Effect of lenperone hydrochloride on gastroesophageal sphincter pressure in healthy dogs.

Treatment of healthy dogs with the butyrophenone derivative, lenperone hydrochloride, at two different doses significantly decreased gastroesophageal sphincter pressure (GESP). No dose-related effect was identified. Individual variation in the response to lenperone hydrochloride was noted which was consistent on a day-to-day basis. Lenperone hydrochloride is unsuitable for chemical restraint of dogs undergoing esophageal manometry because it decreases GESP and because the magnitude of the decrease varies considerably between dogs.     

Cystometry in dogs under oxymorphone and acepromazine restraint

Cystometry was performed in 12 dogs under oxymorphone and acepromazine restraint. A detrusor reflex occurred in 10 of 12 dogs (83%). Mean threshold pressure and volume were 31 cm H2O and 22 ml/kg, respectively. Tonus limb II varied inversely with threshold volume. Threshold volume varied directly with body weight; threshold pressure was independent of body weight.     

Effects of atropine, acepromazine, meperidine, and xylazine on gastroesophageal sphincter pressure in the dog

Gastroesophageal sphincter (GES) pressure was 47.9 +/- 1.2 mm of Hg in nontreated dogs. Treatment with atropine, acepromazine, and xylazine reduced GES pressure to 13.2 +/- 2.03, 18.6 +/- 2.14, and 11.7 +/- 1.19 mm of Hg, respectively. Treatment with meperidine resulted in phasic contractions with minimum and maximum pressures of 27.9 +/- 4.55 and 98.9 +/- 9.16 mm of Hg, respectively. Drugs used in anesthetic procedures can reduce GES pressure in dogs.     

Cardiopulmonary and behavioral effects of combinations of acepromazine/butorphanol and acepromazine/oxymorphone in dogs.

Cardiopulmonary and behavioral effects of the following tranquilizer-opioid drug combinations were compared in conscious dogs: acepromazine (0.22 mg/kg of body weight, IV) and butorphanol (0.22 mg/kg, IV); acepromazine (0.22 mg/kg, IM) and butorphanol (0.22 mg/kg, IM); and acepromazine (0.22 mg/kg, IV) and oxymorphone (0.22 mg/kg, IV). Marked sedation and lateral recumbency that required minimal or no restraint was achieved with every drug combination. Analgesia was significantly better in dogs receiving oxymorphone than in dogs receiving butorphanol, as evaluated by response to toe pinch. There were no significant differences between the effects of the 3 drug combinations on heart rate, respiratory rate, arterial blood pressure, body temperature, and arterial pH, PCO2, PO2, and bicarbonate concentration. Heart rate, respiratory rate, and systolic arterial pressure decreased significantly over time with all drug combinations. Total recovery time (minutes from the initial injection to standing) was significantly longer in the dogs given acepromazine and oxymorphone.     

Sedative effects of hydromorphone or oxymorphone with or without acepromazine in dogs

Hydromorphone is an agonist opioid with potency approximately five times that of morphine and half that of oxymorphone. The purpose of this study was to compare hydromorphone with oxymorphone, with or without acepromazine, for sedation in dogs, and to measure plasma histamine before and after drug administration. Ten dogs received IM hydromorphone (H; 0.2 mg kg^?1), oxymorphone (O; 0.1 mg kg^?1), hydromorphone with acepromazine (H; 0.2 mg kg^?1, A; 0.05 mg kg^?1) or oxymorphone with acepromazine (O; 0.1 mg kg^?1, A; 0.05 mg kg^?1) in a randomized Latin‐square design. Sedation score, heart rate, respiratory rate, blood pressure, and SpO₂ were recorded at baseline and every 5 minutes after drug administration up to 25 minutes. Plasma histamine was measured at baseline and at 25 minutes post‐drug administration. Data were analyzed with repeated measures anova . Mean ± SD body weight was 21.62 ± 1.54 kg. Mean ± SD age was 1.07 ± 0.19 years. Sedation score was significantly greater for OA after 5 minutes than O alone (4.1 ± 3.5 versus 1.9 ± 1.5) and for HA after 15 minutes than H alone (8.6 ± 2.9 versus 5.9 ± 2.5). There was no significant difference in sedation between H and O at any time point. There was no significant difference between groups at any time with respect to heart rate, respiratory rate, blood pressure or SpO₂. Mean ± SD plasma histamine (nM ml^?1) for all groups was 1.72 ± 2.69 at baseline and 1.13 ± 1.18 at 25 minutes. There was no significant change in plasma histamine concentration in any group. Hydromorphone is effective for sedation in dogs and does not cause measurable increase in histamine. Sedation with hydromorphone is enhanced by acepromazine.     

