The Effect of Epidural Anesthesia on Respiratory Distress Induced by Airway Occlusion in Isoflurane-Anesthetized Cats

The role of afferent information from the chest wall in the genesis of dyspnea is not fully elucidated. We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACaor) and the duration from the start of A...

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Veröffentlicht in:Anesthesia and analgesia 2001-03, Vol.92 (3), p.749-754
Hauptverfasser: Ide, Tohru, Okitsu, Yumi, Nehashi, Shino, Yamamoto, Fumiko, Nishino, Takashi
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creator Ide, Tohru
Okitsu, Yumi
Nehashi, Shino
Yamamoto, Fumiko
Nishino, Takashi
description The role of afferent information from the chest wall in the genesis of dyspnea is not fully elucidated. We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACaor) and the duration from the start of AO to the onset of the positive motor response (Doccl) to evaluate respiratory distress quantitatively. We examined the effects of thoracic epidural anesthesia on respiratory distress by using our animal model. Adult cats (n = 24) were anesthetized with isoflurane, and an epidural catheter was placed after T9 laminectomy. After determination of MACaor, Doccl was measured. Animals were then randomly assigned into three groupsthe EPD Group (n = 12) received epidural 1% lidocaine (0.4 mL/kg), IM saline (0.4 mL/kg), and saline infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), IM 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) received epidural 1% lidocaine (0.4 mL/kg) and IV phenylephrine (0.5–1 μg · kg−1 · min−1) to maintain a stable arterial blood pressure. Doccl and MACaor were measured in each animal at 15 min after the administration of drugs. Plasma lidocaine concentrations were measured before and after epidural or IM injection. Doccl was significantly longer after epidural injection in all groups than before the injection. Although there was no significant difference in the values of MACaor between before and after the epidural injection in the EPD Group, the IM administration of lidocaine in the IM Group significantly reduced MACaor. Plasma concentrations of lidocaine were similar in all groups at all measurement points. Our data indicate that thoracic epidural anesthesia using 1% lidocaine significantly reduced respiratory distress induced by AO. This effect is most likely caused by a systemic effect of lidocaine rather than by reduced afferent information from the chest wall.
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We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACaor) and the duration from the start of AO to the onset of the positive motor response (Doccl) to evaluate respiratory distress quantitatively. We examined the effects of thoracic epidural anesthesia on respiratory distress by using our animal model. Adult cats (n = 24) were anesthetized with isoflurane, and an epidural catheter was placed after T9 laminectomy. After determination of MACaor, Doccl was measured. Animals were then randomly assigned into three groupsthe EPD Group (n = 12) received epidural 1% lidocaine (0.4 mL/kg), IM saline (0.4 mL/kg), and saline infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), IM 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) received epidural 1% lidocaine (0.4 mL/kg) and IV phenylephrine (0.5–1 μg · kg−1 · min−1) to maintain a stable arterial blood pressure. Doccl and MACaor were measured in each animal at 15 min after the administration of drugs. Plasma lidocaine concentrations were measured before and after epidural or IM injection. Doccl was significantly longer after epidural injection in all groups than before the injection. Although there was no significant difference in the values of MACaor between before and after the epidural injection in the EPD Group, the IM administration of lidocaine in the IM Group significantly reduced MACaor. Plasma concentrations of lidocaine were similar in all groups at all measurement points. Our data indicate that thoracic epidural anesthesia using 1% lidocaine significantly reduced respiratory distress induced by AO. 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We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACaor) and the duration from the start of AO to the onset of the positive motor response (Doccl) to evaluate respiratory distress quantitatively. We examined the effects of thoracic epidural anesthesia on respiratory distress by using our animal model. Adult cats (n = 24) were anesthetized with isoflurane, and an epidural catheter was placed after T9 laminectomy. After determination of MACaor, Doccl was measured. Animals were then randomly assigned into three groupsthe EPD Group (n = 12) received epidural 1% lidocaine (0.4 mL/kg), IM saline (0.4 mL/kg), and saline infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), IM 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) received epidural 1% lidocaine (0.4 mL/kg) and IV phenylephrine (0.5–1 μg · kg−1 · min−1) to maintain a stable arterial blood pressure. Doccl and MACaor were measured in each animal at 15 min after the administration of drugs. Plasma lidocaine concentrations were measured before and after epidural or IM injection. Doccl was significantly longer after epidural injection in all groups than before the injection. Although there was no significant difference in the values of MACaor between before and after the epidural injection in the EPD Group, the IM administration of lidocaine in the IM Group significantly reduced MACaor. Plasma concentrations of lidocaine were similar in all groups at all measurement points. Our data indicate that thoracic epidural anesthesia using 1% lidocaine significantly reduced respiratory distress induced by AO. This effect is most likely caused by a systemic effect of lidocaine rather than by reduced afferent information from the chest wall.</description><subject>Anesthesia</subject><subject>Anesthesia, Epidural</subject><subject>Anesthesia. Intensive care medicine. Transfusions. 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Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Anesthetics, Inhalation - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Cats</topic><topic>Dyspnea - etiology</topic><topic>Female</topic><topic>Heart Rate - drug effects</topic><topic>Isoflurane - pharmacology</topic><topic>Lidocaine - blood</topic><topic>Lidocaine - pharmacology</topic><topic>Local anesthesia. 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We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACaor) and the duration from the start of AO to the onset of the positive motor response (Doccl) to evaluate respiratory distress quantitatively. We examined the effects of thoracic epidural anesthesia on respiratory distress by using our animal model. Adult cats (n = 24) were anesthetized with isoflurane, and an epidural catheter was placed after T9 laminectomy. After determination of MACaor, Doccl was measured. Animals were then randomly assigned into three groupsthe EPD Group (n = 12) received epidural 1% lidocaine (0.4 mL/kg), IM saline (0.4 mL/kg), and saline infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), IM 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) received epidural 1% lidocaine (0.4 mL/kg) and IV phenylephrine (0.5–1 μg · kg−1 · min−1) to maintain a stable arterial blood pressure. Doccl and MACaor were measured in each animal at 15 min after the administration of drugs. Plasma lidocaine concentrations were measured before and after epidural or IM injection. Doccl was significantly longer after epidural injection in all groups than before the injection. Although there was no significant difference in the values of MACaor between before and after the epidural injection in the EPD Group, the IM administration of lidocaine in the IM Group significantly reduced MACaor. Plasma concentrations of lidocaine were similar in all groups at all measurement points. Our data indicate that thoracic epidural anesthesia using 1% lidocaine significantly reduced respiratory distress induced by AO. This effect is most likely caused by a systemic effect of lidocaine rather than by reduced afferent information from the chest wall.</abstract><cop>Hagerstown, MD</cop><pub>International Anesthesia Research Society</pub><pmid>11226113</pmid><doi>10.1213/00000539-200103000-00037</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Journals@Ovid LWW Legacy Archive; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete
subjects Anesthesia
Anesthesia, Epidural
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Anesthetics, Inhalation - pharmacology
Animals
Biological and medical sciences
Blood Pressure - drug effects
Cats
Dyspnea - etiology
Female
Heart Rate - drug effects
Isoflurane - pharmacology
Lidocaine - blood
Lidocaine - pharmacology
Local anesthesia. Pain (treatment)
Male
Medical sciences
Respiration - drug effects
title The Effect of Epidural Anesthesia on Respiratory Distress Induced by Airway Occlusion in Isoflurane-Anesthetized Cats
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