John A. Reitan, Nguyen D. Kien, Richard W. Martucci, Steven J. Thorup, Paul J. Dennis
{"title":"近无麻醉离体犬后肢模型的建立","authors":"John A. Reitan, Nguyen D. Kien, Richard W. Martucci, Steven J. Thorup, Paul J. Dennis","doi":"10.1016/0160-5402(91)90046-8","DOIUrl":null,"url":null,"abstract":"<div><p>A denervated, isolated canine hindlimb (HL) model was developed to minimize residual anesthetic contamination. To test the preparation, we determined the peripheral arterial vascular effects of atropine sulfate and the effect of the basal anesthetic on arterial resistance. In four dogs that were under halothane and oxygen anesthesia, the HL was prepared to allow either vascular isolation of the limb or continuity with the systemic circulation. During isolation the HL was perfused by roller pump at a preset flow rate through an infant oxygenator. Inspired gas fed to the oxygenator contained either 0%, 1.25%, or 2.5% halothane to determine that anesthetic's effect on HL arterial vascular resistance. No halothane (0%) was used in the oxygenator inflow during the atropine measurements. Vascular resistance was calculated from HL arterial pressure at constant flow. Halothane caused a significant stepwise fall in vascular resistance, with a decrease of 68% at 2.5% inspired concentration (<em>p</em> < 0.01). Atropine produced a progressive attenuation of resistance that decreased by 18% after the 2.5 <span><math><mtext>mg</mtext><mtext>kg</mtext></math></span> dose (<em>p</em>< 0.01). The model proved stable over time and demonstrated an apparent direct, dose-dependent vasodilating effect of both atropine and halothane in the canine HL muscle arterial bed.</p></div>","PeriodicalId":16819,"journal":{"name":"Journal of pharmacological methods","volume":"26 3","pages":"Pages 223-232"},"PeriodicalIF":0.0000,"publicationDate":"1991-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0160-5402(91)90046-8","citationCount":"6","resultStr":"{\"title\":\"Development of a near anesthetic-free isolated canine hindlimb model\",\"authors\":\"John A. Reitan, Nguyen D. Kien, Richard W. Martucci, Steven J. Thorup, Paul J. Dennis\",\"doi\":\"10.1016/0160-5402(91)90046-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>A denervated, isolated canine hindlimb (HL) model was developed to minimize residual anesthetic contamination. To test the preparation, we determined the peripheral arterial vascular effects of atropine sulfate and the effect of the basal anesthetic on arterial resistance. In four dogs that were under halothane and oxygen anesthesia, the HL was prepared to allow either vascular isolation of the limb or continuity with the systemic circulation. During isolation the HL was perfused by roller pump at a preset flow rate through an infant oxygenator. Inspired gas fed to the oxygenator contained either 0%, 1.25%, or 2.5% halothane to determine that anesthetic's effect on HL arterial vascular resistance. No halothane (0%) was used in the oxygenator inflow during the atropine measurements. Vascular resistance was calculated from HL arterial pressure at constant flow. Halothane caused a significant stepwise fall in vascular resistance, with a decrease of 68% at 2.5% inspired concentration (<em>p</em> < 0.01). Atropine produced a progressive attenuation of resistance that decreased by 18% after the 2.5 <span><math><mtext>mg</mtext><mtext>kg</mtext></math></span> dose (<em>p</em>< 0.01). The model proved stable over time and demonstrated an apparent direct, dose-dependent vasodilating effect of both atropine and halothane in the canine HL muscle arterial bed.</p></div>\",\"PeriodicalId\":16819,\"journal\":{\"name\":\"Journal of pharmacological methods\",\"volume\":\"26 3\",\"pages\":\"Pages 223-232\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1991-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0160-5402(91)90046-8\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of pharmacological methods\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0160540291900468\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of pharmacological methods","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0160540291900468","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Development of a near anesthetic-free isolated canine hindlimb model
A denervated, isolated canine hindlimb (HL) model was developed to minimize residual anesthetic contamination. To test the preparation, we determined the peripheral arterial vascular effects of atropine sulfate and the effect of the basal anesthetic on arterial resistance. In four dogs that were under halothane and oxygen anesthesia, the HL was prepared to allow either vascular isolation of the limb or continuity with the systemic circulation. During isolation the HL was perfused by roller pump at a preset flow rate through an infant oxygenator. Inspired gas fed to the oxygenator contained either 0%, 1.25%, or 2.5% halothane to determine that anesthetic's effect on HL arterial vascular resistance. No halothane (0%) was used in the oxygenator inflow during the atropine measurements. Vascular resistance was calculated from HL arterial pressure at constant flow. Halothane caused a significant stepwise fall in vascular resistance, with a decrease of 68% at 2.5% inspired concentration (p < 0.01). Atropine produced a progressive attenuation of resistance that decreased by 18% after the 2.5 dose (p< 0.01). The model proved stable over time and demonstrated an apparent direct, dose-dependent vasodilating effect of both atropine and halothane in the canine HL muscle arterial bed.