Effects of medetomidine premedication on propofol infusion anaesthesia in dogs

Observations of cardiovascular and respiratory parameters were made on six dogs anaesthetized on two separate occasions for 120 minutes with a propofol infusion, once without premedication and once following premedication with 10 μg kg-¹ of intramuscular medetomidine. During anaesthesia the heart rate and cardiac index tended to be lower following medetomidine premedication, while the mean arterial pressure was significantly greater (p<0.05). Although the differences were not statistically significant, the systemic vascular resistance, pulmonary vascular resistance and stroke volume index were also greater in dogs given medetomidine. The mean arterial oxygen and carbon dioxide tensions were similar under both regimens, but in 2 dogs supplementary oxygen had to be administered during anaesthesia to alleviate severe hypoxaemia on both occasions they were anaesthetized. Minute and tidal volumes of respiration tended to be greater in dogs not given medetomidine but medetomidine premedication appeared to have no effect on venous admixture. Dogs given medetomidine received intramuscular atipamezole at the end of the 120 min. propofol infusion; the mean time from induction of anaesthesia to walking without ataxia was 174. min in the unpremedicated dogs and 160 min. in the dogs given atipamezole. The mean blood propofol concentration at which the dogs walked without ataxia was higher in the unpremedicated animals (2.12 ± 0.077 μg. ml-¹ compared with 1.27 ± 0.518 μg. ml-¹ in the premedicated dogs). The oxygen delivery to the tissues was lower after medetomidine premedication (p = 0.03) and the oxygen consumption was generally lower after medetomidine premedication but the difference did not achieve statistical significance. No correlation could be demonstrated between blood propofol concentration and cardiac index, systemic or pulmonary vascular resistance indices, systolic, diastolic or mean arterial blood pressures.     

A comparison of the sedative and analgesic effects of buprenorphine in combination with acepromazine, midazolam or medetomidine in dogs

The effects of buprenorphine in combination with acepromazine, midazolam or medetomidine were compared in dogs. Induction and recovery times, heart rate, respiratory rate and body temperature were measured. Posture, reaction to noise, analgesia and muscle relaxation were assessed and a global score of "sedation-analgesia" was calculated. There were 3 groups of 4 animals: group 1 received 0.1 mg.kg-¹ acepromazine IM and 20 minutes later, 10 g.kg-¹ buprenorphine IV; group 2 received 1 mg.kg-¹ midazolam IV simultaneously with 10 ig.kg-¹ buprenorphine IV and group 3 received 1 mg/m² body surface area medetomidine IM and 20 minutes later, 10 Hg.kg-¹ buprenorphine IV. Only one dog given acepromazine and buprenorphine reached a "sedation-analgesia" stage, denned as the inability to stand together with the absence of reaction to stimulation, including pain. Animals in this group showed a decrease in respiratory rate and in body temperature. None of the dogs given midazolam and buprenorphine became sedated or showed signs of analgesia. Following this combination, the dogs were excited and showed dysphoric reactions which disappeared within 20 minutes.
All of the dogs given medetomidine and buprenorphine showed good sedation and analgesia lasting more than 20 minutes. This drug combination produced a decrease in heart and respiratory rates and body temperature.     

Atipamezole increases medetomidine clearance in the dog: an agonist—antagonist interaction

Medetomidine, an α₂-adrenoceptor agonist, is a potent sedative and analgesic agent in the dog. When necessary, its action can be effectively antagonized by atipamezole. The present work was designed to study the effects of these drugs on each others' pharmacokinetics when a single intramuscular dose of medetomidine (50 μg kg^-1) was followed by a dose of atipamezole (250 μg kg^-1). Three different treatments were used: medetomidine alone, atipamezole alone, and atipamezole after medetomidine. Drug concentrations in plasma were measured by GC-MS. Statistical analysis of the results (anova) revealed significant differences between treatments in the kinetic parameters of medetomidine. Atipamezole decreased the AUC of medetomidine from 41.3 to 28.6 ng h ml"¹(P = 0.005), t_1/4 from 1.44 to 0.87 h ( P = 0.015), and increased Cl from 21 to 31 ml min^-1kg^-1(P = 0.017). Differences in V₂ did not reach statistical significance. The only statistically significant effects of medetomidine on the pharmacokinetics of atipamezole in this study were the slight decrease of Cl and C _max as well as the increase of AUC . It is suggested that the large dose of medetomidine used caused haemodynamic changes, resulting in decreased hepatic circulation and slower drug metabolism. Antagonism by atipamezole restored the hepatic blood flow and, consequently, increased the elimination of medetomidine by biotransformation.     

