Soo Hee Lee, Kyeong-Eon Park, Kibaek Eum, Yeran Hwang, Seong-Ho Ok, Gyujin Sim, Dumidu Perera, Henri K M Ravald, Youngho Park, Susanne K Wiedmer, Ju-Tae Sohn
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The distribution constant (KD: lipid to aqueous phase) of EPI or NOR between a LE (1%) and an aqueous phase was determined.</p><p><strong>Results: </strong>LE (1 and 2%) did not significantly alter vasoconstriction caused by EPI or NOR in isolated endothelium-intact aorta. Moreover, the LE did not significantly alter the increased calcium level caused by EPI or NOR. The log KD of EPI in the LE (1%) was -0.71, -0.99, and -1.00 at 20, 50, and 100 mM ionic strength, respectively. The log KD of NOR in the LE (1%) was -1.22, -1.25, and -0.96 at 20, 50, and 100 mM ionic strength, respectively.</p><p><strong>Conclusions: </strong>Taken together, the Intralipid emulsion did not alter vasoconstriction induced by EPI or NOR that seems to be due to the hydrophilicity of EPI or NOR, leading to sustained hemodynamic support produced by EPI or NOR used during LE resuscitation.</p>","PeriodicalId":17855,"journal":{"name":"Korean Journal of Anesthesiology","volume":" ","pages":"555-564"},"PeriodicalIF":4.2000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11467498/pdf/","citationCount":"0","resultStr":"{\"title\":\"Effect of lipid emulsion on vasoconstriction induced by epinephrine or norepinephrine in isolated rat aorta.\",\"authors\":\"Soo Hee Lee, Kyeong-Eon Park, Kibaek Eum, Yeran Hwang, Seong-Ho Ok, Gyujin Sim, Dumidu Perera, Henri K M Ravald, Youngho Park, Susanne K Wiedmer, Ju-Tae Sohn\",\"doi\":\"10.4097/kja.24093\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Epinephrine (EPI) or norepinephrine (NOR) is widely used to treat cardiovascular collapse during lipid emulsion (LE) resuscitation for drug toxicity. However, the effect of LE on the vasoconstriction caused by EPI or NOR remains unknown. The purpose of this study was to examine the effect of an LE (Intralipid) on the vasoconstriction caused by EPI and NOR in isolated rat aorta.</p><p><strong>Methods: </strong>The effect of LE on the vasoconstriction caused by EPI or NOR in isolated rat aorta was examined. Additionally, the effect of LE on the calcium increase caused by EPI or NOR was investigated. The distribution constant (KD: lipid to aqueous phase) of EPI or NOR between a LE (1%) and an aqueous phase was determined.</p><p><strong>Results: </strong>LE (1 and 2%) did not significantly alter vasoconstriction caused by EPI or NOR in isolated endothelium-intact aorta. Moreover, the LE did not significantly alter the increased calcium level caused by EPI or NOR. The log KD of EPI in the LE (1%) was -0.71, -0.99, and -1.00 at 20, 50, and 100 mM ionic strength, respectively. 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引用次数: 0
摘要
背景：肾上腺素（EPI）或去甲肾上腺素（NOR）被广泛用于治疗药物中毒的脂质乳剂（LE）复苏过程中的心血管衰竭。然而，LE 对 EPI 或 NOR 引起的血管收缩的影响仍然未知。本研究的目的是探讨一种脂质乳剂（Intralipid）对EPI和NOR在离体大鼠主动脉中引起的血管收缩的影响：方法：研究了LE对EPI或NOR引起的离体大鼠主动脉血管收缩的影响。此外，还研究了 LE 对 EPI 或 NOR 引起的钙增加的影响。测定了 EPI 或 NOR 在 LE（1%）和水相之间的分布常数（KD：脂相到水相）：结果：LE（1% 和 2%）没有明显改变 EPI 或 NOR 在离体内皮接触主动脉中引起的血管收缩。此外，LE 对 EPI 或 NOR 引起的钙水平升高也无明显改变。在 20、50 和 100 mM 离子强度下，LE（1%）中 EPI 的对数 KD 分别为-0.71、-0.99 和-1.00。在 20、50 和 100 mM 离子强度下，LE（1%）中 NOR 的对数 KD 分别为-1.22、-1.25 和 -0.96：综上所述，Intralipid乳液不会改变EPI或NOR诱导的血管收缩，这似乎是由于EPI或NOR的亲水性所致，从而导致在LE复苏过程中使用EPI或NOR产生持续的血流动力学支持。
Effect of lipid emulsion on vasoconstriction induced by epinephrine or norepinephrine in isolated rat aorta.
Background: Epinephrine (EPI) or norepinephrine (NOR) is widely used to treat cardiovascular collapse during lipid emulsion (LE) resuscitation for drug toxicity. However, the effect of LE on the vasoconstriction caused by EPI or NOR remains unknown. The purpose of this study was to examine the effect of an LE (Intralipid) on the vasoconstriction caused by EPI and NOR in isolated rat aorta.
Methods: The effect of LE on the vasoconstriction caused by EPI or NOR in isolated rat aorta was examined. Additionally, the effect of LE on the calcium increase caused by EPI or NOR was investigated. The distribution constant (KD: lipid to aqueous phase) of EPI or NOR between a LE (1%) and an aqueous phase was determined.
Results: LE (1 and 2%) did not significantly alter vasoconstriction caused by EPI or NOR in isolated endothelium-intact aorta. Moreover, the LE did not significantly alter the increased calcium level caused by EPI or NOR. The log KD of EPI in the LE (1%) was -0.71, -0.99, and -1.00 at 20, 50, and 100 mM ionic strength, respectively. The log KD of NOR in the LE (1%) was -1.22, -1.25, and -0.96 at 20, 50, and 100 mM ionic strength, respectively.
Conclusions: Taken together, the Intralipid emulsion did not alter vasoconstriction induced by EPI or NOR that seems to be due to the hydrophilicity of EPI or NOR, leading to sustained hemodynamic support produced by EPI or NOR used during LE resuscitation.
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