本文選題：β-腎上腺素受體興奮劑　切入點：異丙腎上腺素　出處：《河北醫(yī)科大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：第一部分β-腎上腺素受體興奮劑對布比卡因中毒心肌心電圖的影響目的:兒茶酚胺因其增加舒張壓和冠狀動脈灌注壓常作為治療心臟衰竭的一線用藥;但是,腎上腺素不但不能改善,反而會加重布比卡因引起的心臟功能不全,甚至引起肺水腫。在前期研究中,本課題組已經(jīng)在單個心肌細(xì)胞水平證實了異丙腎上腺素可加重布比卡因致心肌收縮抑制,而艾司洛爾能逆轉(zhuǎn)這一作用。本實驗將檢測β-腎上腺素受體興奮劑對布比卡因中毒心肌的自律性與傳導(dǎo)能力的影響。方法:動物模型成年雄性SD大鼠,體重200~250g。大鼠經(jīng)10%水合氯醛(0.3ml/100g)腹腔注射麻醉。經(jīng)尾靜脈建立靜脈液體通路后,將大鼠仰臥位固定并連接心電圖。心電圖的探針分別固定于大鼠肢體末端:紅色探針固定于左下肢,綠色探針固定于右上肢,黑色探針固定于右下肢。這種連接方式采集到的是心電圖Ⅱ?qū)?lián)波形。所有大鼠實驗過程中保持自主呼吸。利用RM6420系列多道生理信號采集處理系統(tǒng)采集心電圖并呈現(xiàn)于顯示儀上。實驗分組將大鼠采用隨機(jī)數(shù)字方法分為3組:布比卡因+生理鹽水組、布比卡因+異丙腎上腺素組、布比卡因+腎上腺素組。每組觀察7只大鼠。給藥過程布比卡因+生理鹽水組:經(jīng)尾靜脈勻速給予布比卡因0.75mg/kg/min,持續(xù)時間為12min40s;隨后勻速給予生理鹽水0.4ml,持續(xù)時間為1min30s。布比卡因+異丙腎上腺素組:經(jīng)尾靜脈勻速給予布比卡因0.75mg/kg/min,持續(xù)時間為12min40s;隨后勻速給予異丙腎上腺素(0.08mg/kg,0.4ml),持續(xù)時間為1min30s。布比卡因+腎上腺素組:經(jīng)尾靜脈勻速給予布比卡因0.75mg/kg/min,持續(xù)時間為12min40s;隨后勻速給予腎上腺素(6μg/kg,0.4ml),持續(xù)時間為1min30s。由RM6420系列多道生理信號采集處理系統(tǒng)監(jiān)測大鼠心電圖并分析記錄PR間期、QRS間期和心率等指標(biāo)。結(jié)果:1布比卡因抑制心肌傳導(dǎo)功能;布比卡因中毒心肌可出現(xiàn)PR間期延長、QRS間期增寬,心率下降(P0.05);2異丙腎上腺素(0.08mg/kg)、腎上腺素(6μg/kg)對布比卡因中毒后心肌PR間期和QRS間期無明顯影響。在靜脈輸注1min時,兩組中毒心肌心率增快(P0.05),而在實驗后期與對照組無差異。第二部分β-腎上腺素受體興奮劑加重布比卡因?qū)π募×W(xué)的抑制作用目的:布比卡因中毒在臨床中并不常見但嚴(yán)重影響患者生命。兒茶酚胺類藥物是治療心臟功能衰竭的一線用藥。然而,腎上腺素對于解救布比卡因引起的心臟毒性療效不佳。本課題組在前期研究中采用可視化動緣探測系統(tǒng)動態(tài)跟蹤同步檢測技術(shù),觀察檢測了異丙腎上腺素和艾司洛爾對布比卡因致單心肌細(xì)胞收縮功能抑制的影響。結(jié)果顯示,布比卡因呈濃度依賴性可逆的抑制心肌細(xì)胞收縮功能,異丙腎上腺素可以加重布比卡因抑制心肌細(xì)胞收縮的毒性作用,而艾司洛爾可以逆轉(zhuǎn)此惡化作用。本實驗將在活體動物中檢驗β-腎上腺素受體興奮劑在布比卡因致心肌力學(xué)抑制中的影響。方法:動物模型成年SD大鼠,雄性,體重200g~250g。在10%的水合氯醛(0.3ml/100g)腹腔注射麻醉后,取仰臥位,經(jīng)尾靜脈建立靜脈液體通路。經(jīng)頸總動脈插管并連接于RM6420系列多道生理信號采集處理系統(tǒng),用于測定心室內(nèi)壓,波形記錄于顯示器上。實驗分組采用隨機(jī)數(shù)字方法將大鼠分為3組:布比卡因+生理鹽水組、布比卡因+異丙腎上腺素組、布比卡因+腎上腺素組。每組觀察7只大鼠。給藥過程布比卡因+生理鹽水組:經(jīng)尾靜脈勻速給予布比卡因0.75mg/kg/min,持續(xù)時間為12min40s;隨后勻速給予生理鹽水0.4ml,持續(xù)時間為1min30s。布比卡因+異丙腎上腺素組:經(jīng)尾靜脈勻速給予布比卡因0.75mg/kg/min,持續(xù)時間為12min40s;隨后勻速給予異丙腎上腺素(0.08mg/kg,0.4ml),持續(xù)時間為1min30s。布比卡因+腎上腺素組:經(jīng)尾靜脈勻速給予布比卡因0.75mg/kg/min,持續(xù)時間為12min40s;隨后勻速給予腎上腺素(3μg/kg,0.4ml),持續(xù)時間為1min30s。觀察記錄實驗指標(biāo):給藥過程中,分析并記錄心室收縮壓(left ventricular systolic pressure,LVSP)、心室舒張末壓(left ventricular end-diastolic pressure,LVEDP)、左心室內(nèi)壓最大上升速率(+dp/dt max)、左心室內(nèi)壓最大下降速率(-dp/dt max)等指標(biāo)。結(jié)果:1布比卡因抑制心肌力學(xué),出現(xiàn)LVSP下降、LVEDP上升、+dp/dt max下降、-dp/dt max下降,且結(jié)果有統(tǒng)計學(xué)意義(P0.05)。2β-腎上腺素受體興奮劑異丙腎上腺素、腎上腺素可加重布比卡因?qū)π募×W(xué)的抑制作用,出現(xiàn)LVSP下降、+dp/dt max下降,且上述變化均有統(tǒng)計學(xué)意義(P0.05);而對LVEDP、-dp/dt max未見明顯影響。結(jié)論1布比卡因抑制大鼠心肌傳導(dǎo)功能和心肌力學(xué);2β-腎上腺素能受體興奮劑可加重布比卡因致大鼠心肌力學(xué)抑制,提高布比卡因中毒心肌自律性,但對傳導(dǎo)功能無明顯作用。