Seizures during medetomindine sedation and local anaesthesia in two dogs undergoing skin biopsy

Each of two dogs presented for multiple skin biopsies were sedated with intravenous medetomidine and lignocaine was injected subcutaneously to provide local anaesthesia for skin biopsy. One dog had a seizure during skin biopsy and again immediately following reversal of medetomidine with atipamezole. The other dog developed seizures 2 h following skin biopsy at which time the medetomidine was reversed with atipamezole. Both dogs were neurologically normal with no history of seizures prior to the procedure and remained neurologically normal for 14 weeks and 9 months, respectively, following the procedure. A drug interaction between the α₂-adrenergic agonist medetomidine and lignocaine is suspected and highlights the potential for seizures following the subcutaneous administration of relatively large doses of lignocaine under medetomidine sedation.     

Disposition of propofol after medetomidine premedication in beagle dogs

Propofol by infusion was administered to 6 adult beagle dogs on 2 separate occasions. The dogs received either no premedication or 20 μg/kg im medetomidine 15 min before induction of anaesthesia, with propofol given at 7 mg/kg/min to permit tracheal intubation. After tracheal intubation the infusion rate was maintained for 120 min at 0.4 mg/kg/min in the non-premedicated, and 0.2 mg/kg/min in the premedicated dogs. The latter group received atipamezole 50 μg/kg im immediately at the end of the infusion. After induction of anaesthesia, a 7F balloon catheter designed for thermal dilution measurement of cardiac output was inserted via the right jugular vein. Blood propofol concentrations were measured by HPLC with fluorescence detection and kinetic variables calculated using non-compartmental moment analysis. The induction dose of propofol was 7.00 (sem 0.55) mg/kg in non-premedicated compared with 3.09 (0.25) mg/kg in premedicated dogs. There were differences in systemic clearance and mean residence time (MRT_iv); 47.5 (6.2) ml/kg/min vs 29.0 (4.4) ml/kg/min (non-premedicated vs premedicated) and 132.3 (5.2) min vs 152.4 (3.1) min (P < 0.02 and P < 0.001, respectively). Cardiorespiratory effects were similar in the 2 groups although heart rate was lower in the premedicated dogs. Venous admixture was high (20–45%) but similar in the 2 groups.     

Effects of medetomidine on intestinal and colonic motility in the dog

The motor responses of the jejunum and colon to stimulation of α₂-adrenoceptors by medetomidine and clonidine were investigated in four dogs. In fasting dogs, medetomidine, at a dose rate of 30 μg/kg i.v., disrupted the migrating myoelectric complex (MMC) pattern of the small intestine for about 2 h. Similar, but shorter-lasting effects were also induced by clonidine (30 μg/kg i.v.) on the jejunum. The administration of α₂-agonists inhibited colonic motility in fasting dogs, although medetomidine-induced inhibition was preceded by a short period of increased muscle tone. All these effects were reversed by the α₂-antagonists atipamezole (0.15 mg/kg i.v.) and yohimbine (0.20 mg/kg i.v.). In fed dogs, medetomidine (30 μg/kg i.v.) induced a strong increase of the tone on the proximal colon, while the activity of the medium and distal colon was completely suppressed. Yohimbine (0.50 mg/kg i.v.) immediately restored the activity of the colon and induced a propagated giant contraction and defaecation by the animal. These data confirm the importance of a₂-adrenergic receptors in the control of intestinal and colonic motility in the dog.     

Romifidine as a premedicant to propofol induction and infusion anaesthesia in the dog

The effects of premedication with four different intravenous doses of romifidine (20, 40, 80 and 120 (μg/kg body weight) and a saline placebo were compared in a group of 20 adult beagles of both sexes, undergoing anaesthesia with propofol for a clinical dental procedure. Anaesthesia was induced 10 minutes after premedication and maintained by intravenous infusion of propofol for a period of 30 minutes. Romifidine had a marked synergistic effect with propofol and reduced the required induction and infusion doses by more than 60 per cent for a standard level of anaesthesia; the synergistic effect was dose related. Following premedication, propofol produced no significant alteration of respiratory rate, heart rate or rectal temperature. Anaesthesia was found to be more stable following romifidine premedication at all doses studied. The quality of induction was unaltered by the dose of the romifidine. Recovery from anaesthesia was smooth and of a similar quality in all cases. There were no differences in the recovery times between the unpremedicated group and the dogs premedicated with any dose of romifidine studied. There were no adverse effects noted following this anaesthetic regimen. The marked dose-related synergism with propofol induction and infusion anaesthesia is relevant should romifidine be used in the dog in clinical veterinary practice.     

