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- Author or Editor: Michael J. Woliner x
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Abstract
Objective—To quantitate dose- and time-related anesthetic-sparing effects of xylazine hydrochloride (XYL) during isoflurane-induced anesthesia in horses and to characterize selected physiologic responses of anesthetized horses to administration of XYL.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized 2 times to determine the minimum alveolar concentration (MAC) of isoflurane in O2 and to characterize the anestheticsparing effect (MAC reduction) after IV administration of XYL (0.5 and 1 mg/kg of body weight, random order). Selected measures of cardiopulmonary function, blood glucose concentrations, and urinary output also were measured during the anesthetic studies.
Results—Isoflurane MAC (mean ± SEM) was reduced by 24.8 ± 0.5 and 34.2 ± 1.9% at 42 ± 7 and 67 ± 10 minutes, respectively, after administration of XYL at 0.5 and 1 mg/kg. Amount of MAC reduction by XYL was dose- and time-dependent. Overall, cardiovascular and respiratory values varied little among treatments. Administration of XYL increased blood glucose concentration; the magnitude of change was dose- and time-dependent. Urine volume increased but not significantly.
Conclusions and Clinical Relevance—Administration of XYL reduced the anesthetic requirement for isoflurane in horses. The magnitude of the decrease is dose- and time-dependent. Administration of XYL increases blood glucose concentration in anesthetized horses in a dose-related manner. (Am J Vet Res 2000;61:1225–1231)
Summary
To study behavioral and cardiopulmonary characteristics of horses recovering from inhalation anesthesia, 6 nonmedicated horses were anesthetized under laboratory conditions on 3 different days, with either halothane or isoflurane in O2. Anesthesia was maintained at constant dose (1.5 times the minimum alveolar concentration [mac]) of halothane in O2 for 1 hour (H1), halothane in O2 for 3 hours (H3), or isoflurane in O2 for 3 hours (I3). The order of exposure was set up as a pair of Latin squares to account for horse and trial effects. Circulatory (arterial blood pressure and heart rate) and respiratory (frequency, PaCO2 , PaO2 , pHa) variables were monitored during anesthesia and for as long as possible during the recovery period. End-tidal percentage of the inhaled agent was measured every 15 seconds by automated mass spectrometry, then by hand-sampling after horses started moving. Times of recovery events, including movement of the eyelids, ears, head, and limbs, head lift, chewing, swallowing, first sternal posture and stand attempts, and the number of sternal posture and stand attempts, were recorded.
The washout curve or the et ratio (end-tidal percentage of the inhaled agent at time t to end-tidal percentage of the inhaled agent at the time the anesthesia circuit was disconnected from the tracheal tube) plotted against time was similar for H1 and H3. The slower, then faster (compared with halothane groups) washout curve of isoflurane was explainable by changes in respiratory frequency as horses awakened and by lower blood/gas solubility of isoflurane. The respiratory depressant effects of isoflurane were marked and were more progressive than those for halothane at the same 1.5 mac dose. During the first 15 minutes of recovery, respiratory frequency for group-I3 horses increased significantly (P < 0.05), compared with that for the halothane groups. For all groups, arterial blood pressure increased throughout the early recovery period and heart rate remained constant.
Preanesthesia temperament of horses and the inhalation agent used did not influence the time of the early recovery events (movement of eyelids, ears, head, and limbs), except for head lift. For events that occurred at anesthetic end-tidal percentage < 0.20, or when horses were awake, temperament was the only factor that significantly influenced the nature of the recovery (chewing P = 0.04, extubation P = 0.001, first stand attempt P = 0.008, and standing P = 0.005). The quality of the recoveries did not differ significantly among groups (H1, H3, I3) or horses; however 5 of 6 horses recovering from the H1 exposure had ideal recovery. During recovery, the anesthetic end-tidal percentage did not differ significantly among groups. However, when concentrations were compared on the basis of anesthetic potency (ie, mac multiple) a significantly (P < 0.05) lower MAC multiple of isoflurane was measured for the events ear movement, limb movement, head lift, and first attempt to sternal posture, compared with that for horses given halothane, indicating that isoflurane may be a more-potent sedative than halothane in these horses.