[Abstract]:The first part of the beta adrenergic receptor stimulant of bupivacaine intoxication Objective: ECG myocardial catecholamines due to the increase in diastolic blood pressure and coronary perfusion pressure is often used as a first-line treatment of heart failure; however, epinephrine could improve heart function, it will increase the bupivacaine induced incomplete, even cause pulmonary edema. In previous studies, the research group has confirmed that isoproterenol induced myocardial contraction of bupivacaine can aggravate the inhibition in the level of single cells, and esmolol can reverse this effect. This experiment will affect the self detection of beta adrenoceptor stimulants on bupivacaine and poisoning with myocardial conduction ability. Methods: the animal model of adult male SD rats 10% chloral hydrate by weight of 200~250g. rats (0.3ml/100g) intraperitoneal injection of anesthesia via the tail vein. The establishment of intravenous fluid pathway, the In the supine position fixed and connected. The electrocardiogram ECG probe are respectively fixed on the end of limbs in rats: Red probe fixed on the left lower extremity, green probe fixed to the right upper limb, black probe fixed to the right lower limb. This connection is collected cardiograph waveform. Maintain autonomous breathing in all rats during the experiment using RM6420. A series of multi-channel physiological signal acquisition and processing system of ECG acquisition and presentation on display. Experimental group rats were randomly into 3 groups: bupivacaine + saline + Bupivacaine group, isoproterenol group, bupivacaine and epinephrine group. Each group were 7 rats. Administration of bupivacaine + saline group: intravenous administration of bupivacaine at 0.75mg/kg/min, duration of 12min40s; then the uniform saline 0.4ml, duration 1min30s. bupivacaine + isoproterenol Epinephrine group: intravenous administration of bupivacaine at 0.75mg/kg/min, duration of 12min40s; then the uniform administration of isoprenaline (0.08mg/kg, 0.4ml), duration of 1min30s. bupivacaine and epinephrine group: intravenous administration of bupivacaine 0.75mg/kg/ constant min, duration of 12min40s; then the uniform administration of epinephrine (6 g/kg, 0.4ml). For the duration of 1min30s. by RM6420 series of multi-channel physiological signal acquisition and processing system of ECG monitoring in rats and analysis of PR interval, QRS interval and heart rate. Results: 1 bupivacaine for inhibiting myocardial conduction function; myocardial bupivacaine intoxication can occur with prolonged PR interval, QRS interval widened, heart rate decreased 2 (P0.05); isoproterenol (0.08mg/kg), epinephrine (6 g/kg) had no obvious effect on bupivacaine intoxication after myocardial PR and QRS intervals. After intravenous infusion of 1min, two groups of myocardial poisoning Heart rate (P0.05), and later in the experiment no difference with the control group. The second part of the beta adrenergic receptor stimulant increase inhibitory effect of bupivacaine on myocardial mechanics Objective: bupivacaine intoxication in clinic is not common but serious impact on the lives of patients. Catecholamine drugs as first-line agents in treatment of heart failure. However, for epinephrine effect of bupivacaine induced cardiac toxicity to rescue the poor. The previous studies using visual motion edge detection system of dynamic tracking synchronization detection technology to detect isoproterenol and effect