PubMed Health⌕ Search

Biomedical subjects

C E Short

Publications and source records attributed to C E Short.

At least 19 recordsLinked to original sources
PubMed2006

Clinical efficacy and safety of dexmedetomidine and buprenorphine, butorphanol or diazepam for canine hip radiography.

OBJECTIVES: To investigate the usefulness of dexmedetomidine for restraint and sedation during hip radiographic examination of hip-extended or stress-radiography views when combined with either buprenorphine, butorphanol or diazepam. METHODS: One hundred and twenty-seven client-owned clinically healthy golden retrievers or rottweilers were enrolled in a clinical trial that compared hip-extended and PennHIP methods for diagnosing hip dysplasia and were randomly allocated to receive dexmedetomidine or medetomidine in combination with buprenorphine, butorphanol or diazepam. Subjective assessments were made for response to pain, response to noise, palpebral reflex, muscle tone and overall quality of sedation; non-invasive physiological variables were also recorded. RESULTS: Overall quality of sedation was graded as good or excellent for dogs administered with a combination of butorphanol or diazepam. However, more dogs that received a combination involving buprenorphine had overall a relatively poorer quality of sedation and required additional administration of buprenorphine before the radiographic procedure could commence. Once sedated, clinically sufficient muscle relaxation accompanied by a very low proportion of dogs responding to pain or noise stimuli were observed in all treatment groups. Heart and respiratory rate, and procedure and recovery times were similar for all treatment groups, and no adverse events were observed during the study. CLINICAL SIGNIFICANCE: Dexmedetomidine sedative protocols, particularly in combination with butorphanol and diazepam, can be used effectively and safely in dogs for radiographic procedures.

Animals↗
PubMed2003

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.

Anesthesia↗
PubMed1999

Propofol anesthesia.

Although questions may still remain regarding the use of this unique sedative-hypnotic drug with anesthetic properties in high-risk patients, our studies have provided cardiopulmonary and neurological evidence of the efficacy and safety of propofol when used as an anesthetic under normal and selected impaired conditions in the dog. 1. Propofol can be safely and effectively used for the induction and maintenance of anesthesia in normal healthy dogs. Propofol is also a reliable and safe anesthetic agent when used during induced cardiovascular and pulmonary-impaired conditions without surgery. The propofol requirements to induce the safe and prompt induction of anesthesia prior to inhalant anesthesia with and without surgery have been determined. 2. The favorable recovery profile associated with propofol offers advantages over traditional anesthetics in clinical situations in which rapid recovery is important. Also, propofol compatibility with a large variety of preanesthetics may increase its use as a safe and reliable i.v. anesthetic for the induction and maintenance of general anesthesia and sedation in small animal veterinary practice. Although propofol has proven to be a valuable adjuvant during short ambulatory procedures, its use for the maintenance of general anesthesia has been questioned for surgery lasting more than 1 hour because of increased cost and marginal differences in recovery times compared with those of standard inhalant or balanced anesthetic techniques. When propofol is used for the maintenance of anesthesia in combination with a sedative/analgesic, the quality of anesthesia is improved as well as the ease with which the practitioner can titrate propofol; therefore, practitioners are able to use i.v. anesthetic techniques more effectively in their clinical practices. 3. Propofol can induce significant depression of respiratory function, characterized by a reduction in the rate of respiration. Potent alpha 2 sedative/analgesics (e.g., xylazine, medetomidine) or opioids (e.g., oxymorphone, butorphanol) increase the probability of respiratory depression during anesthesia. Appropriate consideration of dose reduction and speed of administration of propofol reduces the degree of depression. Cardiovascular changes induced by propofol administration consist of a slight decrease in arterial blood pressures (systolic, mean, diastolic) without a compensatory increase in heart rate. Selective premedicants markedly modify this characteristic response. 4. When coupled with subjective responses to painful stimuli, EEG responses during propofol anesthesia provide clear evidence that satisfactory anesthesia has been achieved in experimental dogs. When propofol is used as the only anesthetic agent, a higher dose is required to induce an equipotent level of CNS depression compared with the situation when dogs are premedicated. 5. The propofol induction dose requirement should be appropriately decreased by 20% to 80% when propofol is administered in combination with sedative or analgesic agents as part of a balanced technique as well as in elderly and debilitated patients. As a general recommendation, the dose of propofol should always be carefully titrated against the needs and responses of the individual patient, as there is considerable variability in anesthetic requirements among patients. Because propofol does not have marked analgesic effects and its metabolism is rapid, the use of local anesthetics, nonsteroidal anti-inflammatory agents, and opioids to provide postoperative analgesia improves the quality of recovery after propofol anesthesia. 6. The cardiovascular depressant effects of propofol are well tolerated in healthy animals, but these effects may be more problematic in high-risk patients with intrinsic cardiac disease as well as in those with systemic disease. In hypovolemic patients and those with limited cardiac reserve, even small induction doses of propofol (0.75-1.5 mg/kg i.v.) can produce profound hypotens