Abstract
Objective
To study the effects of inhalation anesthetic agents on the response of horses to 3 hours of hypoxemia.
Design
Controlled crossover study.
Animals
Five healthy adult horses.
Procedure
Horses were anesthetized twice: once with halothane, and once with isoflurane in O2. Anesthetized horses were positioned in left lateral recumbency. Constant conditions for the study began at 2 hours of anesthesia. A constant agent dose of 1.2 minimum alveolar concentration, PaO2 of 50 ± 5 mm of Hg, and PaCO2 of 45 ± 5 mm of Hg were maintained for 3 hours. Circulatory measurements were made at 0.5, 1, 2, and 3 hours of hypoxemia (anesthesia hours 2.5, 3, 4, and 5). Blood was collected from horses for biochemical analyses before anesthesia, within a few minutes after standing, and at 1, 2, 4, and 7 days after anesthesia.
Results
Cardiac index was greater (P = 0.018) during isoflurane than halothane anesthesia. Cardiac index remained constant during the 3 hours of hypoxemia during halothane anesthesia, whereas it decreased from the baseline during isoflurane anesthesia. Marginally nonsignificant P values for an agent difference were detected for arterial O2 content (P = 0.051), and oxygen delivery (P = 0.057). Serum activities of aspartate transaminase (P = 0.050) and sorbitol dehydrogenase (P = 0.017) were higher in halothane-anesthetized horses than in isoflurane-anesthetized horses. Circulatory function was better in hypoxemic horses anesthetized with isoflurane than with halothane. Isoflurane resulted in less muscular injury in hypoxemia horses than did halothane anesthesia. Halothane anesthesia and hypoxemia were associated with hepatic insult.
Conclusion
Isoflurane is better than halothane for hypoxemic horses.(Am J Vet Res 1996;57:351-360)
Abstract
Objective—To quantitate the effects of desflurane and mode of ventilation on cardiovascular and respiratory functions and identify changes in selected clinicopathologic variables and serum fluoride values associated with desflurane anesthesia in horses.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized on 2 occasions: first, to determine the minimum alveolar concentration (MAC) of desflurane in O2 and second, to characterize cardiopulmonary and clinicopathologic responses to 1×, 1.5×, and 1.75× desflurane MAC during both controlled and spontaneous ventilation.
Results—Mean ± SEM MAC of desflurane in horses was 8.06 ± 0.41%; inhalation of desflurane did not appear to cause airway irritation. During spontaneous ventilation, mean PaCO2 was 69 mm Hg. Arterial blood pressure, stroke volume, and cardiac output decreased as the dose of desflurane increased. Conditions of intermittent positive pressure ventilation and eucapnia resulted in further cardiovascular depression. Horses recovered quickly from anesthesia with little transient or no clinicopathologic evidence of adverse effects. Serum fluoride concentration before and after administration of desflurane was below the limit of detection of 0.05 ppm (2.63µM/L).
Conclusions and Clinical Relevance—Results indicate that desflurane, like other inhalation anesthetics, causes profound hypoventilation in horses. The magnitude of cardiovascular depression is related to dose and mode of ventilation; cardiovascular depression is less severe at doses of 1× to 1.5× MAC, compared with known effects of other inhalation anesthetics under similar conditions. Desflurane is not metabolized to an important degree and does not appear to prominently influence renal function or hepatic cellular integrity or function. ( Am J Vet Res 2005;66:669–677)
Summary
A rebreathing method for measurement of pulmonary diffusing capacity for carbon monoxide (Dl CO) and functional residual capacity (frc) was evaluated in conscious horses. Horses were manually ventilated through an endotracheal tube, using a custom-made syringe filled with a gas mixture containing 18-carbon monoxide (18CO) and helium (He). The 18CO and He concentrations were continuously monitored by use of a mass spectrometer connected to the rebreathing circuit. Values for Dl CO and frc were calculated from changes in the concentration of these 2 gases. In 11 Thoroughbreds, mean (± sd) Dl CO was 330.3 ± 56.9 ml•min−1•mm of Hg−1, and frc was 20.21 ± 3 35 L. Body weight normalization yielded mean (± sd) values of 0.652 ± 0.114 ml•min−1•mm of Hg−1•kg−1 for Dl CO, and 39.9 ± 6.4 ml•kg−1 for frc.