Cardiovascular and subjective evaluations of oxymorphone/diazepam and hydromorphone/diazepam induction in experimentally induced hypovolemic dogs

Carprofen is an oral nonsteroidal anti-inflammatory drug commonly used for treatment of chronic osteoarthritic pain. The injectable formulation has some efficacy for treatment of acute surgical orthopedic pain. The purpose of this project was to assess the efficacy of oral preoperative carprofen for control of postoperative pain in dogs undergoing knee surgery for repair of ruptured cranial cruciate ligaments.
This was a randomized, placebo controlled, parallel study that investigated the effectiveness of carprofen compared to placebo. Nineteen dogs, presented to the CSU VTH, were entered into the study and randomly assigned to the carprofen (C) ( n  = 10) or placebo (P) ( n  = 9) group. Dogs received either a loading dose of carprofen (2.2 mg kg⁻¹ PO BID) or placebo starting 24 hours prior to surgery including the morning of surgery. The placebo contained lactose and liver flavoring. Pain was assessed using a pain scoring system, visual analog scale, and a loaded pressure threshold device preoperatively, and at 1, 2, 4, 6, 24, and 48 hours and 10 and 21 days postoperatively. The treatment continued for 21 days. Blood for cortisol analysis was drawn at all assessment times. Data were analyzed using a likelihood-based mixed effect model repeated measures. Data were considered significant if p  < 0.05.
Eight of 10 C dogs and 5/9 P dogs were given at least 1 dose of morphine. The mean relative dose of morphine was greater in the C group at 1 hour ( p  = 0.01) and 24 hours ( p  = 0.02). The heart rate and respiratory rate decreased postoperatively in a similar manner for both groups. There were no significant postoperative differences in cortisol levels or any measured variable. It appears that the scoring system used was not sensitive enough to detect differences in pain between a known analgesic and a placebo.     

Effects of hydromorphone or oxymorphone, with or without acepromazine, on preanesthetic sedation, physiologic values, and histamine release in dogs

OBJECTIVE: To compare hydromorphone with oxymorphone, with or without acepromazine, for preanesthetic sedation in dogs and assess changes in plasma concentration of histamine after drug administration. DESIGN: Randomized clinical study. ANIMALS: 10 healthy mixed-breed dogs. PROCEDURE: Dogs were treated IM with hydromorphone (group H), oxymorphone (group O), hydromorphone with acepromazine (group H/A), or oxymorphone with acepromazine (group O/A). Sedation score, heart rate, respiratory rate, systolic blood pressure, and oxygen saturation were recorded at baseline immediately after drug administration (T0) and every 5 minutes for 25 minutes (T25). Plasma histamine concentration was measured at baseline and T25. RESULTS: Sedation was similar between groups H and 0 at all times. Sedation was significantly greater for groups H/A and O/A from T10 to T25, compared with other groups. Systolic blood pressure was significantly reduced at T25 in group H/A, compared with group H, and in group O/A, compared with group O. Prevalence of panting at T25 was 50% for groups H and O, compared with 20% for group H/A and 30% for group O/A. By T25, heart rate was significantly lower in all groups. Oxygen saturation was unaffected by treatment. Mean +/- SD plasma histamine concentration was 1.72 +/- 2.69 ng/ml at baseline and 1.13 +/- 1.18 ng/ml at T25. There was no significant change in plasma histamine concentration in any group. CONCLUSIONS AND CLINICAL RELEVANCE: Hydromorphone is comparable to oxymorphone for preanesthetic sedation in dogs. Sedation is enhanced by acepromazine. Neither hydromorphone nor oxymorphone caused an increase in plasma histamine concentration.     

