Nitrous Oxide-Induced Analgesia Does Not Influence Nitrous Oxide's Immobilizing Requirements
| Autor: | Steven L. Jinks, Joseph F. Antognini, Earl Carstens |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Male
Pain Threshold medicine.medical_specialty Time Factors Saporin Analgesic Nitrous Oxide Article Rats Sprague-Dawley Immobilization chemistry.chemical_compound Internal medicine Reaction Time medicine Animals Injections Intraventricular Pain Measurement Dose-Response Relationship Drug Isoflurane biology business.industry Immunotoxins Sympathectomy Chemical Withdrawal latency Antibodies Monoclonal Nitrous oxide Analgesics Non-Narcotic Saporins Rats Prolonged exposure Dose–response relationship Anesthesiology and Pain Medicine Endocrinology chemistry Anesthesia Anesthetics Inhalation Anesthetic Ribosome Inactivating Proteins Type 1 biology.protein Adrenergic Fibers business medicine.drug |
| Zdroj: | Anesthesia & Analgesia. 109:1111-1116 |
| ISSN: | 0003-2999 |
| DOI: | 10.1213/ane.0b013e3181b5a2a7 |
| Popis: | Background Nitrous oxide (N(2)O) acts on supraspinal noradrenergic neurons to produce analgesia, but it is unclear if analgesia contributes to N(2)O's immobilizing effects. We tested the hypothesis that N(2)O minimum alveolar anesthetic concentration (MAC) is unchanged after selective ablation of supraspinal noradrenergic neurons, or in naive animals at N(2)O exposure timepoints when analgesia is absent. Methods We determined tailflick latency (TFL) and hindpaw withdrawal latency (HPL) under 70% N(2)O, N(2)O MAC, and isoflurane MAC before and after intracerebroventricular injections of anti-dopamine-beta hydroxylase conjugated to saporin (SAP-DBH; n = 7), or a control antibody conjugated to saporin (n = 5). In a separate group of naive rats (n = 8), N(2)O MAC was determined at 25-45 min after initiation of N(2)O exposure (during peak analgesia) and again at 120-140 min (after TFL and HPL returned to baseline). Results After 30 min of N(2)O exposure, TFL and HPL increased significantly but declined back to baseline within 120 min. N(2)O did not produce analgesia in rats that received SAP-DBH. However, N(2)O and isoflurane MAC were not significantly different between SAP-DBH and control-injected animals (Mean +/- sd for N(2)O: 1.7 +/- 0.1 atm vs 1.7 +/- 0.2 atm; isofurane: 1.6 +/- 0.2% vs 1.7 +/- 0.2%). In naive animals, N(2)O MAC was not different at the 30 min period compared with the 120 min period (1.8 +/- 0.1 atm vs 1.8 +/- 0.2 atm). Conclusions Destroying brainstem noradrenergic neurons or prolonged exposure to N(2)O removes its analgesic effects, but does not change MAC. The immobilizing mechanism of N(2)O is independent from its analgesic effects. |
| Databáze: | OpenAIRE |
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