本文選題：乙醇　切入點：血清鉀離子　出處：《河北醫(yī)科大學》2017年碩士論文　論文類型：學位論文

【摘要】：目的:在法醫(yī)實踐中,因酒后自制力失控、乙醇對機體的損傷等原因造成的外傷、意外、交通事故甚至死亡等案件逐年增多。有臨床研究發(fā)現(xiàn)過量飲酒所致的酒精中毒患者時常出現(xiàn)電解質(zhì)紊亂,特別是血清鉀離子降低,表現(xiàn)為肌無力和發(fā)作性軟癱,食欲缺乏,腹脹,惡心和便秘;嚴重缺鉀者可引起麻痹性腸梗阻,甚至導致死亡。本室在前期觀察人飲酒后對電解質(zhì)、血糖、血脂、凝血功能、肝功能影響時發(fā)現(xiàn),幾乎所有飲酒者都有血清鉀降低的趨勢。目前,飲酒后血鉀降低的變化規(guī)律以及乙醇導致血清鉀離子降低的機制前尚不清楚。本研究擬從探究乙醇導致血清鉀離子的降低現(xiàn)象為切入點,從以下兩個方面研究乙醇對鉀離子的作用及其機制:(1)收集急慢性飲酒人體標本,觀察血清鉀離子的變化規(guī)律;(2)建立急慢性飲酒大鼠模型,探討血清鉀離子降低的機制。方法:1觀察人體急性飲酒后血生化指標的變化1.1人體標本采集征集急性飲酒志愿者22名,年齡在20-50歲之間,征集要求:(1)男性;(2)無基礎疾病;(3)未服用特殊藥物(影響電解質(zhì)、血壓、血糖等的藥物);(4)如實填寫知情同意書。1.2試驗分組及方法志愿者隨機分為兩組,其中低劑量組10人,飲酒(飲用白酒56%v/v)100ml,飲酒后1h采血,高劑量組12人,飲酒150ml,飲酒后1.5h采血。對各志愿者飲酒前和飲酒后的血乙醇濃度、電解質(zhì)、凝血功能、肝功能、乙醇脫氫酶(ADH)、乙醛脫氫酶(ALDH)進行監(jiān)測,以觀察急性飲酒對上述血生化指標的影響。2觀察急慢性飲酒后人體血清鉀離子的變化規(guī)律2.1急性飲酒人體標本采集及分組:征集急性飲酒志愿者5名,志愿者要求:(1)男性;(2)年齡在20-30歲之間,其他要求同前。因?qū)嶒灁?shù)據(jù)均為志愿者飲酒前后自身的對照,在統(tǒng)計學上所收集案例數(shù)量能夠滿足統(tǒng)計學要求。然后,對各志愿者飲酒(飲用白酒56%v/v)前和飲酒后0.5 h、1 h、2 h、3 h的血乙醇濃度和血清鉀離子(Serum potassium,SP)進行監(jiān)測,以觀察急性飲酒后SP的變化規(guī)律。2.2慢性飲酒人體標本采集及分組:征集慢性中重度飲酒和不飲酒或輕度飲酒志愿者60名,志愿者要求:(1)男性;(2)年齡在20-50歲之間;其他要求同前。試驗分組:分為20-30歲組、30-40歲組、40-50歲組,每組20人;每組中慢性中重度飲酒者10人,不飲酒或輕度飲酒者10人。抽血檢測各志愿者SP,以觀察慢性中重度飲酒對SP的影響。2.3采血方式:抽血前安靜休息15分鐘,肘正中靜脈穿刺抽血。2.4檢測:采用離子選擇電極法檢測SP;采用頂空氣相色譜法檢測BAC。3急慢性飲酒動物模型建立及實驗分組3.1急性飲酒動物模型建立及實驗分組:(1)對照組(n=36):隨機分為Control組、0.5 h、1 h、1.5 h、2 h、2.5 h組,每組6只。Control組用蒸餾水灌胃(1.2 ml/100 g)后,于0.5 h、1 h、1.5 h、2 h、2.5 h內(nèi)眥靜脈取血測定血清鉀離子濃度;(2)急性飲酒組(n=30):隨機分為0.5 h、1 h、1.5 h、2 h、2.5 h組,每組6只。給予飲用白酒(56%v/v)灌胃(1.2 ml/100g)制備急性飲酒組模型。各組分別于灌胃后0.5 h、1 h、1.5 h、2 h、2.5 h內(nèi)眥取血測定血乙醇濃度和血清鉀離子濃度;(3)鈉-鉀ATP酶抑制劑組(以下簡稱抑制劑組)(n=18):隨機分為1 h、1.5 h、2 h組,每組6只。腹腔注射給予鈉-鉀ATP酶抑制劑哇巴因溶液(Oua)(60μg/100 g)進行干預。各組分別于腹腔注射Oua后1 h、1.5 h、2 h內(nèi)眥取血測定血清鉀離子濃度;(4)抑制劑+飲酒組(n=18),隨機分為1 h、1.5 h、2 h組,每組6只。在腹腔注射給予Oua(60μg/100 g)后,隨即給予飲用白酒(56%v/v)灌胃(1.2 ml/100 g)。各組分別于灌胃后1 h、1.5 h、2 h進行內(nèi)眥取血測定血乙醇濃度和血清鉀離子濃度。3.2慢性飲酒動物模型建立及實驗分組:(1)慢性飲酒組(n=18):隨機分為1 w、2 w、4 w組,每組6只。分別給予飲用白酒(56%v/v)灌胃(1.2 ml/100 g/d)1 w、2 w、4 w制備慢性飲酒組模型。各組分別于末次灌胃后12 h進行內(nèi)眥取血測定血鉀含量;(2)慢性+急性飲酒組(n=18):隨機分為1 w、2 w、4 w組,每組6只。各組分別于末次灌胃后12 h再次進行急性飲用白酒(56%v/v)灌胃(1.2 ml/100 g),并于灌胃后1.5h進行內(nèi)眥取血測定血乙醇濃度和血清鉀離子濃度。3.3檢測:采用離子選擇電極法檢測SP;采用頂空氣相色譜法檢測BAC。結(jié)果:1人體急性飲酒后血生化指標的變化:急性飲酒后血鈉、血氯、血鈣、血鎂、血磷、ADH、ALDH含量,凝血功能,肝功能,與飲酒前均無顯著性差異(P0.05),而血鉀比飲酒前顯著降低(P0.05)。2飲酒對人體血清鉀離子的影響:(1)急性飲酒志愿者0.5 h、1 h、2 h的SP均比飲酒前顯著降低(P0.05)。飲酒后3 h的SP與飲酒前比無顯著性差異(P0.05)。飲酒后3 h內(nèi)的BAC與SP的Pearson相關(guān)系數(shù)為-0.67;(2)慢性中重度飲酒和不飲酒或輕度飲酒志愿者,各年齡段組內(nèi)組間SP均無顯著性差異(P0.05);3飲酒對大鼠血清鉀離子的影響:(1)大鼠急性飲酒后0.5h、1 h、1.5 h、2 h組SP比對照組顯著降低(P0.05),2.5 h組SP與對照組相比無顯著性差異(P0.05)。BAC與SP的Pearson相關(guān)系數(shù)為-0.68;(2)抑制劑組大鼠各時間點SP比對照組顯著升高(P0.05);(3)抑制劑+急性飲酒組大鼠SP比急性飲酒組顯著升高(P0.05),但較抑制劑組顯著降低(P0.05);(4)大鼠慢性飲酒1 w、2 w、4 w對SP無顯著影響(P0.05);(5)大鼠慢性+急性飲酒后1 w、2 w、4 w組SP比對照組顯著降低(P0.05),與急性飲酒1.5h組相比無顯著變化。上述結(jié)果提示,鈉-鉀ATP酶抑制劑拮抗了急性飲酒所致鉀離子的降低。結(jié)論:1飲酒后人體血清鉀濃度短暫降低為急性乙醇作用所致,并隨乙醇濃度呈現(xiàn)規(guī)律性變化,而慢性飲酒對血清鉀濃度無影響。2急性乙醇作用所致血清鉀濃度降低與細胞內(nèi)外鉀離子轉(zhuǎn)運功能有關(guān)。