Anesthesia, General↗
PubMed1997

The use of propofol for induction of anaesthesia in dogs premedicated with acepromazine, butorphanol and acepromazine-butorphanol.

Cardiovascular, pulmonary and anaesthetic-analgesic responses were evaluated in 18 male and female dogs to determine the effect of the injectable anaesthetic propofol used in conjuction with acepromazine and butorphanol. The dogs were randomly divided into three groups. Dogs in Group A were premeditated with 0.1 mg/kg of intramuscular acepromazine followed by an induction dose of 4.4 mg/kg of intravenous propofol; Group B received 0.2 mg/kg of intramuscular butorphanol and 4.4 mg/kg of intravenous propofol; dogs in Group AB were administered a premeditation combination of 0.1 mg/kg of intramuscular acepromazine and 0.2 mg/kg of intramuscular butorphanol, followed by induction with 3.3 mg/kg of intravenous propofol. The induction dose of propofol was given over a period of 30-60 seconds to determine responses and duration of anaesthesia. Observations recorded in the dogs included heart and respiratory rates, indirect arterial blood pressures (systolic, diastolic and mean), cardiac rhythm, end-tidal CO, tension, oxygen saturation, induction time, duration of anaesthesia, recovery time and adverse reactions. The depth of anaesthesia was assessed by the response to mechanical noxious stimuli (tail clamping), the degree of muscle relaxation and the strength of reflexes. Significant respiratory depression was seen after propofol induction in both groups receiving butorphanol with or without acepromazine. The incidence of apnea was 4/6 dogs in Group B, and 5/6 dogs in Group AB. The incidence of apnea was also correlated to the rate of propofol administration. Propofol-mediated decreases in arterial blood pressure were observed in all three groups. Moderate bradycardia (minimum value > 55 beats/min) was observed in both Groups B and AB. There were no cardiac dysrhythmias noted in any of the 18 dogs. The anaesthetic duration and recovery times were longer in dogs premeditated with acepromazine/butorphanol.

Journal Article↗
PubMed1997

Evaluation of selected cardiopulmonary and cerebral responses during medetomidine, propofol, and halothane anesthesia for laparoscopy in dogs.

