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Biomedical subjects

G J Benson

Publications and source records attributed to G J Benson.

At least 19 recordsLinked to original sources
PubMed2000

Evaluation of short-term increased intraocular pressure on flash- and pattern-generated electroretinograms of dogs.

OBJECTIVE: To determine the electrodiagnostic and histologic response of short-term increases of intraocular pressure (IOP) on transient pattern electroretinograms (PERG) and flash electroretinograms (FERG) in the eyes of dogs. ANIMALS: 8 healthy mixed-breed dogs. PROCEDURE: Transient PERG and FERG waveforms were recorded from dogs (while anesthetized) as IOP was increased from baseline (7 to 19 mm Hg) to 90 mm Hg. One hundred mean PERG responses and a single FERG response were recorded at each step during 3 recording sessions. Globes of each dog were enucleated after euthanasia on posttreatment day 7 and evaluated by a pathologist. RESULTS: Increases in spatial frequency resulted in decreased amplitudes of N2 (second negative PERG peak). Increases in IOP resulted in decreases in all 3 PERG waveforms and the FERG waveform. All values began to return to baseline after short-term increases in IOP on day 0, and waveforms were not significantly different on posttreatment days 3 and 7 CONCLUSIONS: Data suggest that short-term increases in IOP affect PERG and FERG waveforms, and PERG waveforms are more sensitive to increases in IOP Differences were not detected between treated and control eyes on histologic examination. Further studies are necessary to determine at what IOP permanent damage to ganglion and photoreceptor cells will develop and whether PERG is a reliable clinical diagnostic technique for use in dogs to reveal retinal damage that is secondary to increased IOP prior to changes in waveforms generated by FERG in dogs.

Animals↗
PubMed2000

Duration of nonresponse to noxious stimulation after intramuscular administration of butorphanol, medetomidine, or a butorphanol-medetomidine combination during isoflurane administration in dogs.

OBJECTIVE: To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO). ANIMALS: 6 healthy dogs. PROCEDURE: Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 microg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 microg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, end-tidal CO2 and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected. RESULTS: Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean +/- SD) was 0.0+/-0.0, 1.5+/-1.5, 2.63+/-0.49, and 5.58+/-2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone. CONCLUSION AND CLINICAL RELEVANCE: During ISO-induced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone.

Analgesics, Non-Narcotic↗
PubMed1999

Techniques for evaluation of right ventricular relaxation rate in horses and effects of inhalant anesthetics with and without intravenous administration of calcium gluconate.

OBJECTIVES: To determine the most repeatable method for evaluating right ventricular relaxation rate in horses and to determine and compare effects of isoflurane or halothane with and without the added influence of intravenously administered calcium gluconate on right ventricular relaxation rates in horses. ANIMALS: 6 Thoroughbred horses from 2 to 4 years old. PROCEDURE: 6 models (2 for monoexponential decay with zero asymptote, 3 for monoexponential decay with variable asymptote, and 1 for biexponential decay) for determining right ventricular relaxation rate were assessed in conscious and anesthetized horses. The 2 methods yielding the most repeatable results then were used to determine right ventricular relaxation rates in horses anesthetized with isoflurane or halothane before, during, and after i.v. administration of calcium gluconate. Right ventricular pressure was measured, using a catheter-tip high-fidelity pressure transducer, and results were digitized at 500 Hz from minimum rate of change in ventricular pressure. RESULTS: 2 models that used monoexponential decay with zero asymptote repeatedly produced an estimate for relaxation rate and were used to analyze effects of anesthesia and calcium gluconate administration on relaxation rate. Isoflurane and halothane each prolonged right ventricular relaxation rate, with greater prolongation evident in halothane-anesthetized horses. Calcium gluconate attenuated the anesthesia-induced prolongation in right ventricular relaxation rate, with greater response obtained in isoflurane-anesthetized horses. CONCLUSIONS AND CLINICAL RELEVANCE: Right ventricular relaxation rate in horses is assessed best by use of a monoexponential decay model with zero asymptote and nonlinear regression. Intravenous administration of calcium gluconate to isoflurane-anesthetized horses best preserves myocardial relaxant function.

Anesthetics, Inhalation↗
PubMed1999

Hemodynamic effects of ionized calcium in horses anesthetized with halothane or isoflurane.

