發(fā)布時間：2018-11-06 17:10

【摘要】：背景：癌癥的發(fā)生發(fā)展與免疫功能失調(diào)息息相關(guān)。自然殺傷細胞（naturalkiller cell, NK細胞）在負責(zé)腫瘤的監(jiān)督、識別、殺傷及控制感染中起主要作用。已知手術(shù)創(chuàng)傷性應(yīng)激反應(yīng)與相關(guān)的麻醉因素都明顯抑制手術(shù)期NK細胞活性及數(shù)量。部分麻醉藥物本身對免疫系統(tǒng)有直接或間接抑制作用，術(shù)中、術(shù)后鎮(zhèn)痛不全會通過激活HPA軸（下丘腦-垂體-腎上腺軸）釋放皮質(zhì)醇等應(yīng)激激素更進一步抑制免疫功能。既往對麻醉與免疫關(guān)系的研究多集中于麻醉藥物本身和麻醉方式，而對于在麻醉下癌與非癌癥患者的免疫影響未見報道。本實驗采用對NK細胞無影響的鎮(zhèn)靜藥丙泊酚及具有免疫保護作用的右美托咪定輔助鎮(zhèn)靜、復(fù)合靶控輸注相同血漿靶濃度的瑞芬太尼麻醉，觀察實施甲狀腺手術(shù)的甲狀腺癌癥患者及非癌癥患者行相同的麻醉時術(shù)中、術(shù)后24小時NK細胞數(shù)量變化有無不同。 方法：40名ASA分級I-II級擇期行甲狀腺手術(shù)的患者，麻醉誘導(dǎo)前以負荷量1ug/kg泵入右美托咪定10min后改維持量全程輸注，麻醉誘導(dǎo)靜注丙泊酚、苯磺酸順式阿曲庫銨及靶控輸注瑞芬太尼，麻醉維持采用丙泊酚靜脈泵入和瑞芬太尼靶控輸注，術(shù)中麻醉藥物維持劑量及血藥濃度根據(jù)BIS值及血流動力學(xué)指標(biāo)進行調(diào)整。根據(jù)患者術(shù)中病理結(jié)果分成兩組，即癌癥組和非癌組，，分別于入室時（T1）、插管時（T2）、術(shù)畢（T3）、術(shù)后24h（T4）抽取外周靜脈血利用流式細胞儀檢測NK細胞數(shù)量、用電化學(xué)發(fā)光法測皮質(zhì)醇（COR）數(shù)值。 結(jié)果：NK細胞結(jié)果顯示：兩組術(shù)前（T1）18.85±4.15與15.79±4.64均在正常范圍，組間比較無統(tǒng)計學(xué)差異；癌癥組誘導(dǎo)后插管時（T2）10.52±5.32與術(shù)前（T1）18.85±4.15組內(nèi)比較、非癌癥組（T2）9.91±2.34與術(shù)前（T1）15.79±4.64組內(nèi)比較均有統(tǒng)計學(xué)差異（P0.05）；癌癥組術(shù)畢（T3）15.49±7.10與T210.52±5.32組內(nèi)比較、與非癌組T37.21±4.04組間比較均有統(tǒng)計學(xué)差異（P0.05）；癌癥組術(shù)后24小時（T4）10.56±2.85與T118.85±4.15及T315.49±7.10組內(nèi)比較均有統(tǒng)計學(xué)差異（p0.05）；非癌組T414.73±5.12與T115.79±4.64組內(nèi)比較無統(tǒng)計學(xué)差異，與T37.21±4.04比較有統(tǒng)計學(xué)差異（p0.05）；兩組T410.56±2.85與14.73±5.12組間比較有統(tǒng)計學(xué)差異（p0.05）。COR結(jié)果顯示： T1時癌癥組671.33±15.45與非癌癥組472.23±19.36組間比較有統(tǒng)計學(xué)差異（p0.05）,T2時癌癥組498.56±14.75與非癌癥組350.25±14.96組間比較有統(tǒng)計學(xué)差異（p0.05），總體數(shù)值顯示癌癥組各時間點COR數(shù)值略高于非癌癥組。 結(jié)論：7ng/ml瑞芬太尼靶控輸注對甲狀腺癌和良性腫物患者術(shù)中NK細胞數(shù)目均有抑制作用，這種抑制作用在非癌癥患者術(shù)后24小時恢復(fù)至術(shù)前水平，而癌癥患者NK細胞的抑制作用持續(xù)至術(shù)后24小時仍未恢復(fù)，但這種抑制一部分歸結(jié)于手術(shù)因素，另外亦不排除癌癥患者本身對瑞芬太尼導(dǎo)致的NK細胞的抑制作用恢復(fù)較差。
[Abstract]:Background: the occurrence and development of cancer is closely related to immune dysfunction. Natural killer cells (naturalkiller cell, NK cells) play a major role in tumor surveillance, identification, killing and control of infection. All known traumatic stress responses and related anesthetic factors significantly inhibited the activity and number of NK cells during surgery. Part of the anesthetic itself has direct or indirect inhibitory effect on the immune system. During the operation, postoperative analgesia is not complete by activating the HPA axis (hypothalamus-pituitary-adrenal axis) release of cortisol and other stress hormones to further inhibit the immune function. Previous studies on the relationship between anesthesia and immunity have focused on the anesthetic drugs themselves and anaesthesia methods, but the immune effects on cancer and non-cancer patients under anesthesia have not been reported. In this experiment, propofol, a sedative agent with no effect on NK cells, and dexmetomidine, which has immune protective effect, were used to assist sedation, and remifentanil with the same plasma target concentration was administered by target controlled infusion. To observe the changes of the number of NK cells 24 hours after thyroidectomy in patients