OBJECTIVES: To compare the dose-sparing effect of medetomidine on the propofol induction dose and concentration of halothane for maintenance of anesthesia during laparoscopy and to provide guidelines for effective and safe use of these anesthetics in dogs to ensure desirable perioperative analgesia. ANIMALS: 14 purpose-bred dogs. PROCEDURE: Cardiopulmonary and electroencephalographic responses were determined during 2 anesthesia protocols in dogs scheduled for laparoscopy. Fifteen minutes before anesthesia induction, all dogs received atropine sulfate (0.02 mg/kg of body weight, i.m.). Seven dogs were then given propofol (6.6 mg/kg, i.v.); anesthesia was maintained with halothane in oxygen. The other dogs were given medetomidine hydrochloride (10 micrograms/kg, i.m.) 5 minutes after administration of atropine sulfate; anesthesia was then induced by administration of propofol (2.8 mg/kg, i.v.) and was maintained with halothane in oxygen. RESULTS: The halothane concentration required for laparoscopy was lower in dogs given medetomidine. Anesthetic requirements were significantly increased during abdominal manipulation in both groups. Total amplitude of the electroencephalograph in medetomidine-treated dogs was not significantly lower than that in dogs not given medetomidine. Pulmonary responses were stable throughout all procedures. The primary cardiovascular response was an increase in blood pressure associated with the medetomidine-atropine preanesthetic combination. Significant differences in total amplitude or frequency shifts (spectral edge) of brain wave activity were not associated with surgical stimulation. CONCLUSION: Lack of neurologic changes during laparoscopy supports the efficacy of either medetomidine-propofol-halothane or propofol-halothane combinations at higher concentrations to provide desirable analgesia and anesthesia in this group of dogs.

Adrenergic alpha-Agonists↗
PubMed1996

Comparative responses to propofol anaesthesia alone and with alpha 2-adrenergic medications in a canine model.

Cardiovascular and pulmonary effects of propofol, a relatively new nonbarbiturate intravenous anaesthetic, were assessed and compared in 22 male and female dogs. Dogs in group 1 did not receive any premedication prior to 6.6 mg/kg IV propofol, group 2 was premedicated with atropine (0.02 mg/kg IM) and the alpha 2-agonist medetomidine (10 micrograms/kg IM), and group 3 received the same premedication agents as group 2, but the medetomidine effects were reversed by the alpha 2-antagonist atipamezole (30 micrograms/kg IV) after 30 min of anaesthesia. Each dog in groups 2 and 3 received a propofol induction dose of 2.2 mg/kg IV. The anaesthetic duration was shortest with propofol alone and prolonged with medetomidine as a premedication which was reversible with atipamezole. In group 1, the most prominent effects were a temporary drop in diastolic arterial blood pressure (26% and 24%) at 2 and 5 min post-propofol, respectively and a drop in respiratory frequency (41%) 2 min after propofol induction. Similar respiratory depression was observed in groups 2 and 3 (20% and 48%, respectively) at the same time. Apnea was not observed. An increase in systemic arterial blood pressure was observed throughout the trial in groups 2 and 3 until dogs recovered or were reversed with atipamezole. Medetomidine significantly reduces propofol dosage requirements. Safe and effective injectable anaesthesia was produced by propofol in this group of dogs. The frequency of respiratory depression would suggest in clinical usage, the practitioner should be aware oxygen supplementation is the treatment of choice should apnea occur.

Adjuvants, Anesthesia↗
PubMed1995

Effects of medetomidine administration on intracranial pressure and cardiovascular variables of isoflurane-anesthetized dogs.

Intracranial pressure and cardiovascular variables after IV administration of medetomidine (0.03 mg/kg of body weight) were evaluated in 6 healthy, mixed-breed dogs anesthetized with 1.3% end-tidal isoflurane concentration and mechanically ventilated to normocapnia (PaCO2, 35 to 45 mm of Hg). Baseline values were determined for intracranial pressure, heart rate, arterial blood pressure, cardiac output, mean pulmonary artery pressure, pulmonary capillary wedge pressure, central venous pressure, end-tidal CO2 tension and isoflurance concentration, arterial pH and CO2 and O2 tensions, and core body temperature. Cerebral perfusion pressure, cardiac index, systemic and pulmonary vascular resistances, plasma HCO3- concentration, and base excess were calculated. Intracranial pressure was measured, using a calibrated, fiberoptic transducer placed within the brain parenchyma and secured to the calvarium by means of a subarachnoid bolt. Cardiac output was determined by thermodilution. End-tidal CO2 tension and isoflurane concentration were determined, using an infrared gas analyzer. Administration of medetomidine did not change intracranial pressure, but was associated with significant (P < 0.05) decreases in values for heart rate, cardiac index, end-tidal CO2, and HCO3- and with significant increases in systolic, mean, and diastolic pressure; pulmonary artery pressure; systemic vascular resistance; central venous pressure; and pulmonary capillary wedge pressure.

