20 min (20.95 micrograms/kg +/- 2.28 SEM) compared to CNTL (6.64 micrograms/kg +/- 1.09), xylazine at 20 min (5.82 micrograms/kg +/- 0.95) and 4 h (6.13 micrograms/kg +/- 1.05), and acepromazine at 4 h (7.32 micrograms/kg +/- 0.34). No other significant differences existed (P < 0.05). In this study we were unable to show any sensitization to epinephrine following xylazine administration during halothane anesthesia, while a protective effect was shown with a low dose of acepromazine.

The effect of carotid artery occlusion on lingual arterial blood pressure in dogs.

Although temporary occlusion of the carotid arteries is commonly done to reduce blood loss during nasal surgery in the dog, data supporting its use are mostly anecdotal and subjective. Twelve dogs were placed under general inhalation anesthesia and mechanically ventilated to maintain normocapnea and an end-tidal halothane concentration equivalent to 1.3 times the minimum alveolar concentration. Tourniquets were placed around both carotid arteries of each dog. Both lingual arteries were cannulated in each dog and their heart rate and blood pressure were measured bilaterally. During unilateral carotid artery occlusion, the blood pressures in the ipsilateral lingual artery were significantly (P < 0.05) lower than the preocclusion control pressures and pressures recorded in the contralateral vessel. Bilateral carotid artery occlusion resulted in a further significant (P < 0.05) fall in all lingual arterial pressures. The recorded heart rates only varied significantly from preocclusion control values when they increased during bilateral carotid occlusion (P < 0.05). The results of this study confirm that carotid artery occlusion has the potential to reduce intraoperative blood loss during oronasal surgery in the dog.

The arrhythmogenic dose of epinephrine in halothane and isoflurane anesthetized dogs: an assessment of repeatability.

Repeat determinations of the arrhythmogenic dose of epinephrine (ADE) were made over two 6 h periods on 2 separate days during halothane and isoflurane anesthesia. Each of 6 dogs underwent 4 trials (2 halothane and 2 isoflurane). During each trial, the ADE was determined at baseline, 3 and 6 h. Epinephrine was infused for 3.0 min at increasing dose rates (2.5, 5.0, 10.0 and 20.0 mg/kg/min) until the arrhythmia criterion (4 or more intermittent or continuous premature ventricular contractions) was reached. The inter-infusion interval was 20 min. There were no significant differences in the measured cardiovascular parameters (SBP, DBP, MBP, and HR), arterial blood gases, or acid-base status prior to each determination during a single trial. The cardiovascular responses to epinephrine infusion were not significantly different between inhalants or determinations. The range of the ADE determined over both trials during isoflurane anesthesia was 30.12 +/- 12.21 micrograms/kg to 50.83 +/- 9.17 micrograms/kg. The baseline ADE during Day 1 of halothane anesthesia (6.70 +/- 1.36 micrograms/kg) was significantly greater than ADE determinations at 3 (4.65 +/- 0.88 micrograms/kg) and 6 h (4.61 +/- 0.87 micrograms/kg). The reduction in the ADE over time during day 2 of halothane anesthesia was not statistically significant (P = 0.0669). These results suggest that during halothane anesthesia, the ADE is not repeatable over time, and they may influence our interpretation of the results of investigations that measure alterations in the ADE due to pharmacological manipulations without repeated control ADE determinations.

An evaluation of the influence of medetomidine hydrochloride and atipamezole hydrochloride on the arrhythmogenic dose of epinephrine in dogs during halothane anesthesia.

Alterations in the arrhythmogenic dose of epinephrine (ADE) were determined following administration of medetomidine hydrochloride (750 micrograms/M2) and a saline placebo, or medetomidine hydrochloride (750 micrograms/M2), followed by specific medetomidine reversal agent, atipamezole hydrochloride (50 micrograms/kg) 20 min later, in halothane-anesthetized dogs (n = 6). ADE determinations were made prior to the administration of either treatment, 20 min and 4 h following medetomidine/saline or medetomidine/atipamezole administration. Epinephrine was infused for 3 min at increasing dose rates (2.5 and 5.0 micrograms/kg/min) until the arrhythmia criterion (4 or more intermittent or continuous premature ventricular contractions) was reached. The interinfusion interval was 20 min. There were no significant differences in the amount of epinephrine required to reach the arrhythmia criterion following the administration of either treatment. In addition, the ADE at each determination was not different between treatment groups. In this study, the administration of medetomidine to halothane-anesthetized dogs did not alter their arrhythmogenic response to infused epinephrine.

Comparison of medetomidine and fentanyl-droperidol in dogs: sedation, analgesia, arterial blood gases and lactate levels.

Medetomidine and fentanyl-droperidol (Innovar-vet) were assessed over a three hour period in 80 healthy dogs. Following physical examination, electrocardiogram (ECG), arterial blood sample analysis, and dynamometer pressure threshold (analgesia score), the dogs were randomly assigned to one of four treatments: Miv--medetomidine (750 micrograms/M2) administered intravenously (IV), Mim--medetomidine (1000 micrograms/M2) administered intramuscularly (IM), Iiv--Innovar-vet IV (0.05 mL/kg) or Iim--Innovar-vet IM (0.1 mL/kg). All assessments were carried out by a single individual unaware of the treatment used. Objective assessments included temperature, heart and respiratory rates, analgesia score, arterial blood gases, acid-base and lactate levels. Subjective evaluation included degree of sedation, response to various clinical procedures, noise responsiveness, posture, and the incidence of side effects. Onset and duration of effect were also recorded. The ECG strips were assessed for arrhythmias. Data was analyzed using a 3-way analysis of variance for continuous variables and a Chi-square analysis of frequencies. A p value < or = 0.05 was considered significant. Medetomidine-treated animals had a decreased respiratory rate, longer duration of analgesic effect, increased incidence of bradycardia, vomiting and twitching, were less noise responsive and shivered less throughout the study. An increased incidence of second degree heart block with Miv (15 min), a delayed onset and recovery with Mim and increased lactate levels following Iiv (15 min) were observed. No differences were found in other measurements and good to excellent chemical restraint was produced with all treatments in 65% or more cases.