Reversal of medetomidine-induced sedation in reindeer (Rangifer tarandus tarandus) with atipamezole increases the medetomidine concentration in plasma

The pharmacokinetics of two potent α₂-adrenoceptor agents that can be used for immobilization (medetomidine) and reversal (atipamezole) of the sedation in mammals, were studied in three reindeer ( Rangifer tarandus tarandus) in winter and again in summer. Medetomidine (60 μg/kg) was injected intravenously (i.v.), followed by atipamezole (300 μg/kg) intravenously 60 min later. Drug concentrations in plasma were measured by HPLC. The administration of atipamezole resulted in an immediate 2.5–3.5 fold increase in the medetomidine concentration in plasma. Clearance for medetomidine (median 19.3 mL/min·kg) was lower than clearance for atipamezole (median 31.0 mL/min·kg). The median elimination half-lives of medetomidine and atipamezole in plasma were 76.1 and 59.9 min, respectively. The animals became resedated 0.5–1 h after the reversal with atipamezole. Resedation may be explained by the longer elimination half-life of medetomidine compared to atipamezole.     

Effects of metaraminol bitartrate on intraocular pressure in dogs under halothane anesthesia

The effects of metaraminol bitartrate on intraocular pressure (IOP) were studied in dogs anesthetized with halothane. Forty-five healthy, adult, mixed-breed dogs, of both sexes, were divided into three groups of 15 dogs each (GI, GII and GIII) and maintained under general anesthesia with halothane after tranquilization with levomepromazine and induction with thiopental. Saline (0.9%) was administered intravenously (IV) to GI through continuous infusion, at a velocity of 0.125 mL kg⁻¹ min⁻¹. GII and GIII received metaraminol 0.004% IV, at a dose of 5 μg kg⁻¹ min⁻¹, at 0.125 mL kg⁻¹ min⁻¹ and at a dose of 2 μg kg⁻¹ min⁻¹, at 0.06 mL kg⁻¹ min⁻¹, respectively. IOP was measured by applanation tonometry (Tono-Pen) before and during anesthesia. Results showed that IOP decreased in GI, increased in GII, and remained at basal levels in GIII. Continuous infusion of metaraminol at 2 μg kg min⁻¹ maintained IOP at pretest levels, while infusion at 5 μg kg⁻¹ min⁻¹ produced an elevation of IOP.     

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.     

The pharmacodynamics of thiopental, medetomidine, butorphanol and atropine in beagle dogs

This study evaluated the quality of anaesthesia and some of the haemodynamic effects induced by a combination of thiopental, medetomidine, butorphanol and atropine in healthy beagle dogs ( n  = 12). Following premedication with atropine (ATR, 0.022 mg/kg intravenously (i.v.)) and butorphanol (BUT, 0.22 mg/kg i.v.), medetomidine (MED, 22 μg/kg intramuscularly (i.m.)) was administered followed in 5 min by thiopental (THIO, 2.2 mg/kg i.v.). Heart rate, systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial blood pressure (MBP) were monitored continuously with an ECG and direct arterial blood pressure monitor. Atipamezole (ATI, 110 μg/kg i.v.) was administered to half of the dogs ( n  = 6) following surgery to evaluate the speed and quality of arousal from anaesthesia. Anaesthesia was characterized by excellent muscle relaxation, analgesia and absence of purposeful movement in response to surgical castration. Arousal following antagonism of mede­tomidine was significantly faster ( P  < 0.05) than in unantagonized dogs. Recoveries were smooth but recovery times following atipamezole administration were highly variable among dogs (sternal time range 6–38 min, standing time range 9–56 min). Medetomidine caused a significant ( P  < 0.05) increase in SBP, DBP and MBP. Atropine prevented the medetomidine induced bradycardia. In conclusion, this combination provided adequate surgical anaesthesia in healthy beagle dogs. At the dosages used in this study, it seems prudent that this combination should be reserved for dogs free of myocardial disease.     