OBJECTIVES: To evaluate the effects of halothane and isoflurane on cardiovascular function and serum total and ionized calcium concentrations in horses, and to determine whether administration of calcium gluconate would attenuate these effects. ANIMALS: 6 clinically normal adult Thoroughbreds. PROCEDURE: Catheters were inserted for measurement of arterial blood pressures, pulmonary arterial blood pressures, right ventricular pressure (for determination of myocardial contractility), right atrial pressure, and cardiac output and for collection of arterial blood samples. Anesthesia was then induced with xylazine hydrochloride and ketamine hydrochloride and maintained with halothane or isoflurane. An i.v. infusion of calcium gluconate was begun 75 minutes after anesthetic induction; dosage of calcium gluconate was 0.1 mg/kg of body weight/min for the first 15 minutes, 0.2 mg/kg/min for the next 15 minutes, and 0.4 mg/kg/min for an additional 15 minutes. Data were collected before, during, and after administration of calcium gluconate. RESULTS: Halothane and isoflurane decreased myocardial contractility, cardiac index, and mean arterial pressure, but halothane caused greater depression than isoflurane. Calcium gluconate attenuated the anesthetic-induced depression in cardiac index, stroke index, and maximal rate of increase in right ventricular pressure when horses were anesthetized with isoflurane. When horses were anesthetized with halothane, a higher dosage of calcium gluconate was required to attenuate the depression in stroke index and maximal rate of increase in right ventricular pressure; cardiac index was not changed with calcium administration. CONCLUSIONS AND CLINICAL RELEVANCE: I.v. administration of calcium gluconate may support myocardial function in horses anesthetized with isoflurane.

Anesthesia, Inhalation↗
PubMed1999

Hemodynamic effects of thyroidectomy in sedentary horses.

OBJECTIVE: To investigate hemodynamic effects of thyroidectomy in horses at rest. ANIMALS: 6 healthy aged Quarter Horse mares. PROCEDURE: Horses were monitored for 5 months before and 4 weeks after thyroidectomy and for an additional 4 weeks after administration of thyroid hormone supplement (2.5 microg of thyroxine/kg of body weight, PO, q 12 h, and 0.6 microg of triiodothyronine/kg, PO, q 12 h). Responses to thyroid-stimulating hormone (TSH) were measured before and 4 weeks after thyroidectomy. Other variables monitored daily were resting rectal temperature (T), heart rate (HR), respiratory rate (RR), and body weight (BW). Monthly cardiac output (Q), blood volume (BV), plasma volume (PV), standard electrocardiographic measures, systolic and right ventricular blood pressure, and HR responses were determined after IV administration of isoproterenol and phenylephrine. Variables were analyzed by use of repeated-measures ANOVA. RESULTS: Complete thyroidectomy was confirmed by minimal response to TSH 4 weeks after surgery. Resting HR, RR, T, Q, and beta-adrenergic responsiveness to isoproterenol decreased significantly after thyroidectomy. Resting T, Q, and beta-adrenergic responsiveness increased after administration of supplement and was not significantly different from euthyroid values. Blood volume and PV increased significantly after thyroidectomy but did not return to euthyroid values despite administration of supplement. Response to phenylephrine was minimally different between treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Thyroidectomy in horses caused decreased resting HR, RR, T, Q, and isoproterenol responsiveness and increased BV, PV, PQ interval, and QT interval corrected for HR. Some of these surgically induced changes appeared to be partially reversed by administration of thyroid hormone supplement.

Adrenergic alpha-Agonists↗
PubMed1998

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 micrograms/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 micrograms/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.

Adjuvants, Anesthesia↗
PubMed1996

Ability of flumazenil, butorphanol, and naloxone to reverse the anesthetic effects of oxymorphone-diazepam in dogs.

