Search PubMed⌕ Search

Biomedical subjects

W McDonell

Publications and source records attributed to W McDonell.

15 recordsLinked to original sources

Assessment of lithium dilution cardiac output as a technique for measurement of cardiac output in dogs.

OBJECTIVES: To determine agreement of cardiac output measured by use of lithium dilution cardiac output (LiDCO) and thermodilution cardiac output (TDCO) techniques in dogs and to determine agreement of low- and high-dose LiDCO with TDCO. ANIMALS: 10 dogs (7 males, 3 females). PROCEDURE: Cardiac output was measured in anesthetized dogs by use of LiDCO and TDCO techniques. Four rates of cardiac output were induced by occlusion of the caudal vena cava, changes in depth of anesthesia, or administration of dobutamine. Lithium dilution cardiac output was performed, using 2 doses of lithium chloride (low and high dose). Each rate of cardiac output allowed 4 comparisons between LiDCO and TDCO. RESULTS: 160 comparisons were determined of which 68 were excluded. The remaining 92 comparisons had values ranging from 1.10 to 12.80 L/min. Intraclass correlation coefficient (ICC) between low-dose LiDCO and TDCO was 0.9898 and between high-dose LiDCO and TDCO was 0.9896. When all LiDCO determinations were pooled, ICC was 0.9894. For determinations of cardiac output < 5.0 L/min, ICC was 0.9730. Mean +/- SD of the differences of TDCO minus LiDCO for all measurements was -0.084+/-0.465 L/min, and mean of TDCO minus LiDCO for cardiac outputs < 5.0 L/min was -0.002+/-0.245 L/min. CONCLUSIONS AND CLINICAL RELEVANCE: The LiDCO technique is a suitable substitute for TDCO to measure cardiac output in dogs. Use of LiDCO eliminates the need for catheterization of a pulmonary artery and could increase use of cardiac output monitoring, which may improve management of cardiovascularly unstable animals.

Anesthesia↗

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.

Analgesics, Non-Narcotic↗

Diagnostic evaluation of cats with seizure disorders: 30 cases (1991-1993).

OBJECTIVE: To investigate causes of seizure disorders in cats. DESIGN: Case series. ANIMALS: 30 cats referred to the Ontario Veterinary College for recurrent seizures. PROCEDURES: Signalment and seizure pattern were evaluated. Diagnostic procedures included physical, neurologic, and fundic examinations; CBC; serum biochemical analyses, including determination of pre- and postprandial bile acid concentrations; urinalysis; serologic assays for FeLV and feline immunodeficiency virus, feline infectious peritonitis, and Toxoplasma gondii, magnetic resonance imaging of the brain; CSF analysis; and neuropathologic examination of euthanatized cats and of surgical biopsy specimens. RESULTS: All cats were found to have structural brain diseases; nonsuppurative meningoencephalitis of unknown cause was found in 14 cats, feline ischemic encephalopathy in 6, meningioma in 2, polycythemia vera with secondary brain lesions in 2, posttraumatic epilepsy in 1, and cerebral abscess in 1. A definitive diagnosis could not be reached in 4 cats. CLINICAL IMPLICATIONS: The most common cause of seizures in cats is structural brain disease. Structural brain lesions often can be detected on the basis of seizure pattern and results of neurologic examination. Cerebrospinal fluid analysis and brain imaging are essential to determine the cause of these lesions. Causes of seizures found in the cats of this study differ from those reported to be the most common. Nonsuppurative meningoencephalitis of unknown origin appears to be a frequent cause of neurologic disorders in cats, including seizure disorders. Feline ischemic encephalopathy appears to exist in a milder form than the classic disease and may be a common cause of seizures in cats.

Animals↗

Clinical management and outcome of cats with seizure disorders: 30 cases (1991-1993).

OBJECTIVE: To determine outcome of clinical management of cats with seizure disorders. DESIGN: Case series. ANIMALS: 30 cats referred to the Ontario Veterinary College for recurrent seizures. PROCEDURES: Treatment was dictated by the cat's seizure frequency and by the underlying cause. Cats that were having cluster seizures or status epilepticus at the time of admission were treated orally with phenobarbital and with constant IV administration of diazepam. The other cats were treated with long-term oral administration of phenobarbital if the frequency of their seizures justified it. Follow-up included evaluation of seizure frequency, serum antiepileptic drug concentrations, and hematologic and serum biochemical values. Outcome was documented on the basis of survival and seizure frequency at the end of the followup period, which ranged from 3 to 21 months. RESULTS: 6 cats were euthanatized without any therapeutic attempts at the owners' request. Twenty of the remaining 24 cats were alive at the time of final follow-up. Seventeen had a good outcome; 11 were not having any more seizures and 6 were having a low frequency of seizures. For 3 other cats, seizures were not well controlled. Four cats had been euthanatized (2 because of intractable seizures, 1 because of postcraniotomy complications, and 1 because the owners did not want to pursue treatment). CLINICAL IMPLICATIONS: Results suggest that severity of seizure disorder in cats is not a good predictor of outcome and that aggressive treatment is often rewarding, even in the most severe cases.