Adrenergic alpha-Agonists↗
PubMed1995

Quantitative electroencephalographic evaluation to determine the quality of analgesia during anesthesia of horses for arthroscopic surgery.

We compared the anesthetic combination of detomidine, ketamine, and halothane in control horses not undergoing apparently painful procedures with that in horses during arthroscopic surgery. The effectiveness of this regimen in suppressing neurologic response to surgery was, thus, evaluated. In this study, significant differences were not observed in electroencephalographic total amplitude, spectral edge, or beta-to-delta frequency ratio between surgically treated and nonsurgically treated (control) horses. On the basis of its attenuation of encephalographic responses, we conclude that detomidine (20 micrograms/kg of body weight, IV) and ketamine (2.2 mg/kg, IV) induction of anesthesia followed by maintenance with halothane is an effective regimen for control of pain in horses during arthroscopic surgery. The insignificant frequency changes observed without any other signs of inadequate anesthesia or pain may indicate a surgical stress response. We hypothesize that brain activity monitoring may give an earlier index to initiation of surgically induced stress than do hormonal responses, because endocrine alterations are not as rapidly perceived as is the electroencephalogram. Analysis of spectral edge frequency changes could be used to evaluate anesthetic regimens to find those that cause the least stress to the CNS during surgery in horses. Differences in species responses to an anesthetic agent or the regimen's effectiveness in prevention of pain during surgery may be identified by adoption of the study model. Evaluation of cardiopulmonary variables during anesthesia, with and without surgery, did not reveal any alterations that would be relevant to CNS responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1993

Reduction of isoflurane anesthetic requirement by medetomidine and its restoration by atipamezole in dogs.

The isoflurane-sparing effect of the alpha 2-adrenergic agonist medetomidine (30 micrograms/kg of body weight, IV) was tested in 7 dogs, using a blinded, randomized-block study design. The baseline minimal alveolar concentration (MAC) of isoflurane was 1.18 vol% (95% confidence interval [0.97,1.39]). Medetomidine significantly (P < 0.003) reduced isoflurane MAC by 47.2%. Atipamezole (0.3 mg/kg, IV), an alpha 2-adrenergic antagonist, completely reversed the effect of medetomidine on isoflurane MAC. Atipamezole alone did not significantly alter isoflurane MAC. After medetomidine administration, marked bradycardia developed in all dogs and persisted for more than 2 hours. Mean arterial blood pressure increased acutely, but later decreased, and hypotension persisted for more than 2 hours. Atipamezole reversed the bradycardic and hypotensive effects of medetomidine. Results of this study indicate that medetomidine may be useful in clinical cases in which isoflurane MAC-reduction is desirable and that atipamezole might be used to reverse desirable and undesirable effects of medetomidine during isoflurane anesthesia.

Adrenergic alpha-Agonists↗
PubMed1992

Advantages and guidelines for using halothane.

Halothane is a frequently used agent. Its cost is inexpensive. Halothane is a safe and effective anesthetic agent if used properly. Proper usage includes adjusting the concentration administered to produce adequate anesthesia for the procedure without excess depression of cardiac, respiratory, and neurologic function. Proper monitoring of the patient indicates the adjustments needed in concentration or needed medications or procedures to increase safe usage. Potent tranquilizers, sedatives, and analgesics used as preanesthetics during halothane anesthesia or the early postanesthetic period may produce profound changes in anesthetic concentrations required or physiologic responses to the combined medications.