OBJECTIVE: To evaluate the ability of flumazenil (FLU), butorphanol (BUT), and naloxone (NAL) to reverse the anesthetic effects of oxymorphone-diazepam in dogs. ANIMALS: 6 healthy adult mixed-bread dogs. PROCEDURE: Dogs were randomly assigned to each of 6 reversal treatment groups. In each experiment, oxymorphone (0.22 mg/kg of body weight, i.v.) and diazepam (0.22 mg/kg. i.v.) were given sequentially 15 minutes after glycopyrrolate (0.01 mg/kg, i.v.) administration. Physiologic saline solution (SAL; 1 ml), FLU (0.01 mg/kg), BUT (0.44 mg/kg), or NAL (0.06 mg/kg) alone, or FLU-BUT or FLU-NAL (same dosages) was given i.v. as a reversal treatment 15 minutes after oxymorphone-diazepam administration. An individual unaware of the treatment protocol recorded time to extubation, sternal recumbency, and walking. RESULTS: Time to extubation was significantly (P < 0.05) less with BUT, NAL, FLU-BUT, or FLU-NAL treatment, compared with that for SAL treatment. Time to sternal recumbency was less with BUT, NAL, FLU-BUT, or FLU-NAL treatment, compared with that for SAL treatment. Time to walking was less with FLU-BUT or FLU-NAL treatment, compared with that for SAL treatment. CLINICAL IMPLICATIONS: Flumazenil, in combination with BUT or NAL, can be used to reverse the anesthetic effects of oxymorphone-diazepam in dogs.

Adjuvants, Anesthesia↗
PubMed1996

Acid-base and electrolyte effects of shortening steeplechase in a three-day-event.

This study was designed to characterise the acid-base and electrolyte effects of shortening the distance required during steeplechase (Phase B) in the face of hot and humid weather conditions during a treadmill-simulated Speed and Endurance test. Eight conditioned Thoroughbred horses underwent 3 randomised permutations of a standardised exercise test on a high speed treadmill. Each test consisted of trotting at 3.7 m/s for 10 min (Phase A); galloping at 11 m/s (Phase B) for 4 (cool laboratory conditions), 3 (hot and humid), or 2 (hot and humid) min; trotting at 3.7 m/s for 30 min (Phase C); and walking at 1.8 m/s for 10 min (Phase X). The treadmill slope was 4% for trotting and galloping and 0% for walking. Cool versus hot and humid conditions were 20 degrees C and 50-60% relative humidity vs. 26-28 degrees C and 80-85% relative humidity, respectively. Pulmonary artery blood samples were obtained at rest prior to exercise (Rest); at the end of Phases A (A10) and B (B2-4); at 10 (C10), 20 (C20) and 30 (C30) min through Phase C; and at 5 min into Phase X (X5). Additional samples for lactate (LA) and glucose (GLC) analysis were obtained 5 min into Phase C (C5) and at the end of Phase X (X10). Samples were analysed for packed cell volume (PCV), haemoglobin (HB), total plasma protein (TP), sodium (Na), potassium (K), chloride (Cl), anion gap (AG), plasma glucose (GLC) and lactate (LA), pH, PCO2, bicarbonate (HCO3) and base excess (BE). Shortening steeplechase distance by 50% under hot and humid conditions (2 min B) resulted in a consistent return to control measurements (4 min B) only for plasma LA. Changes in PCV, HB, TP, K and Cl were related more to the longer galloping distance in the 4 min B trials than to hot vs. cold laboratory conditions. Alternatively, changes in LA, GLC, pH, PCO2 and AG were more related to hot and humid laboratory conditions than they were to galloping distance. These latter variables, when combined with physical measures such as core temperature, bodyweight loss, point of fatigue on Phase C and recovery heart rates may serve as the best monitors of positive responses in future studies of proposed modifications to Phase C, rather than those variables which were more distance than weather-related.

Acid-Base Equilibrium↗
PubMed1995

Physiological effects of shortening steeplechase in a 3-day-event.