Effect of gastrin, histamine, serotonin, and adrenergic amines on gastroesophageal sphincter pressure in the dog

In nonrestrained dogs that had not been given chemicals and that were in the fasted and fed state, gastroesophageal sphincter pressure (GESP) was measured; results were compared with GESP induced in the same dogs by drugs that modified activity at cholinergic, adrenergic, histaminic, and gastrin receptors. Atropine reduced GESP from 38.5 +/- 1.3 (mean +/- SE) and 55.5 +/- 2.0 mm of Hg to 11.3 +/- 2.0 and 14.5 +/- 2.4 mm of Hg in fasted and fed dogs, respectively. Histamine induced phasic contractions that were not affected by anticholinergics or cimetidine. Iphenhydramine eliminated the phasic contractions and reduced GESP to 18.2 +/- 3.9 mm of Hg. In fed dogs, diphenhydramine reduced GESP to 37.0 +/- 2.5 mm of Hg, but cimetidine did not. Pentagastrin induced increases in GESP that were inversely related to basal GESP. Pentagastrin given during histamine infusion eliminated histamine-induced phasic contractions. In fed dogs, metoclopramide increased GESP from 48.8 +/- 4.0 mm of Hg to 76.0 +/- 4.0 mm of Hg; this increment was eliminated by diphenhydramine. Administration of atropine after metoclopramide reduced GESP the same as for dogs given atropine alone. An adrenergic amine with only alpha-adrenergic effects induced phasic contractions, and an adrenergic amine with only beta-adrenergic effects reduced GESP. Blockers of alpha and beta effects did not change GESP in fed dogs. Domperidone induced phasic contractions that were eliminated by feeding. Serotonin increased GESP. Canine GESP may be maintained in fed dogs by chemicals interacting with cholinergic, histaminic, gastrin, and serotonin receptors, but not by chemicals interacting with adrenergic receptors.     

Relationship of plasma gastrin immunoreactivity and gastroesophageal sphincter pressure in clinically normal dogs and in dogs with previous gastric dilatation-volvulus

Fasting and postprandial gastroesophageal sphincter pressure (GESP) and plasma gastrin immunoreactivity were measured in 6 dogs from 9 through 60 months after treatment for and recovery from gastric dilatation-volvulus (GDV). The GESP was not significantly increased in these dogs, compared with that in clinically normal dogs in either the fasting or postprandial state. Corresponding plasma gastrin immunoreactivity was not significantly increased in dogs of the GDV-recovered group, compared with that in clinically normal dogs (fasting or postprandial). An exaggerated increase in GESP in response to food-induced gastrin release was not observed in dogs of the GDV-recovered group. Exogenously administered pentagastrin (3-micrograms/kg bolus, IV) increased fasting GESP in clinically normal dogs over a 4-minute test period (P = 0.01). Gastric distention in response to oral administration of isosmolar saline solution (500 ml) did not significantly increase GESP or plasma gastrin immunoreactivity in clinically normal dogs. In anesthetized clinically normal dogs, gastric distention in response to use of balloons filled to exert intragastric pressure of 30 mm of Hg also did not cause significant increase in plasma gastrin immunoreactivity. Increased GESP, secondary to hypergastrinemia or gastric distention, is an unlikely cause of eructation failure in dogs with GDV.     

Comparison of intraocular pressure and pupil diameter after sedation with either acepromazine or dexmedetomidine in healthy dogs

Objective

To compare intraocular pressure (IOP) and pupillary diameter (PD) following intravenous (IV) administration of dexmedetomidine and acepromazine in dogs.