Anesthesia, Inhalation↗
PubMed1992

The case for high gas flows.

High gas flows provide a higher margin of safety and fewer physiologic complications for extended anesthetic periods. The veterinarian should consider personnel, anesthetic, and monitoring equipment and the surgical procedure requiring anesthesia before making a final decision on which flow rates are appropriate.

Anesthesia, Inhalation↗
PubMed1992

Comparison of neurologic responses to the use of medetomidine as a sole agent or preanesthetic in laboratory beagles.

Different dose regimens of medetomidine (a potent alpha 2-adrenergic agonist), adding up to a combined dose of 80 micrograms/kg, were administered to laboratory beagles to determine physiologic responses including neurologic. The study was intended to determine EEG responses where sufficient sedative and analgesic effects are reached with medetomidine and in contrast its effects when used with ketamine or halothane. Cardiopulmonary responses were very similar in each dose regimen, showing the characteristic properties of single doses of 80 micrograms/kg of medetomidine. Effective sedative and analgesic duration seemed to be a function of when the largest dose was administered. Adequate additional sedative and analgesic could be gained from injections at doses of half of the initial one. The potent sedative and analgesic effects of medetomidine confirmed by neurologic evaluation supports its potential use as a premedication to general anesthesia in dogs. In this study, 2 different doses of medetomidine were also tested as premedication to both ketamine HCI and halothane anesthesia. Neorologic responses were determined at the same time cardiopulmonary parameters, anesthetic quality, and dose requirements were recorded. Medetomidine was found to have favorable qualities in conjunction with these anesthetics. Cardiopulmonary parameters remained satisfactory in both groups as preanesthetic medication prior to halothane, but no additional benefits could be seen from doses of 40 micrograms/kg medetomidine compared to 20 micrograms/kg, except a significant 30% reduction in halothane requirement. The positive chronotropic and inotropic properties of ketamine restored the medetomidine-induced bradycardia and produced a short anesthetic period of 15 to 30 min depending on the dose of medetomidine. The quality of anesthesia was better when 40 micrograms/kg medetomidine was used, but recovery was quicker with 20 micrograms/kg medetomidine. Medetomidine significantly reduced cerebral activity as demonstrated by recordings of total amplitude and frequency evaluation of the EEG with compressed spectral analysis. This analytical method was effective in confirming clinical signs of sedation, analgesia, and anesthesia in canine subjects.

Analgesia↗
PubMed1991

Effects of anticholinergic treatment on the cardiac and respiratory systems in dogs sedated with medetomidine.

Alpha 2-adrenergic agonists are often used for sedation and, or, analgesia in dogs, but they are often associated with bradycardia and in some animals with atrioventricular heart block. In this study, atropine or glycopyrrolate either helped to maintain the heart rates or were effective in increasing reduced heart rates of dogs treated with medetomidine. In the process, however, cardiac dysrhythmias often developed. These dysrhythmias were predominantly associated with the combined responses to the medetomidine and the anticholinergic agent because there were no significant changes in respiratory function. A reduced blood oxygen content or increased blood carbon dioxide can contribute to cardiac irritability. Atropine and glycopyrrolate were more effective in preventing bradycardia and had less undesirable side effects when they were given before the administration of medetomidine.

Adrenergic alpha-Agonists↗
PubMed1989

Medetomidine as a preanesthetic prior to ketamine-HCL and halothane anesthesia in laboratory beagles.