Medetomidine/propofol anaesthesia for gastroduodenal endoscopy in dogs

This study was performed to evaluate clinically the level of analgesia obtained during fibre optic gastroduodenal examination with an anaesthetic regimen consisting of 1000 μg/m²b.s.a. medetomidine premedica-tion (equivalent to 30–50 μg/kg b.w, IM) followed by induction and maintenance of anaesthesia with propofol (1–2 mg/kg, IV), with spontaneous respiration of room air. Following premedication, all the dogs (n=20) were connected to an E.C.G. monitor (lead II) and a femoral artery catheter was placed for continuous recording of blood pressure and to allow sampling for arterial blood gas analysis. The mean values for heart rate and arterial blood pressure following medetomidine administration were 55 b.p.m. and 121 mm Hg, respectively, and these values remained unchanged during the procedure. Blood gas data all remained within physiological limits. Fibre optic gastroduodenoscopy could be performed without the occurrence of “pain” responses. In all but one dog, the pyloric sphincter was relaxed and it was easy to pass the endoscope into the duodenum. All the dogs recovered rapidly and smoothly from anaesthesia, following administration of atipamezole 2500 μg/m² b.s.a. (equivalent to 75–125 μg/kg b.w.) IM to reverse the effects of the medetomidine.     

Effects of combinations of medetomidine/pethidine when used for sedation and pre-anaesthetic medication in dogs

Medetomidine, either 5, 10 or 20 (μg/kg, was administered together with pethidine, 2 mg/kg, by either the intramuscular or subcutaneous route to 88 dogs from a clinical population. Administration of all the drug combinations consistently produced profound sedation in the dogs, accompanied by dramatic reductions in heart rate. The degree of sedation was similar to that seen after 40 μg/kg medetomidine is administered on its own to dogs. Intramuscular administration produced more reliable sedation, but was associated with more pain than subcutaneous administration. In a number of dogs, sedation permitted the completion of various diagnostic or therapeutic procedures. Several dogs were anaesthetised with thiopentone and the induction doses required were characteristically low (mean doses between 2 to 3·3 mg/kg depending on the dose of medetomidine and the route of administration). Administration of atipamezole at the termination of sedation or anaesthesia, produced a rapid and full recovery (mean time to standing between seven and 11 minutes).     

A comparison of propofol infusion and propofol/isoflurane anaesthesia in dexmedetomidine premedicated dogs

The effects of propofol infusion were compared with propofol/isoflurane anaesthesia in six beagles premedicated with 10 microg/kg intramuscular (i.m.) dexmedetomidine. The suitability of a cold pressor test (CPT) as a stress stimulus in dogs was also studied. Each dog received isoflurane (end tidal 1.0%, induction with propofol) with and without CPT; propofol (200 microg/kg/min, induction with propofol) with and without CPT; premedication alone with and without CPT in a randomized block study in six separate sessions. Heart rate and arterial blood pressures and gases were monitored. Plasma catecholamine, beta-endorphin and cortisol concentrations were measured. Recovery profile was observed. Blood pressures stayed within normal reference range but the dogs were bradycardic (mean heart rate < 70 bpm). PaCO2 concentration during anaesthesia was higher in the propofol group (mean > 57 mmHg) when compared with isoflurane (mean < 52 mmHg). Recovery times were longer with propofol than when compared with the other treatments. The mean extubation times were 8 +/- 3.4 and 23 +/- 6.3 min after propofol/isoflurane and propofol anaesthesia, respectively. The endocrine stress response was similar in all treatments except for lower adrenaline level after propofol infusion at the end of the recovery period. Cold pressor test produced variable responses and was not a reliable stress stimulus in the present study. Propofol/isoflurane anaesthesia was considered more useful than propofol infusion because of milder degree of respiratory depression and faster recovery.     

The effects of medetomidine hydrochloride on the electroretinogram of normal dogs

Purpose  To determine the effects of a standardized intravenous dose of an α-2 agonist (Domitor^®, Orion Pharma, distributed by Pfizer Animal Health, Exton, PA) on the electroretinogram (ERG) response in normal dogs.
Methods  Twenty-five normal dogs were used to collect ERG responses including a- and b-wave implicit times (IT) and amplitudes (AMP) before and after administration of medetomidine. Dogs were dark adapted for 20 min and ERGs were obtained using the HMsERG (RetVetCorp Inc., Columbia, MO). The QuickRetCheck protocol (Narfström) was employed to provide the following flash intensities: 10 mcd s/m², 3 cd s/m², and 10 cd s/m². ERGs were repeated after 375 µg/m² of medetomidine intravenously. Statistical analysis of the difference between the responses before and after medetomidine at all flash intensities was performed using a mixed effects model for anova .
Results  The P value for the effect of medetomidine on each of the ERG responses was < 0.01. The estimates of the effect of medetomidine were (+)1.35 ms, (–)23 µV, (+)3.16 ms, and (–)47 µV for the a-wave IT, a-wave AMP, b-wave IT, and the b-wave AMP, respectively.
Conclusions  Medetomidine significantly prolongs the implicit time and lowers the amplitude response of both the a- and b-waves in normal dogs at all flash intensities examined. Clinically, however, medetomidine only minimally affects the retinal responses and is a viable choice for use in dog ERGs.     