Various methods for modifying the Speed and Endurance portion (Day 2) of the 3-day-event have been proposed to aid horses in dealing with the hot and humid conditions expected during the next Olympic 3-day-events in Atlanta, Georgia USA in 1996. This study was designed to characterise the effects of shortening the distance required during the steeplechase (Phase B) in the face of Atlanta-like hot and humid weather conditions. Eight conditioned Thoroughbred horses (mean +/- s.e.m. age 3.75 years, range 3-5 years) underwent 3 randomised permutations of a standardised exercise test on a high speed treadmill. Each test consisted of trotting at 3.7 m/s for 10 min (Phase A); galloping at 11 m/s (Phase B) for 4 (cool, control laboratory conditions), 3 (hot and humid), or 2 (hot and humid) min; trotting at 3.7 m/s for 30 min (Phase C); and walking at 1.8 m/s for 10 min (Phase X). Subjects had Swan-Ganz catheters inserted into the pulmonary artery (PA) for measuring core temperature (PAT) in mixed venous blood every 2 min. Heart rate (HR) was measured by an on-board HR computer every 2 min. Rectal temperature (RT) was measured at the beginning (RTzero) and end (RT10) of Phase X using a mercury rectal thermometer as under typical field conditions. Pre- and post exercise bodyweights (bwt) were determined on a digital electronic scale. The point on Phase C at which each horse visibly fatigued and drifted toward the back of the treadmill was defined as the point of fatigue. Differences between treatments were tested for significance (P < 0.05) by repeated measures, Student-Neuman-Keul's and Student's tests where appropriate. Heart rate increased (mean 115.7-136.1) with the onset of trotting exercise in Phase A (P < 0.05), increased further with Phase B galloping (mean +/- s.e.m. 187.8-193.7, P < 0.05) and decreased with a return to trotting during Phase C (mean 108-130.5, P < 0.05) for all 3 treatments. Through the end of Phase C, there were no differences in HR between treatments (P > 0.05). From 3-10 min in Phase X (recovery), HR after 2 min B (mean 81.3-91) were lower than after 3 min B (mean +/- s.e.m. 98.4-100.5, P < 0.05) and were no different than 4 min B HR (mean 85.9-94.8, P > 0.05). Pulmonary artery blood temperature increased (mean 38.1-38.7) with trotting in Phase A (P < 0.05), increased further with Phase B galloping (mean 39.4-40.2, P < 0.05) for all 3 treatments and then decreased (mean +/- s.e.m. 39.3-39.9, P < 0.05) during Phase C under cool conditions (4 min B) but plateaued or continued to rise slightly under hot and humid conditions (mean 39.7-40.2). Throughout Phases C and X, PAT was lower for 4 min B than for either hot and humid treatment (P < 0.05). Bodyweight decreased after exercise for all treatments (P < 0.05) with the largest bwt loss (mean 10.9 kg) after 3 min B (P < 0.05) followed by 2 min B (8.3 kg) and then by 4 min cool B (6.5 kg). Point of fatigue was different between the 3 treatments (P < 0.05), with 4 min B the longest (mean +/- s.e. 24.8 min), followed by 2 min B (21.8 min), and then 3 min B (16.3 min). Rectal temperature was not different between the 3 treatments (P > 0.05), but there was a trend for both RTzero and RT10 to be highest after the 3 min B, lower after the 2 min B, and lowest after the 4 min cool B. It was concluded that there was a progressive gain in restoring cool weather performance and recovery by a progressive shortening of Phase B under hot and humid conditions, based on net weight loss, point of fatigue and recovery HR. Shortening Phase B by as much as 50% under hot and humid conditions still did not allow a complete return to cool weather performance and recovery. Further modifications to Phase C will be required in order to aid horses in net heat loss during Phases B and C.

Animals↗
PubMed1994

Hemodynamic and anesthetic effects of etomidate infusion in medetomidine-premedicated dogs.

Hemodynamic and analgesic effects of medetomidine (15 micrograms/kg of body weight, IM) and etomidate (0.5 mg/kg, IV, loading dose; 50 micrograms/kg/min, constant infusion) were evaluated in 6 healthy adult Beagles. Instrumentation was performed during isoflurane/oxygen-maintained anesthesia. Before initiation of the study, isoflurane was allowed to reach end-tidal concentration < or = 0.5%, when baseline measurements were recorded. Medetomidine and atropine (0.044 mg/kg) were given IM after recording of baseline values. Ten minutes later, the loading dose of etomidate was given IM, and constant infusion was begun and continued for 60 minutes. Oxygen was administered via endotracheal tube throughout the study. Analgesia was evaluated by use of the standard tail clamp technique and a direct-current nerve stimulator. Sinoatrial and atrial-ventricular blocks occurred in 4 of 6 dogs within 2 minutes after administration of a medetomidine-atropine combination, but disappeared within 8 minutes. Apnea did not occur after administration of the etomidate loading dose. Analgesia was complete and consistent throughout 60 minutes of etomidate infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output. Etomidate infusion caused a decrease in respiratory function, but minimal changes in hemodynamic values. Time from termination of etomidate infusion to extubation, sternal recumbency, standing normally, and walking normally were 17.3 +/- 9.4, 43.8 +/- 14.2, 53.7 +/- 11.9, and 61.0 +/- 10.9 minutes, respectively. All recoveries were smooth and unremarkable. We concluded that this anesthetic drug combination, at the dosages used, is a safe technique in healthy Beagles.

