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- Author or Editor: Tatsushi Mutoh x
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Abstract
Objective—To determine the effects of nitrous oxide (N2O) on the speed and quality of mask induction with sevoflurane or isoflurane in dogs.
Animals—7 healthy Beagles.
Procedure—Anesthesia was induced with sevoflurane or isoflurane delivered in 100% oxygen or in a 2:1 mixture of N2O and oxygen via a face mask. Each dog received all treatments with at least 1 week between treatments. Initial vaporizer settings were 0.8% for sevoflurane and 0.5% for isoflurane (0.4 times the minimum alveolar concentration [MAC]). Vaporizer settings were increased by 0.4 MAC at 15-second intervals until settings were 4.8% for sevoflurane and 3.0% for isoflurane (2.4 MAC). Times to onset and cessation of involuntary movements, loss of the palpebral reflex, negative response to tail-clamp stimulation, and endotracheal intubation were recorded, and cardiopulmonary variables were measured.
Results—Administration of sevoflurane resulted in a more rapid induction, compared with isoflurane. However, N2O had no effect on induction time for either agent. Heart rate, mean arterial blood pressure, cardiac output, and respiratory rate significantly increased and tidal volume significantly decreased from baseline values immediately after onset of induction in all groups. Again, concomitant administration of N2O had no effect on cardiopulmonary variables.
Conclusions and Clinical Relevance—Administration of N2O did not improve the rate or quality of mask induction with sevoflurane or isoflurane. The benefits provided by N2O attributable to concentrating and second gas effects appear minimal in healthy dogs when low solubility inhalation agents such as isoflurane and sevoflurane are used for mask induction. (Am J Vet Res 2001;62:1727–1733).
Abstract
Objective—To characterize the effects of medetomidine- midazolam, midazolam-butorphanol, or acepromazine- butorphanol as premedicants for mask induction of anesthesia with sevoflurane in dogs.
Animals—10 healthy Beagles.
Procedure—The following premedicants were administered intramuscularly: medetomidine-midazolam (20 µg/kg and 0.3 mg/kg, respectively), midazolambutorphanol (0.1 and 0.2 mg/kg, respectively), and acepromazine-butorphanol (0.05 and 0.2 mg/kg, respectively). Saline (0.9% NaCl) solution (0.1 ml/kg) was administered intramuscularly as a control. Anesthesia was induced in each dog with sevoflurane in a 100% O2 at a flow rate of 4 L/min developed by a facemask. Vaporizer settings were increased by 0.8% at 15-second intervals until the value corresponding to 4.8% sevoflurane was achieved. Time to onset and cessation of involuntary movements, loss of the palpebral reflex, negative response to tail-clamp stimulation, and endotracheal intubation were recorded, and the cardiopulmonary variables were measured.
Results—Mask induction with sevoflurane in dogs that received each premedicant resulted in a shorter induction time and milder changes in heart rate, mean arterial blood pressure, cardiac output, and respiratory rate, compared with mask induction without premedicants. Treatment with medetomidine-midazolam resulted in a shorter and smoother induction, compared with acepromazine-butorphanol or midazolambutorphanol treatment, whereas the cardiovascular changes were greater. Cardiopulmonary variables of dogs during induction following treatment with acepromazine- butorphanol or midazolam-butorphanol were maintained close to the anesthetic maintenance values for sevoflurane, with the exception of mild hypotension that was observed in dogs following acepromazine-butorphanol treatment.
Conclusion and Clinical Relevance—In dogs use of premedicants provides a smoother and better quality mask induction with sevoflurane. (Am J Vet Res 2002;63:1022–1028)
Abstract
Objective—To characterize and determine the sensory innervation of respiratory reflexes elicited by nasal administration of halothane to dogs.
Animals—10 healthy Beagles.
Procedure—Dogs underwent permanent tracheostomy and, 2 to 3 weeks later, were anesthetized with thiopental and α-chloralose administered IV. The nasal passages were functionally isolated so that halothane could be administered to the nasal passages while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of halothane at concentrations of 1.25, 1.75, and 2.5 times the minimum alveolar concentration (MAC), and 5% (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of 5% halothane were also recorded following transection of the infraorbital nerve, transection of the caudal nasal nerve, and nasal administration of lidocaine.
