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氨基胍对中暑休克大鼠血压波形的影响
引用本文:宋旭东,陈爱华,李志樑,罗炳德,邹飞. 氨基胍对中暑休克大鼠血压波形的影响[J]. 中华劳动卫生职业病杂志, 2006, 24(8): 475-478
作者姓名:宋旭东  陈爱华  李志樑  罗炳德  邹飞
作者单位:1. 510282,广州,南方医科大学附属珠江医院心内科
2. 510282,广州,南方医科大学附属珠江医院热卫系高温医学研究所
摘    要:目的 探讨中暑休克大鼠的血压、心电图(ECG)、一氧化氮(NO)水平变化及氨基胍(AG)可能具有的抗中暑休克作用.方法 将SD雄性大鼠随机分为对照组及AG组,每组10只,给予温度41℃、相对湿度65%的环境进行热暴露诱发中暑休克,连续记录动脉血压、结肠温度(Tco)、ECG变化情况.取SD雄性大鼠随机分为对照组及AG组,每组10只,处理同前,热暴露0、60min时各取血1 ml,测大鼠血浆NO浓度.结果 两组大鼠血压在热暴露0~50 min时差异无统计学意义(P>0.05),在热暴露50 min时平均动脉压(MAP)升至最高,热暴露55~60min时MAP出现下降(中暑休克形成),对照组MAP下降较AG组明显.热暴露后两组K值及重搏切迹相对高度(hD/H)逐渐下降,尤其在热暴露40 min时对照组K值低于AG组,差异有统计学意义(P<0.05).热暴露之后,两组动物心率(HR)及QT间期延长,PR间期缩短.热暴露之后,两组动物Tco均升高,但差异无统计学意义(P>0.05).AG组中暑休克形成时间(TOHS)及生存时间(ST)较对照组明显延长.两组大鼠血浆NO浓度在热暴露0min时差异无统计学意义(P>0.05),热暴露60 min时两组血浆NO浓度均升高,对照组明显高于AG组,差异有统计学意义(P<0.05).结论 氨基胍可能对中暑休克出现的血压降低有一定的保护性影响,这种影响可能是通过对可诱导型一氧化氮合酶(iNOS)的抑制而体现的.

关 键 词:中暑 一氧化氮合酶 血压 氨基胍
收稿时间:2005-11-03
修稿时间:2005-11-03

Effects of selective iNOS inhibitor aminoguanidine on waveform of blood pressure in rat heat stroke
SONG Xu-dong,CHEN Ai-hua,LI Zhi-liang,LUO Bing-de,ZOU Fei. Effects of selective iNOS inhibitor aminoguanidine on waveform of blood pressure in rat heat stroke[J]. Chinese journal of industrial hygiene and occupational diseases, 2006, 24(8): 475-478
Authors:SONG Xu-dong  CHEN Ai-hua  LI Zhi-liang  LUO Bing-de  ZOU Fei
Affiliation:Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China
Abstract:OBJECTIVE: To evaluate the change of blood pressure, ECG and nitric oxide (NO) in rat heat stroke and effects of aminoguanidine (AG) against heatstroke. METHODS: The male SD rats were randomly assigned into 1 of the following 2 groups: control group or AG group. The rats of control group (n = 10) and AG group (n = 10) were exposed to high ambient temperature (41 degrees C, relative humidity 65%) to induce heatstroke, arterial blood pressures, colonic temperature (T(co)), electrocardiograph (ECG) were monitored. The other rats of both groups (both n = 10) were exposed to high ambient temperature (41 degrees C, relative humidity 65%), and the blood samples were taken at 0, 60 min after the start of heat exposure for determination of the plasma NO concentrations. RESULTS: (1) From 0 min to 50 min after heat exposure, MAPs of two groups were not significantly different, but at about 55 approximately 60 min after the start of heat exposure, MAPs of control group were decreased significantly differently from that of AG group, K value and dicrotic pulse relative height (h(D)/H) were gradually decreased, especially at 40 min after the start of heat exposure, K value of control group decreased significantly comparison with that of AG group; (2) Heart rate (HR) and QT interval of both groups were increased, while PR interval were decreased after the start of heat exposure; (3) T(co) of both groups were increased after the start of heat exposure until T(co) increased to 42 degrees C (the onset of heatstroke), but there was not significantly difference between the two groups; (4) The time of the onset of heatstroke (TOHS) and survival time (ST) of AG group were significantly longer than those of control group; (5) The plasma NO concentrations of the two groups were significantly higher at 60 min than at 0 min after the start of heat exposure, and the plasma NO concentrations of control group were significantly higher than that of AG group at 60 min after the start of heat exposure. CONCLUSION: iNOS may contribute to heatstroke, and aminoguanidine can provide protective effects on heatstroke as a selective iNOS inhibitor.
Keywords:Heat stroke  Nitric-oxide synthase  Blood pressure  Aminognanidine
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