Effect of intravenous propofol and remifentanil on heart rate, blood pressure and nociceptive response in acepromazine premedicated dogs

ObjectiveTo investigate the cardiorespiratory, nociceptive and endocrine effects of the combination of propofol and remifentanil, in dogs sedated with acepromazine.Study designProspective randomized, blinded, cross-over experimental trial.AnimalsTwelve healthy adult female cross-breed dogs, mean weight 18.4 ± 2.3 kg.MethodsDogs were sedated with intravenous (IV) acepromazine (0.05 mg kg^?1) followed by induction of anesthesia with IV propofol (5 mg kg^?1). Anesthesia was maintained with IV propofol (0.2 mg kg^?1 minute^?1) and remifentanil, infused as follows: R1, 0.125 μg kg^?1 minute^?1; R2, 0.25 μg kg^?1 minute^?1; and R3, 0.5 μg kg^?1 minute^?1. The same dogs were administered each dose of remifentanil at 1-week intervals. Heart rate (HR), mean arterial pressure (MAP), respiratory rate (f_R), end tidal CO₂ (Pe′CO₂), arterial hemoglobin O₂ saturation, blood gases, and rectal temperature were measured before induction, and 5, 15, 30, 45, 60, 75, 90, and 120 minutes after beginning the infusion. Nociceptive response was investigated by electrical stimulus (50 V, 5 Hz and 10 ms). Blood samples were collected for plasma cortisol measurements. Statistical analysis was performed by anova (p < 0.05).ResultsIn all treatments, HR decreased during anesthesia with increasing doses of remifentanil, and increased significantly immediately after the end of infusion. MAP remained stable during anesthesia (72–98 mmHg). Antinociception was proportional to the remifentanil infusion dose, and was considered satisfactory only with R2 and R3. Plasma cortisol concentration decreased during anesthesia in all treatments. Recovery was smooth and fast in all dogs.Conclusions and clinical relevanceInfusion of 0.25–0.5 μg kg^?1 minute^?1 remifentanil combined with 0.2 mg kg^?1 minute^?1 propofol produced little effect on arterial blood pressure and led to a good recovery. The analgesia produced was sufficient to control the nociceptive response applied by electrical stimulation, suggesting that it may be appropriate for performing surgery.     

Effect of medetomidine-butorphanol and dexmedetomidine-butorphanol combinations on intraocular pressure in healthy dogs

ObjectiveTo assess the effects of intravenous (IV) medetomidine-butorphanol and IV dexmedetomidine-butorphanol on intraocular pressure (IOP).Study designProspective, randomized, blinded clinical study.AnimalsForty healthy dogs. Mean ± SD body mass 37.6 ± 6.6 kg and age 1.9 ± 1.3 years.MethodsDogs were allocated randomly to receive an IV combination of dexmedetomidine, 0.3 mg m^?2, combined with butorphanol, 6 mg m^?2, (group DEX) or medetomidine 0.3 mg m^?2, combined with butorphanol 6 mg m^?2, (group MED). IOP and pulse (PR) and respiratory (f_R) rates were measured prior to (baseline) and at 10 (T10), 20 (T20), 30 (T30) and 40 (T40) minutes after drug administration. Oxygen saturation of hemoglobin (SpO₂) was monitored following sedation. Data were analyzed by anova followed by Dunnett's tests for multiple comparisons. Changes were considered significant when p < 0.05.ResultsFollowing drug administration, PR and f_R were decreased significantly at all time points but did not differ significantly between groups. Baseline IOP in mmHg was 14 ± 2 for DEX and 13 ± 2 for MED. With both treatments, at T10, IOP increased significantly (p < 0.001), reaching 20 ± 3 and 17 ± 2 for DEX and MED respectively. This value for DEX was significantly higher than for MED. There were no significant differences in IOP values between groups at any other time points. At T30 and T40, IOP in both groups was below baseline (DEX, 12 ± 2 and 11 ± 2: MED 12 ± 2 and 11 ± 2) and this was statistically significant, for DEX.Conclusions and clinical relevanceAt the documented doses, both sedative combinations induced a transient increase and subsequent decrease of IOP relative to baseline, which must be taken into consideration when planning sedation of animals in which marked changes in IOP would be undesirable.     

Effect of propofol and ketamine-diazepam on intraocular pressure in healthy premedicated dogs

Objective

To compare the effect of propofol and ketamine/diazepam for induction following premedication on intraocular pressure (IOP) in healthy dogs.