[Abstract]:Objective: in forensic practice, drunken self-control is out of control, causing ethanol injury to the body due to trauma, accidents, traffic accidents and even death cases increased year by year. Clinical studies have found that alcohol poisoning caused by excessive drinking often occurs in electrolyte disorder, especially serum potassium decreased, showed weakness and seizures soft paralysis, loss of appetite, abdominal distension, nausea and constipation; severe potassium deficiency can cause paralytic ileus, and even lead to death. The room in the early observation of drinking on blood glucose, blood lipid, electrolyte, blood coagulation function, found that the influence of liver function, almost all drinkers have decreased serum potassium current. Changes of serum potassium, decreased after drinking and ethanol induced mechanism of serum potassium decreased before is not clear. This study intends to explore ethanol leads to the decrease of serum potassium phenomenon as the breakthrough point, from the following Two aspects of ethanol on the potassium ion effect and its mechanism: (1) from acute and chronic alcohol consumption in human specimens, observe the changes of serum potassium ion; (2) the establishment of acute and chronic drinking rat model, and explore the mechanism of serum potassium decreased. Methods: the changes of biochemical indexes of 1 acute human blood after 1.1 drinks the human body specimens collection of acute alcohol intake of 22 volunteers, collecting requirements at the age of 20-50, (1): male; (2) basic diseases; (3) did not take special drugs (blood pressure, blood glucose and electrolyte effects, drugs); (4) fill in the informed consent of volunteers.1.2 test group and method were randomly divided into two groups, including low dose group (10 people, drinking liquor drinking 56%v/v 100ml, 1H) after drinking blood, the high dose group of 12 people, drinking 150ml, after drinking 1.5h blood. The blood alcohol concentration, the volunteers before and after drinking alcohol electrolytes, coagulation function, liver function, Alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH) were monitored to observe the acute effects of alcohol on the blood biochemical.2 observation of human serum potassium changes after acute and chronic alcohol drinking 2.1 acute human specimen collection and grouping: for acute alcohol 5 volunteers, volunteer requirements: (1) (2 men; at the age of 20-30), with other requirements. Because the experimental data are in its own volunteers before and after drinking, collected the number of cases can meet the statistical requirements in statistics. Then, the volunteers (alcohol drinking liquor 56%v/v) before and after drinking 0.5 h, 1 h, 2 h, and the blood alcohol concentration the serum potassium ion of 3 h (Serum potassium SP) were monitored to observe the acute SP after drinking.2.2 changes of chronic alcohol consumption of human specimen collection and grouping: for chronic heavy drinking and non drinking or mild drinking 60 volunteers, volunteer 鑰呰姹，

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