with thyroid cancer and non-cancer patients undergoing the same anesthesia. Methods: 40 ASA grade I-II patients undergoing selective thyroid surgery were injected with load 1ug/kg before anesthesia induction and then injected with dexmetomidine 10min. Propofol was injected intravenously after anesthesia induction, and propofol was injected intravenously. The anesthesia was maintained by intravenous infusion of propofol and target controlled infusion of remifentanil. The maintenance dose and blood concentration of the anesthetic were adjusted according to BIS and hemodynamic indexes. The patients were divided into two groups according to the pathological results during operation: cancer group and non-cancer group. The number of NK cells was detected by flow cytometry at the time of entry (T1), intubation (T2), the end of operation (T3), and 24 hours after operation (T4). The (COR) value of cortisol was measured by electrochemiluminescence. Results: the results of NK cells showed that before operation (T1) 18.85 鹵4.15 and 15.79 鹵4.64 in normal range, there was no statistical difference between the two groups. There were significant differences between the cancer group (T _ 2) 10.52 鹵5.32 and preoperative (T _ 1) 18.85 鹵4.15, and the non-cancer group (T _ 2) 9.91 鹵2.34 and preoperative (T _ 1) 15.79 鹵4.64 (P0.05). After operation (T3) 15.49 鹵7.10 and T210.52 鹵5.32 in cancer group, there were significant differences between T37.21 鹵4.04 and T37.21 鹵4.04 groups (P0.05). 24 hours after operation (T4) 10.56 鹵2.85 in cancer group, T118.85 鹵4.15 and T315.49 鹵7.10 in T315.49 鹵7.10 group, there were significant differences (p0.05). There was no statistical difference between T414.73 鹵5.12 and T115.79 鹵4.64 in non-cancer group, but there was statistical difference between T37.21 鹵4.04 and T37.21 鹵4.04 (p0.05). There was significant difference between the two groups in T410.56 鹵2.85 and 14.73 鹵5.12 (p0.05). COR). The results showed that there was significant difference between the cancer group (671.33 鹵15.45) and the non-cancer group (472.23 鹵19.36) at T1 (p0.05). There was statistical difference between cancer group (498.56 鹵14.75) and non-cancer group (350.25 鹵14.96) at T2. The total value of COR in cancer group was slightly higher than that in non-cancer group. Conclusion: target-controlled infusion of 7ng/ml remifentanil can inhibit the number of NK cells in thyroid carcinoma and benign tumor patients during operation, and the inhibitory effect is restored to the preoperative level 24 hours after operation in non-cancer patients. However, the inhibition of NK cells in cancer patients did not recover until 24 hours after operation, but the inhibition was partly attributed to surgical factors, and it was not excluded that the inhibition of remifentanil induced NK cells in cancer patients was poor.
【學(xué)位授予單位】：大連醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R614

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相關(guān)期刊論文 前1條

1 耿志宇,宋琳琳,許幸,吳新民;異丙酚復(fù)合芬太尼或瑞芬太尼靶控靜脈麻醉與靜吸復(fù)合麻醉的比較[J];中華麻醉學(xué)雜志;2004年01期

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