Effects of diazepam, ketamine, and their combination on intraocular pressure in normal dogs

Ketamine has been implicated as causing increases in intraocular pressure. The purpose of this study is to document the effects of ketamine, diazepam, and their combination on intraocular pressure (IOP) in normal, unpremedicated dogs. Random-source dogs were assigned to one of five groups of 10 dogs each: ketamine 5 mg kg^–1 (KET5), ketamine 10 mg kg^–1 (KET10), diazepam 0.5 mg kg^–1 (VAL), ketamine 10 mg kg^–1 with diazepam 0.5 mg kg^–1 (KETVAL), saline 0.1 mL kg^–1 (SAL), all given intravenously. A baseline IOP was measured before injection, immediately after injection, and at 5, 10, 15, and 20 minutes following injection. IOP was increased over baseline immediately after injection in the KET5, KET10, and KETVAL groups; at 5, 10, and 15 minutes in the KET5 group; and at 20 minutes in the KETVAL group. The mean IOP change compared to SAL increased immediately after injection and at 5 minutes in the KET5, KET10, and KETVAL groups; at 10 and 15 minutes in the KET5 group, and at 20 minutes in the KETVAL group. The mean IOP increased up to 5.7, 3.2, and 3.1 mm Hg over mean baseline in the KET5, KET10, and KETVAL groups, respectively. All dogs in the KET5 group and the majority in the KETVAL and KET10 groups had an increase in their IOP over baseline. Ketamine caused a clinically and statistically significant elevation in IOP over baseline and compared to SAL. The concurrent addition of diazepam did not blunt this increase. Ketamine should be avoided in dogs with corneal trauma, glaucoma, or in those undergoing intraocular surgery.     

Effects of ketamine‐diazepam and ketamine‐acepromazine combinations on intraocular pressure in rabbits

ObjectiveTo determine the effects of ketamine-diazepam and ketamine-acepromazine combinations on intraocular pressure (IOP) in rabbits.Study designRandomized clinical trial.AnimalsSixteen adult New Zealand white rabbits approximately one year old, weighing 2.3 ± 0.2 kg were used in this study.MethodsThe animals were randomly divided into two groups of eight each (KA and KD). The pre-treatment IOPs were recorded in both groups (T0). All rabbits in group KA received intramuscular ketamine-acepromazine (ketamine 30 mg kg^?1+ acepromazine 0.5 mg kg^?1). Ketamine-diazepam (ketamine 30 mg kg^?1 + diazepam 1 mg kg^?1) was administered intramuscularly in members of group KD. The IOP values were measured at 5 (T₅), 15 (T₁₅), and 20 (T₂₀) minutes after drug administration in both treatment groups.ResultsSignificant increases in IOP values were observed in both treatment groups at T_5, T₁₅, and T₂₀ in comparison to the baseline values. In group KA the mean ± SD IOP at T_5, T₁₅, and T₂₀ were 37 ± 13 (p < 0.001), 35 ± 4 (p < 0.001) and 34 ± 4 mmHg (p < 0.001). The post-treatment mean ± sd values in group KD were 23 ± 8 (p = 0.002), 23 ± 5 (p < 0.001) and 23 ± 6 mmHg (p = 0.001) at 5, 15, and 20 minutes respectively.Conclusion and clinical relevanceBoth ketamine-diazepam and ketamine-acepromazine combinations increased IOP after intramuscular administration in rabbits.     