Adrenergic alpha-Agonists↗
PubMed1994

Hemodynamic and analgesic effects of propofol infusion in medetomidine-premedicated dogs.

Hemodynamic and analgesic effects of medetomidine (30 micrograms/kg of body weight, IM), atropine (0.044 mg/kg, IM), and propofol (2 mg/kg, IV, as a bolus, and 165 micrograms/kg/min, IV, for 60 minutes, as an infusion) were evaluated in 6 healthy adult Beagles. Catheters were placed while the dogs were anesthetized with isoflurane in oxygen. Administration of isoflurane was then discontinued, and dogs were allowed to breath oxygen until end-tidal isoflurane concentration was < or = 0.5%. At this time, baseline measurements were recorded and medetomidine and atropine were administered. Ten minutes later, the bolus of propofol was given and the infusion was begun. Analgesia was evaluated with a tail clamp test and by use of a direct-current nerve stimulator. Sinoatrial and atrioventricular blockade developed in all 6 dogs within 2 minutes of administration of medetomidine and atropine, but disappeared within 10 minutes. Apnea did not develop after administration of propofol. Analgesia was strong and consistent throughout the entire 60-minute period of propofol infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output, compared with baseline values. Propofol infusion appeared to alleviate medetomidine-induced vasoconstriction. Recovery was smooth and uncomplicated. All dogs were able to walk normally at a mean time (+/- SEM) of 88.2 +/- 20.6 minutes after termination of propofol infusion. It was concluded that medetomidine, atropine, and propofol, as given in the present study, is a safe combination of anesthetic drugs for use in healthy Beagles.

Analgesics↗
PubMed1993

Immobilization and anesthesia of two hand-reared zebras.

This report describes our experiences with 2 drug combinations that were used safely and effectively to immobilize and anesthetize 2 hand-reared zebras. Zebras were sedated with xylazine hydrochloride or detomidine. The latter is more potent and of more use in healthy, vigorous animals. Anesthesia was induced with thiamylal/guaifenesin or tiletamine/zolazepam. The latter is more convenient because a quick, simple IV injection will preclude the necessity for physical restraint required to administer a large volume of guaifenesin/thiobarbiturate combination. Tracheal intubation was easily accomplished with either induction regimen, and inhalation anesthetic was used for longer periods of anesthesia.

Anesthesia↗
PubMed1993

Alterations in the arrhythmogenic dose of epinephrine after xylazine or medetomidine administration in halothane-anesthetized dogs.

Eight dogs (12.5 to 21.5 kg) were assigned at random to each of 3 groups that were not given glycopyrrolate (HS, HX, HM) and to each of 3 groups that were given glycopyrrolate (HGS, HGX, HGM). Dogs were anesthetized with halothane (1.31% end-tidal concentration), and ventilation was controlled (PCO2 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline arrhythmogenic dose of epinephrine (ADE) determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0 and 2.5 micrograms/kg/min. The ADE was defined as the total dose of epinephrine inducing at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline ADE and posttreatment ADE for groups HS, HX, and HM was performed by use of one-way ANOVA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1993

Alterations in the arrhythmogenic dose of epinephrine after xylazine or medetomidine administration in isoflurane-anesthetized dogs.

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (IS, IX, IM) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (IGS, IGX, IGM). Dogs were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (PCO2, 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline ADE determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 micrograms/kg/min. The ADE was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ADE values was performed by use of one-way ANOVA. Mean +/- SEM baseline ADE values for groups IS, IX, and IM were 1.55 +/- 0.23, 1.61 +/- 0.28, and 1.95 +/- 0.65 micrograms/kg, respectively. Differences for groups IS, IX, and IM were -0.12 +/- 0.05, -0.31 +/- 0.40, and -0.17 +/- 0.26, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1993

Influence of anesthetic regimens on the perioperative catecholamine response associated with onychectomy in cats.