The potent sedative and analgesic effects of medetomidine confirm its potential use as a premedication to general anesthesia in dogs. In this study two different doses of medetomidine were tested as premedication to both ketamine HCl and halothane anesthesia in groups consisting of 4 laboratory beagles each. Cardiopulmonary parameters, anesthetic quality and dose requirements were recorded. Medetomidine was found to have favorable qualities in conjunction with these anesthetics. Atropine prevented the profound bradycardia and sinus arrhythmia seen with medetomidine alone. Cardiopulmonary parameters remained satisfactory in both groups, but no additional benefits could be seen from doses of 40 micrograms/kg medetomidine compared to 20 micrograms/kg, except a significant 30% reduction in halothane requirement. The positive chronotropic and inotropic properties of ketamine restored the medetomidine induced bradycardia and produced a short anesthetic period of 15-30 min depending on the dose of medetomidine. The quality of anesthesia was good in both groups, but recovery was quicker and smoother in the group with 20 micrograms/kg medetomidine.

Adrenergic alpha-Agonists↗
PubMed1989

Comparison of three different dose regimes of medetomidine in laboratory beagles.

Different dose regimes of medetomidine (a potent alpha 2-adrenergic agonist), adding up to a combined dose of 80 micrograms/kg, were administered to laboratory beagles to determine the possible superiority of any particular regime. The study was intended to mimic a clinical situation where sufficient sedative and analgesic effect was not reached with the initial dose and an additional dose would have to be administered. Cardiopulmonary responses were very similar in each dose regime, showing the characteristic properties of single doses of 80 micrograms/kg of medetomidine as reported in the literature. Effective sedative and analgesic duration seemed to be a function of when the largest dose was administered. Adequate additional sedative and analgesic effect could be gained from the second injection at doses of half of the initial one.

Adrenergic alpha-Agonists↗
PubMed1989

A comparison of xylazine, acepromazine, meperidine and medetomidine as preanesthetics to halothane anesthesia in dogs.

The preanesthetic properties of medetomidine, a novel alpha 2-adrenergic agonist, were compared to the preanesthetic properties of acepromazine, zylazine and meperidine prior to halothane anesthesia. The premedications were given to 23 randomly selected laboratory beagles in doses with sedative effects equal to the 10 micrograms/kg used in the medetomidine group. These dogs also received 0.04 mg/kg of atropine prior to the preanesthetic. A group of 7 dogs with a high medetomidine dose (40 micrograms/kg) was included in the study. Cardiopulmonary and respiratory parameters were recorded at 10 min intervals during surgical stimulus. Dogs receiving 40 micrograms/kg of medetomidine showed bradycardia, but higher blood pressures than dogs in the other groups. Adequate oxygen saturations and perfusion were recorded in all groups. The low 10 micrograms/kg dose of medetomididine had a halothane sparing effect comparable to the other premedications, while the 40 micrograms/kg of medetomidine group showed a clear decrease in halothane consumption. The sedative effect of 10 micrograms/kg of medetomidine was in some instances inadequate for proper manipulation of the dogs, but 40 micrograms/kg produced excessive sedation. Atropine was found to counteract the medetomidine induced bradycardia.

Acepromazine↗
PubMed1988

Cardiac dysrhythmias during anesthesia for cervical decompression in the dog.

In a retrospective study, the risk for cardiac dysrhythmias was evaluated in dogs undergoing ventral decompression and/or fenestration of the cervical spine (CERV) and compared with that for dogs undergoing dorsal laminectomy for decompression of the thoracic or lumbar spine (TL). The dogs in the CERV subset (48 dogs) tended to be heavier and older than the dogs in the TL subset (111 dogs). There was no apparent bias detected in treatment before anesthesia and surgery. The risk for dysrhythmias was 2.5 times greater in the CERV subset, compared with that in the TL subset (P less than 0.01). The risk for ventricular premature contraction was 3.5 times higher in the CERV group (P less than 0.05). Bradycardia was found in 6 dogs from the CERV subset and was not found in any dogs from the TL subset. A logistic model was derived from the data and may be used to evaluate the risk for dysrhythmias in similar patients undergoing similar surgery and anesthesia. This model uses age, preoperative heart rate, and site of surgery (CERV or TL) to estimate the risk.

Anesthesia↗