Summary
The effect of 3 plasma concentrations of alfentanil on the minimum alveolar concentration (mac) of halothane in horses was evaluated. Five healthy geldings were anesthetized on 3 occasions, using halothane in oxygen administered through a mask. After induction of anesthesia, horses were instrumented for measurement of blood pressure, airway pressure, and end-tidal halothane concentrations. Blood samples, for measurement of pH and blood gas tensions, were taken from the facial artery. Positive pressure ventilation was begun, maintaining PaCO 2, at 49.1 ± 3.3 mm of Hg and airway pressure at 20 ± 2 cm of H2O. The mac was determined in triplicate, using a supramaximal electrical stimulus of the oral mucous membranes. Alfentanil infusion was then begun, using a computer-driven infusion pump to achieve and maintain 1 of 3 plasma concentrations of alfentanil. Starting at 30 minutes after the beginning of the infusion, mac was redetermined in duplicate. Mean ± sd measured plasma alfentanil concentration during the infusions were 94.8 ± 29.0, 170.7 ± 29.2 and 390.9 ± 107.4 ng/ml. Significant changes in mac were not observed for any concentration of alfentanil. Blood pressure was increased by infusion of alfentanil and was dose-related, but heart rate did not change. Pharmacokinetic variables of alfentanil were determined after its infusion and were not significantly different among the 3 doses.
Abstract
Objective—To quantitate effects of dose of sevoflurane and mode of ventilation on cardiovascular and respiratory function in horses and identify changes in serum biochemical values associated with sevoflurane anesthesia.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized twice: first, to determine the minimum alveolar concentration (MAC) of sevoflurane and second, to characterize cardiopulmonary and serum biochemical responses of horses to 1.0, 1.5, and 1.75 MAC multiples of sevoflurane during controlled and spontaneous ventilation.
Results—Mean (± SEM) MAC of sevoflurane was 2.84 ± 0.16%. Cardiovascular performance during anesthesia decreased as sevoflurane dose increased; the magnitude of cardiovascular depression was more severe during mechanical ventilation, compared with spontaneous ventilation. Serum inorganic fluoride concentration increased to a peak of 50.8 ± 7.1 µmol/L at the end of anesthesia. Serum creatinine concentration and sorbitol dehydrogenase activity reached their greatest values (2.0 ± 0.8 mg/dL and 10.2 ± 1.8 U/L, respectively) at 1 hour after anesthesia and then returned to baseline by 1 day after anesthesia. Serum creatine kinase, aspartate aminotransferase, and alkaline phosphatase activities reached peak values by the first (ie, creatine kinase) or second (ie, aspartate aminotransferase and alkaline phosphatase) day after anesthesia.
Conclusions and Clinical Relevance—Sevoflurane causes dose-related cardiopulmonary depression, and mode of ventilation further impacts the magnitude of this depression. Except for serum inorganic fluoride concentration, quantitative alterations in serum biochemical indices of liver- and muscle-cell disruption and kidney function were considered clinically unremarkable and similar to results from comparable studies of other inhalation anesthetics. (Am J Vet Res 2005;66:606–614)
Abstract
Objectives
To evaluate the role of nitric oxide (NO), vasoactive intestinal peptide (VIP), and a transmitter acting through an apamin-sensitive mechanism in mediating inhibitory transmission in the equine jejunal circular muscle, and to determine the distribution of VIP-and NO-producing nerve fibers in the myenteric plexus and circular muscle.
Procedure
Circular muscle strips were suspended in tissue baths containing an oxygenated modified Krebs solution and attached to isometric force transducers. Responses to electrical field stimulation (EFS), tetrodotoxin, the NO antagonists l-N-nitro-arginine-methyl-ester (L-NAME) and N-nitro-l-arginine, apamin, VIP, authentic NO, and the NO donar sodium nitroprusside were tested. Immunostaining for VIP-like and NADPH diaphorase histochemical staining were performed on paraformaldehyde-fixed tissue.