Plasma catecholamine concentrations in response to onychectomy were examined in 27 cats receiving different anesthetic regimens. Each cat was anesthetized with a dissociative-tranquilizer combination, and onychectomy was performed on 1 forefoot. One week later, each cat was anesthetized with the same dissociative-tranquilizer combination plus either butorphanol or oxymorphone, and onychectomy was performed on the other forefoot. Four treatment groups were studied: tiletamine-zolazepam and tiletamine-zolazepam-butorphanol combinations were administered to group-1 cats, ketamine-acepromazine and ketamine-acepromazine-butorphanol combinations were administered to group-2 cats, tiletamine-zolazepam and tiletamine-zolazepam-oxymorphone combinations were administered to group-3 cats, and ketamine-acepromazine and ketamine-acepromazine-oxymorphone combinations were administered to group-4 cats. All drug combinations were administered IM. Central venous blood samples were drawn for catecholamine analysis after injection of drug(s), after onychectomy, and 1, 2, and 4 hours after injection. Tiletamine-zolazepam alone or tiletamine-zolazepam-butorphanol prevented epinephrine release for 2 hours after injection of drug(s). Norepinephrine concentration increased significantly (P < 0.05) from baseline after onychectomy for tiletamine-zolazepam-butorphanol and at 4 hours for tiletamine-zolazepam and tiletamine-zolazepam-butorphanol. After onychectomy, there was no difference in epinephrine values between tiletamine-zolazepam and tiletamine-zolazepam-oxymorphone. Ketamine-acepromazine prevented increases in norepinephrine and epinephrine concentrations for up to 2 hours after surgery. Addition of butorphanol to ketamine-acepromazine decreased norepinephrine values immediately after onychectomy. Addition of oxymorphone to ketamine-acepromazine resulted in lower epinephrine values 4 hours after surgery.

Anesthesia, General↗
PubMed1992

Yohimbine/flumazenil antagonism of hemodynamic alterations induced by a combination of midazolam, xylazine, and butorphanol in dogs.

Reversal of hemodynamic alterations induced by midazolam maleate (1.0 mg/kg of body weight), xylazine hydrochloride (0.44 mg/kg), and butorphanol tartrate (0.1 mg/kg) with yohimbine (0.1 mg/kg) and flumazenil (0.25 mg/kg) was evaluated in 5 dogs. The dogs were anesthetized with isoflurane for instrumentation. With return to consciousness, baseline values were recorded, and the midazolam/xylazine/butorphanol mixture with glycopyrrolate was administered IV. Hemodynamic data were recorded for 60 minutes, and then a reversal mixture of yohimbine and flumazenil was administered IV. All variables were measured 1 minute from beginning of the reversal injection. Mean arterial pressure, pulmonary arterial pressure, systemic vascular resistance, and right ventricular stroke work index increased significantly (P < 0.05) above baseline at 60 minutes. Cardiac index and central venous pressure significantly decreased below baseline at 60 minutes. After reversal, mean arterial pressure and central venous pressure significantly decreased from baseline, whereas cardiac index, pulmonary arterial pressure, and right ventricular stroke work index increased significantly above baseline. Heart rate, cardiac index, and right ventricular stroke work index increased significantly above the 60-minute value after reversal. Mean arterial pressure and systemic vascular resistance decreased significantly (P < 0.05) below the 60-minute value after reversal. The hemodynamic alterations accompanying midazolam/xylazine/butorphanol sedation-anesthesia may be rapidly reversed with a combination of yohimbine and flumazenil.

Anesthesia↗
PubMed1992

Advantages and guidelines for using alpha-2 agonists as anesthetic adjuvants.

Xylazine and medetomidine produce reliable sedation, muscle relaxation, and analgesia in dogs and cats. In addition, alpha-2 agonists have proved very effective as sedative-analgesic adjuncts when coadministered with benzodiazepine or opioid agonists. Alpha-2 agonists should not be classified as monoanesthetics. They are excellent anesthetic adjuncts when combined with dissociatives and opioids. Because of the acute alterations in cardiopulmonary function commonly induced by alpha-2 agonists, it is suggested that their use be restricted to the young healthy patient undergoing routine surgical or diagnostic procedure. The development of more specific and selective alpha-2 agonists will continue to enhance the safety and reliability of this novel class of compounds. The unique spectrum of anesthetic properties induced by alpha-2 agonists has assured them of an increasingly prominent role in the development of new and sophisticated ways of achieving anesthesia.

Adjuvants, Anesthesia↗