Administration, Oral↗

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.

Acid-Base Equilibrium↗

Evidence that halothane anaesthesia induces intracellular translocation of surface coat and Golgi response in equine pulmonary intravascular macrophages.

The pulmonary intravascular macrophages (PIMs) of horse contain a unique electron-dense globular surface-coat which is arranged in a linear fashion in conformity with the contours of the cell membrane. The coat is sensitive to heparin treatment and to the digestive effect of lipolytic lipase, suggesting that the coat is predominantly composed of lipoproteins. During the present study, ultrastructural features of PIMs were analysed after exposing horses to halothane inhalation which was chosen as the model agent of lipid-soluble anaesthetic. The surface-coat showed acute sensitivity to halothane by disappearing almost completely from the surface after 1-2 h of exposure. The cell membranes were thrown into extraordinary arrays of lamellipods, pseudopods and veils. Concurrently, the globular units of the coat were translocated into the endosomal-lysosomal system, most probably via receptor-mediated endocytosis. There was a high profile of the expanded Golgi apparatus especially the trans Golgi network (TGN) in close association with the centrioles and microtubules. Cytochemistry revealed an enrichment of the Golgi complex with acid phosphatase activity. On the other hand, halothane showed an inhibitory effect on the lysosomal acid phosphatase of the PIMs. It is proposed that the Golgi response occurred as an obligatory concomitant of internalization of the surface-coat and its subsequent passage through endosomal-lysosomal system. The acid phosphatase activity as a marker enzyme of the expanded Golgi is correlated with metabolic effects of the internalized coat which is unique to the pulmonary intravascular macrophages. Furthermore, the intense expression of acid phosphatase at the Golgi level of the PIMs may signify a component of secretory phenotype in order to produce vasoactive mediators at the onset of stressful stimuli triggered by the halothane anesthesia.

Acid Phosphatase↗

Influenza hemagglutination inhibiting activity in respiratory mucus from horses with chronic obstructive pulmonary disorders (heaves syndrome).

Samples of mucus from the lower trachea were collected from 53 horses with chronic obstructive pulmonary disease and from 24 clinically normal horses. Serum samples were collected from 35 of the horses with chronic obstructive pulmonary disease and from the 24 normal horses. Samples were tested for inhibition of hemagglutination by influenza A equine 1 and 2 viruses. There were high levels of hemagglutination inhibiting activity against influenza A equine 1 in mucus samples from horses with chronic obstructive pulmonary disease.

Animals↗

Equine postanesthetic forelimb lameness: intracompartmental muscle pressure changes and biochemical patterns.

Intracompartmental muscle pressures were recorded from the right and left forelimbs (extensor carpi radialis, triceps brachii) of healthy horses maintained in left lateral recumbency while under deep halothane anesthesia for 180 to 240 minutes. Cardiac output, blood pressure, blood gases, and acid-base status were monitored throughout the anesthesia, and electrolyte levels (Ca2+, P+, K+, Cl-, Na+) and enzyme activities (aspartate aminotransferase (AST), creatine phosphokinase (CPK), and blood lactate) were monitored for 7 days. Postanesthetic forelimb lameness was produced in 5 of the 6 horses with this prolonged anesthetic regime. This lameness was associated with muscle plaque formation and clinical signs which were similar to the forelimb lameness sometimes seen in horses after surgical anesthesia. Plasma protein, serum calcium, plasma sodium, and blood urea nitrogen concentrations did not change, whereas significantly increased hematocrit, plasma potassium, and serum inorganic phosphate values were seen at the end of anesthesia, along with a decrease in plasma chloride values. Blood lactate, serum AST, and serum CPK activities were significantly high in the postanesthetic period, although the sequence of the changes differed. Intracompartmental muscle pressures were higher in the left forelimb adjacent to the floor (contact limb), and in the instance of the triceps of the contact limb, the pressures were sufficiently high (greater than 30 mm of Hg) that they may have compromised capillary blood flow. However, these high intracompartmental muscle pressures did not persist when positional changes of the horses were introduced at the end of the anesthetic period. There was no correlation between the severity of postanesthetic lameness and any of the measured values. The results demonstrate an experimentally induced postanesthetic lameness which was primarily related to the development of a myositis. Although the causative factors of this myositis may be multiple, the present study implicates local hypoxia in that increased blood lactate and inorganic phosphate values preceded that increased CPK activity. Intracompartmental muscle pressure in the contact limb were possibly high enough to have restricted local capillary blood flow.

Anesthesia, Inhalation↗