The cardiovascular and respiratory effects of medetomidine and thiopentone anaesthesia in dogs breathing at an altitude of 1486 m

The purpose of this study was to evaluate the cardio-respiratory effects of the combination of medetomidine and thiopentone followed by reversal with atipamezole as a combination for anaesthesia in 10 healthy German Shepherd dogs breathing spontaneously in a room at an altitude of 1486 m above sea level with an ambient air pressure of 651 mmHg. After the placement of intravenous and intra-arterial catheters, baseline samples were collected. Medetomidine (0.010 mg/kg) was administered intravenously and blood pressure and heart rate were recorded every minute for 5 minutes. Thiopentone was then slowly administered until intubation conditions were ideal. An endotracheal tube was placed and the dogs breathed room air spontaneously. Blood pressure, pulse oximetry, respiratory and heart rate, capnography, blood gas analysis and arterial lactate were performed or recorded every 10 minutes for the duration of the trial. Thiopentone was administered to maintain anaesthesia. After 60 minutes, atipamezole (0.025 mg/kg) was given intramuscularly. Data were recorded for the next 30 minutes. A dose of 8.7 mg/kg of thiopentone was required to anaesthetise the dogs after the administration of 0.010 mg/kg of medetomidine. Heart rate decreased from 96.7 at baseline to 38.5 5 minutes after the administration of medetomidine (P < 0.05). Heart rate then increased with the administration of thiopentone to 103.2 (P < 0.05). Blood pressure increased from 169.4/86.2 mmHg to 253.2/143.0 mmHg 5 minutes after the administration of medetomidine (P < 0.05). Blood pressure then slowly returned towards normal. Heart rate and blood pressure returned to baseline values after the administration of atipamezole. Arterial oxygen tension decreased from baseline levels (84.1 mmHg) to 57.8 mmHg after the administration of medetomidine and thiopentone (P < 0.05). This was accompanied by arterial desaturation from 94.7 to 79.7% (P < 0.05). A decrease in respiratory rate from 71.8 bpm to 12.2 bpm was seen during the same period. Respiratory rates slowly increased over the next hour to 27.0 bpm and a further increases 51.4 bpm after the administration of atipamezole was seen (P < 0.05). This was maintained until the end of the observation period. Arterial oxygen tension slowly returned towards normal over the observation period. No significant changes in blood lactate were seen. No correlation was found between arterial saturation as determined by blood gas analysis and pulse oximetry. Recovery after the administration of atipamezole was rapid (5.9 minutes). In healthy dogs, anaesthesia can be maintained with a combination of medetomidine and thiopentone, significant anaesthetic sparing effects have been noted and recovery from anaesthesia is not unduly delayed. Hypoxaemia may be problematic. Appropriate monitoring should be done and oxygen supplementation and ventilatory support should be available. A poor correlation between SpO2 and SaO2 and ETCO2 and PaCO2 was found.     

Medetomidine, levo-methadone and diazepam as premedication for lumbosacral epidural anaesthesia in dogs

The effect of medetomidine (40 μg/ kg) together with levo-methadone (0.5 mg/kg) was evaluated in dogs as a sedative and analgesic premedication followed by a lumbosacral epidural block with mepivacaine 2% or bupi-vacaine 0.5% (0.3–0.5 ml/10cm crown-rump length). When sedation became insufficient in the course of surgery, additional diazepam (0.1–0.2 mg/kg) was administered. Only in 43% of the dogs could surgery be performed without additional sedation. Medetomidine and levo-methadone influenced the cardio-respiratory system markedly. Hypoxaemia as well as hypercarbia were evident. Diazepam had no additional effect on these respiratory changes. After surgery 19 dogs were given atipamezole, 18 received atipamezole and naloxone while 17 received no antagonists. In 10 out of the 19 dogs receiving only atipamezole, fits of excitability were seen, but those receiving atipamezole and naloxone had a quiet recovery.     