Results
Subpopulations of myenteric neurons and nerve fibers in the circular muscle were positive for NADPH diaphorase and VIP-like staining. EFS caused a frequency-dependent inhibition of contractile activity. Tetrodotoxin prevented the EFS-induced inhibition of contractions. L-NAME (200 μM) and apamin 0.3 μM) significantly (P < 0.01) reduced EFS-stimulated inhibition of contractile activity at most frequencies tested. The effects of L-NAME and apamin were additive. In their combined presence, EFS induced excitation instead of inhibition (196.7% increase at 5 Hz, n = 28, P < 0.01). Inhibition of contractile activity by EFS was mimicked by sodium nitroprusside. Authentic NO (3-6 μM) abolished contractile activity. VIP induced a dose-dependent inhibition of contractile activity (89.1 ± 6.3% reduction at approximately 0.3 μM, n = 16). Antagonism of NO synthesis did not alter the response to VIP.
Conclusion
NO, VIP, and a substance acting through an apamin-sensitive mechanism appear to comediate inhibitory transmission in the equine jejunal circular muscle.
Clinical Relevance
These findings may suggest new therapeutic targets for motility disorders, such as agents that inhibit the synthesis or actions of NO. (Am J Vet Res 1996;57:1206-1213)
Abstract
Objective
To determine whether xanthine oxidase and dehydrogenase activities are altered during low flow ischemia and reperfusion of the small intestine of horses.
Animals
5 clinically normal horses without histories of abdominal problems.
Procedure
With the horse under general anesthesia, a laparotomy was performed and blood flow to a segment of the distal jejunum was reduced to 20% of baseline for 120 minutes and was then reperfused for 120 minutes. Biopsy specimens were obtained before, during, and after ischemia for determination of xanthine oxidase and dehydrogenase activities, and for histologic and morphometric analyses.
Results
Percentage of xanthine oxidase activity (as a percentage of xanthine oxidase and dehydrogenase activity) was not altered during ischemia and reperfusion. An inflammatory response developed and progressed during ischemia and reperfusion. Mucosal lesions increased in severity after ischemia and reperfusion. Mucosal surface area and volume decreased during ischemia and continued to decrease during reperfusion. Submucosal volume increased slightly during ischemia, and continued to increase during reperfusion.
Conclusions and Clinical Relevance
Evidence for conversion of xanthine dehydrogenase to xanthine oxidase during ischemia was not found. Factors other than production of reactive oxygen metabolites may be responsible for progressive epithelial loss, decrease in mucosal surface area and volume, and increase in submucosal volume observed in this study. Other methods of determining xanthine oxidase activity that detect the enzyme in sloughed epithelial cells should be used to better define the importance of this pathway in jejunal reperfusion injury in horses. (Am J Vet Res 1998;59:772-776)
Summary
Sixteen horses were allotted at random to 3 groups: vehicle only; low dosage (vehicle and 3 mg of U-74389G/kg of body weight); high dosage (vehicle and 10 mg of U-74389G/kg). These solutions were given prior to reperfusion. The ascending colon was subjected to 2 hours of ischemia followed by 2 hours of reperfusion. Before, during, and after ischemia, full-thickness colonic tissue biopsy specimens were obtained for measurement of malondealdehyde (mda) concentration and myeloperoxidase activity and for morphologic evaluation.
Although increases were not significant, mda concentration and myeloperoxidase activity increased during ischemia and reperfusion. Administration of U-74389G did not have significant effects on mda concentration and myeloperoxidase activity. However, the lower dosage tended (P = 0.08) to reduce myeloperoxidase activity at 30 and 60 minutes of reperfusion.
In horses of the vehicle-only group, ischemia induced a decrease in mucosal surface area that was continued into the reperfusion period (P ≤ 0.05). Administration of U-74389G at both dosages (3 and 10 mg/kg) prevented the reperfusion-induced reduction in mucosal surface area, which was significant at 60 minutes (high dosage; P = 0.05) and 90 minutes (low and high dosages; P = 0.02). After initial reduction in horses of all groups, mucosal volume increased for the initial 60 minutes of reperfusion.
Our results indicate that lipid peroxidation may be partially involved in continued cellular death after ischemia of the ascending colon of horses. The 21-aminosteroid, U-74389G, prevented further loss of mucosa and partially attenuated the induced increase in myeloperoxidase activity during reperfusion of the ascending colon.