of esmolol single myocardial cell contraction function on inhibition of bupivacaine induced by bupivacaine. The results showed that the contraction of myocardial cell concentration dependent reversible inhibition function the toxic effects of isoproterenol, bupivacaine can aggravate the inhibition of myocardial cell contraction, and AI division Los You can reverse this deterioration effect. This experiment will test the beta adrenergic receptor in the effect of doping of bupivacaine in inhibiting myocardial mechanics in vivo animal. Methods: the animal model of adult SD rats, male, weight 200g~250g. of 10% chloral hydrate (0.3ml/100g) intraperitoneal injection of anesthesia, supine position, the tail the establishment of vein intravenous fluid pathway. The common carotid artery and connected to the RM6420 series of multi-channel physiological signal collecting and processing system for the determination of ventricular pressure waveforms, recorded on display. Experimental groups by using random number method the rats were divided into 3 groups: bupivacaine + bupivacaine + saline group, isoproterenol group, bupivacaine + epinephrine group. 7 rats of each group were observed. Administration of bupivacaine + saline group: intravenous administration of bupivacaine at 0.75mg/kg/min, duration of 12min40s; then give uniform Physiological saline 0.4ml, duration 1min30s. bupivacaine + isoproterenol group: intravenous administration of bupivacaine at 0.75mg/kg/min, duration of 12min40s; then the uniform administration of isoprenaline (0.08mg/kg, 0.4ml), duration of 1min30s. bupivacaine and epinephrine group: intravenous administration of bupivacaine at 0.75mg/kg/min, duration of 12min40s and uniform; epinephrine (3 g/kg, 0.4ml), duration of 1min30s. observed experimental indicators: administration process, analysis and record the ventricular systolic pressure (left ventricular systolic pressure, LVSP), left ventricular end diastolic pressure (left ventricular end-diastolic pressure, LVEDP), left ventricular pressure maximal rate of rise (+dp/dt max). Left ventricular pressure decline rate (-dp/dt max) and other indicators. Results: 1 bupivacaine inhibits myocardial mechanics, LVSP decreased, LVEDP increased, +d P/dt Max -dp/dt decreased, Max decreased, and the results are statistically significant (P0.05).2 beta adrenergic receptor stimulant isoproterenol and epinephrine can increase the inhibitory effect of bupivacaine on myocardial mechanics, LVSP decreased, +dp/dt Max decreased, and the changes were statistically significant (P0.05); while the LVEDP, Max was -dp/dt obvious effect. Conclusion 1 bupivacaine inhibits myocardial conduction function and myocardial mechanics in rats; 2 beta adrenergic receptor agonists can aggravate myocardial mechanics in rats induced by bupivacaine inhibited, improve myocardial bupivacaine self-discipline, but no obvious effect on the conduction function.

【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R965

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本文編號：1562217