The effects of medetomidine and xylazine on gastrointestinal motility and gastrin release in the dog

The effect of medetomidine, a potent and highly selective α₂-adrenoceptor agonist, on the motility of the gastric antrum, duodenum, mid-jejunum and ileum was investigated in ten dogs. Its effect on the release of gastrin was also determined. Administration of medetomidine intramuscularly (i.m.) at a dose of 40 μg/kg inhibited the motility of the gastric antrum, duodenum, mid-jejunum and ileum significantly, in comparison to administration of xylazine intramuscularly at a dose of 2.0 mg/kg. The release of gastrin was also significantly decreased in dogs receiving medetomidine. It was found to inhibit the motility in the gastric antrum and duodenum longer than in the mid-jejunum and ileum, presumably by acting specifically on α₂-adrenoceptors, likely at the peripheral level. Medetomidine also inhibited the gastric contraction associated with gastrin secretion.     

The effect of body condition on propofol requirement in dogs

ObjectiveTo determine if body condition score (BCS) influences the sedative effect of intramuscular (IM) premedication or the dose of intravenous (IV) propofol required to achieve endotracheal intubation in dogs.Study designProspective clinical study.AnimalsForty–six client–owned dogs undergoing general anaesthesia.MethodsDogs were allocated to groups according to their BCS (BCS, 1 [emaciated] to 9 [obese]): Normal–weight Group (NG, n = 25) if BCS 4–5 or Over–weight Group (OG, n = 21) if BCS over 6. Dogs were scored for sedation prior to IM injection of medetomidine (5 μg kg^?1) and butorphanol (0.2 mg kg^?1) and twenty minutes later anaesthesia was induced by a slow infusion of propofol at 1.5 mg kg^?1 minute^?1 until endotracheal intubation could be achieved. The total dose of propofol administered was recorded. Data were tested for normality then analyzed using Student t–tests, Mann–Whitney U tests, chi–square tests or linear regression as appropriate.ResultsMean ( ± SD) propofol requirement in NG was 2.24 ± 0.53 mg kg^?1 and in OG was 1.83 ± 0.36 mg kg^?1. The difference between the groups was statistically significant (p = 0.005). The degree of sedation was not different between the groups (p = 0.7). Post–induction apnoea occurred in 11 of 25 animals in the NG and three of 21 in OG (p = 0.052).ConclusionsOverweight dogs required a lower IV propofol dose per kg of total body mass to allow tracheal intubation than did normal body condition score animals suggesting that IV anaesthetic doses should be calculated according to lean body mass. The lower dose per kg of total body mass may have resulted in less post–induction apnoea in overweight/obese dogs. The effect of IM premedication was not significantly affected by the BCS.Clinical relevanceInduction of general anaesthesia with propofol in overweight dogs may be expected at lower doses than normal–weight animals.     

Prothrombotic and Inflammatory Effects of Intravenous Administration of Human Immunoglobulin G in Dogs

Background: Intravenous administration of human immunoglobulin G (hIVIgG) has been suggested to potentiate thromboembolism in dogs, but supportive scientific reports are lacking.
Objectives: To determine if hIVIgG therapy promotes hypercoagulability and inflammation in dogs.
Animals: Twelve healthy Beagle dogs.
Methods: Prospective, experimental trial. An hIVIgG/saline solution was infused IV at 1 g/kg BW over 8 hours to 6 dogs, and physiological saline was infused to the other 6 dogs. Blood samples were drawn before, during, and after infusion for serial measurement of indicators of coagulation and inflammation. Data were analyzed by 2-way repeated measures analysis of variance.
Results: Dogs administered hIVIgG developed mildly decreased blood platelet concentrations without thrombocytopenia (median, 200 × 10³/μL; range, 150–302 × 10³/μL; P < .01), leukopenia (median, 3.5 × 10³/μL; range, 20–62 × 10³/μL; P < .001), and mildly increased plasma total protein concentrations (median, 6.3 g/dL; range, 5.6–6.7 g/dL; P < .001). Administration of hIVIgG was also associated with increases in fibrin/fibrinogen degradation products in all dogs (either 5 μg/mL or 10 μg/dL), thrombin-antithrombin III complexes (median, 7.2 ng/mL; range, 4.9–14.2 ng/mL; P < .001), and C-reactive protein concentrations (median, 2.5 mg/dL; range, 0.5–4.3 mg/dL; P < .01).
Conclusion and Clinical Importance: Administration of hIVIgG to dogs promotes hypercoagulability and an inflammatory state. This should be further evaluated and considered when using hIVIgG in dogs with IMHA or other prothrombotic conditions.