Results—Nasal administration of halothane induced an inhibition of breathing characterized by a dosedependent increase in expiratory time and a resultant decrease in expired volume per unit time. Effects were noticeable immediately after the onset of halothane administration and lasted until its cessation. Reflex responses to halothane administration were attenuated by transection of the caudal nasal nerve and by nasal administration of lidocaine, but transection of the infraorbital nerve had no effect.
Conclusions and Clinical Relevance—Nasal administration of halothane at concentrations generally used for mask induction of anesthesia induces reflex inhibition of breathing. Afferent fibers in the caudal nasal nerve appear to play an important role in the reflex inhibition of breathing induced by halothane administration. (Am J Vet Res 2000;61:260–267)
Abstract
Objective—To evaluate dose-sparing effects of medetomidine-midazolam (MM), acepromazinebutorphanol (AB), and midazolam-butorphanol (MB) on the induction dose of thiopental and propofol and to examine cardiopulmonary changes in dogs.
Animals—23 healthy Beagles.
Procedure—Dogs were administered MM, AB, MB, or physiologic saline (0.9% NaCl) solution (PS) IM, and anesthesia was induced with thiopental or propofol. Cardiopulmonary measurements were obtained before and after administration of medication and 0, 5, 10, and 15 minutes after endotracheal intubation.
Results—Induction doses were reduced significantly by preanesthetic administration of MM, AB, and MB (thiopental, 20, 45, and 46% after administration of PS; propofol, 42, 58, and 74% after administration of PS, respectively). Recovery time in dogs administered MM-thiopental or MM-propofol and AB-propofol were significantly prolonged, compared with recovery time in dogs administered PS-thiopental or PS-propofol. Relatively large cardiovascular changes were induced by administration of MM, which were sustained even after the induction of anesthesia. Administration of AB and MB induced cardiovascular changes during and immediately after endotracheal intubation that were significantly decreased by induction with thiopental or propofol. However, mild hypotension developed with AB-propofol. Apnea was observed in dogs administered MM during induction of anesthesia, but most respiratory variables did not change significantly.
Conclusions and Clinical Relevance—Preanesthetic medication with MM greatly reduced the anesthesia induction dose of thiopental and propofol but caused noticeable cardiopulmonary changes. Preanesthetic medication with AB and MB moderately reduced the induction dose of thiopental and propofol and ameliorated cardiovascular changes induced by these anesthetics, although AB caused mild hypotension. (Am J Vet Res 2002;63:1671–1679)
Abstract
Objective—To characterize respiratory reflexes elicited by nasal administration of sevoflurane (Sevo), isoflurane (Iso), or halothane (Hal) in anesthetized dogs.
Animals—8 healthy Beagles.
Procedure—A permanent tracheostomy was created in each dog. Two to 3 weeks later, dogs were anesthetized by IV administration of thiopental and α-chloralose. Nasal passages were isolated such that inhalant anesthetics could be administered to the nasal passages while the dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of each anesthetic at 1.2 and 2.4 times the minimum alveolar concentration (MAC) and the full vaporizer setting (5%) were recorded. Reflexes in response to administration of 5% of each anesthetic also were recorded following administration of lidocaine to the nasal passages.
Results—Nasal administration of Sevo, Iso, and Hal induced an immediate ventilatory response characterized by a dose-dependent increase in expiratory time and a resulting decrease in expired volume per unit of time. All anesthetics had a significant effect, but for Sevo, the changes were smaller in magnitude. Responses to administration of each anesthetic were attenuated by administration of lidocaine to the nasal passages.
Conclusions and Clinical Relevance—Nasal administration of Sevo at concentrations generally used for mask induction of anesthesia induced milder reflex inhibition of breathing, presumably via afferent neurons in the nasal passages, than that of Iso or Hal. Respiratory reflexes attributable to stimulation of the nasal passages may contribute to speed of onset and could promote a smoother induction with Sevo, compared with Iso or Hal. (Am J Vet Res 2001;62:311–319)