Effects of sedation with acepromazine maleate and buprenorphine hydrochloride on femoral artery blood flow in healthy dogs

The purpose of this study was to qualify and quantify the femoral artery blood flow by duplex Doppler ultrasonography (DDU) in healthy dogs, before and after the administration of a combination of acepromazine maleate and buprenorphine hydrochloride (ACP-BPN). Seven healthy adult mongrel dogs and three adult beagles were used. Heart rate, arterial blood pressure and measurement of femoral artery blood flow by DDU were also recorded. The DDU measurements were: femoral artery diameter (FAD), peak systolic velocity (PSV), early retrograde (EDV) and end diastolic velocities (EnDV), mean velocity (BMV), pulsatility index (PI), flow velocity integral (FVI) and femoral blood flow (FBF). After 30 min, combination ACP-BPN was administered intramuscularly, and all the measurements were recorded again. The ACP-BPN protocol induced a significant decrease in systolic, mean, and diastolic arterial blood pressure, and heart rate. A significant increase in peak systolic velocity and integral flow velocity integral of the femoral blood were obtained. The Doppler spectra of the blood flow in the femoral artery revealed a spectral dispersion pattern after ACP-BPN administration in all the dogs. These results demonstrate that despite quantitative and qualitative changes, the overall femoral blood flow (FBF) is not significantly modified.     

Evaluation of the analgesic properties of acepromazine maleate, oxymorphone, medetomidine and a combination of acepromazine-oxymorphone

Objective To determine the presence and duration of analgesia after oxymorphone, acepromazine maleate, acepromazine‐oxymorphone combination and medetomidine administration in dogs. Study design Blinded, controlled study. Animals Six adult beagle dogs. Methods Each dog participated in five trials receiving acepromazine maleate (0.2 mg kg^?1 IM), oxymorphone (0.2 mg kg^?1 IM), acepromazine‐oxymorphone drug combination (0.2 mg kg^?1 each IM), medetomidine (20 µg kg^?1 IM) and sterile saline (control). Two specially designed instruments were used for analgesia determination: a heat device (HD) utilized a linear ramped intensity incandescent bulb and a pressure device (PD) consisted of a pneumatic cylinder that protruded a 2.5‐cm bolt. The minimum pressure and heat necessary to produce an avoidance response were determined. Analgesia testing was performed prior to and at 30‐minute intervals for six hours after drug administration. Results Oxymorphone, acepromazine‐oxymorphone and medetomidine significantly elevated both pressure and heat response thresholds compared to controls and acepromazine. Both medetomidine and acepromazine‐oxymorphone provided a significantly longer duration of analgesia than oxymorphone. No adverse effects were observed at any of the thermal or pressure application sites. Conclusions Oxymorphone, medetomidine and acepromazine‐oxymorphone produced significant analgesia with medetomidine and acepromazine‐oxymorphone providing the longest duration of analgesia.     

Eructation of gas through the gastroesophageal sphincter before and after truncal vagotomy in dogs

The function of the gastroesophageal sphincter (GES) to eructate gas before and after vagotomy was investigated in conscious, fed dogs. Gastric and GES pressures were measured in 5 dogs, using a perfused 4-lumen catheter with a Dent sleeve. To induce eructation, nitrogen gas was insufflated (440 ml/min) into the stomach through 1 channel of the catheter. After base-line studies were completed on each dog, bilateral truncal vagotomy was performed 5 cm cranial to the diaphragm. Mean (+/- SE) GES pressure was 51.5 +/- 1 mm of Hg before vagotomy and 28 +/- 1.7 mm of Hg after vagotomy (P less than 0.001). Mean gastric contraction rates were the same, 4.91 +/- 0.11/min and 4.78 +/- 0.06/min in dogs before and after vagotomy, respectively. During insufflation, gastric pressures increased to 11.8 +/- 0.7 mm of Hg before eructation in dogs before vagotomy and to 18.4 +/- 0.8 mm of Hg in dogs after vagotomy (P less than 0.001). Eructation occurred at intervals of 1.79 +/- 0.09 minutes before vagotomy and 5.71 +/- 0.41 minutes after vagotomy (P less than 0.001). Atropine resulted in an interval of 1.98 +/- 0.18 minutes before vagotomy. Eructation was not seen in 2 dogs after vagotomy and was sometimes not seen in the 3 others. Gastroesophageal sphincter pressure in dogs before vagotomy began to decrease 4.5 +/- 0.2 s before the GES-pressure gradient disappeared, and GES pressure remained there for 5.3 +/- 0.3 s before the gradient began to return.(ABSTRACT TRUNCATED AT 250 WORDS)