中华烧伤杂志
中華燒傷雜誌
중화소상잡지
16
2010年
6期
435-438
,共4页
邱啸臣%金以超%孙瑜%罗鹏飞%付晋凤%陈斌%夏照帆
邱嘯臣%金以超%孫瑜%囉鵬飛%付晉鳳%陳斌%夏照帆
구소신%금이초%손유%라붕비%부진봉%진빈%하조범
烧伤%活性氧%肺%血压%富氢盐水%延迟复苏
燒傷%活性氧%肺%血壓%富氫鹽水%延遲複囌
소상%활성양%폐%혈압%부경염수%연지복소
Burns%Reactive oxygen species%Lung%Blood pressure%Hydrogen-rich saline%Delayed resuscitation
目的 观察富氢盐水对延迟复苏烫伤大鼠血压和肺组织抗氧化能力的影响.方法 制备富氢盐水(即氢气溶解度达到饱和的生理盐水,氢浓度为0.6 mmol/L).采用随机数字表法将20只SD大鼠分为富氢盐水组和生理盐水组,每组10只.2组大鼠背部致30%TBSAⅢ度烫伤,伤后7、9、17 h,分别经腹腔给予相当于总补液量体积1/2、1/4、1/4的富氢盐水或者生理盐水,补液总量按照4 mL·kg-1·%TBSA-1(Parkland公式)计算.观察实验过程中大鼠总体情况;伤后6、24 h测收缩压;伤后24 h取大鼠肺组织,检测S0D抑制率和丙二醛含量.对实验结果进行t检验.结果 2组大鼠实验过程中无一只死亡.富氢盐水组和生理盐水组伤后6 h的收缩压分别为(87±4)、(86±5)mm Hg(1 mm Hg=0.133 kPa),2组水平接近(t=0.213,P=0.834);伤后24 h,富氢盐水组收缩压[(124±7)mm Hg]高于生理盐水组[(115±6)mm Hg,t=2.958,P=0.008].富氢盐水组肺组织SOD抑制率为(0.465±0.014)%,高于生理盐水组[(0.358±0.021)%,t=11.767,P=0.000].富氢盐水组的肺组织丙二醛含量[(922±196)pmol/mg]低于生理盐水组[(1118±212)pmol/mg,t=-2.142,P=0.046].结论 用富氢盐水对烫伤大鼠行延迟复苏,更有助于其血压恢复,并通过增强抗氧化酶的作用,减轻再灌注引起的肺组织细胞损伤.
目的 觀察富氫鹽水對延遲複囌燙傷大鼠血壓和肺組織抗氧化能力的影響.方法 製備富氫鹽水(即氫氣溶解度達到飽和的生理鹽水,氫濃度為0.6 mmol/L).採用隨機數字錶法將20隻SD大鼠分為富氫鹽水組和生理鹽水組,每組10隻.2組大鼠揹部緻30%TBSAⅢ度燙傷,傷後7、9、17 h,分彆經腹腔給予相噹于總補液量體積1/2、1/4、1/4的富氫鹽水或者生理鹽水,補液總量按照4 mL·kg-1·%TBSA-1(Parkland公式)計算.觀察實驗過程中大鼠總體情況;傷後6、24 h測收縮壓;傷後24 h取大鼠肺組織,檢測S0D抑製率和丙二醛含量.對實驗結果進行t檢驗.結果 2組大鼠實驗過程中無一隻死亡.富氫鹽水組和生理鹽水組傷後6 h的收縮壓分彆為(87±4)、(86±5)mm Hg(1 mm Hg=0.133 kPa),2組水平接近(t=0.213,P=0.834);傷後24 h,富氫鹽水組收縮壓[(124±7)mm Hg]高于生理鹽水組[(115±6)mm Hg,t=2.958,P=0.008].富氫鹽水組肺組織SOD抑製率為(0.465±0.014)%,高于生理鹽水組[(0.358±0.021)%,t=11.767,P=0.000].富氫鹽水組的肺組織丙二醛含量[(922±196)pmol/mg]低于生理鹽水組[(1118±212)pmol/mg,t=-2.142,P=0.046].結論 用富氫鹽水對燙傷大鼠行延遲複囌,更有助于其血壓恢複,併通過增彊抗氧化酶的作用,減輕再灌註引起的肺組織細胞損傷.
목적 관찰부경염수대연지복소탕상대서혈압화폐조직항양화능력적영향.방법 제비부경염수(즉경기용해도체도포화적생리염수,경농도위0.6 mmol/L).채용수궤수자표법장20지SD대서분위부경염수조화생리염수조,매조10지.2조대서배부치30%TBSAⅢ도탕상,상후7、9、17 h,분별경복강급여상당우총보액량체적1/2、1/4、1/4적부경염수혹자생리염수,보액총량안조4 mL·kg-1·%TBSA-1(Parkland공식)계산.관찰실험과정중대서총체정황;상후6、24 h측수축압;상후24 h취대서폐조직,검측S0D억제솔화병이철함량.대실험결과진행t검험.결과 2조대서실험과정중무일지사망.부경염수조화생리염수조상후6 h적수축압분별위(87±4)、(86±5)mm Hg(1 mm Hg=0.133 kPa),2조수평접근(t=0.213,P=0.834);상후24 h,부경염수조수축압[(124±7)mm Hg]고우생리염수조[(115±6)mm Hg,t=2.958,P=0.008].부경염수조폐조직SOD억제솔위(0.465±0.014)%,고우생리염수조[(0.358±0.021)%,t=11.767,P=0.000].부경염수조적폐조직병이철함량[(922±196)pmol/mg]저우생리염수조[(1118±212)pmol/mg,t=-2.142,P=0.046].결론 용부경염수대탕상대서행연지복소,경유조우기혈압회복,병통과증강항양화매적작용,감경재관주인기적폐조직세포손상.
Objective To study the effect of hydrogen-rich saline on blood pressure and antioxidant ability of lung tissue in scalded rats following delayed resuscitation. Methods The hydrogen-rich saline was prepared ( hydrogen-saturated normal saline with hydrogen concentration of 0.6 mmol/L). Twenty SD rats were divided into hydrogen-rich saline group (HS) and normal saline group (NS) according to the random number table, with 10 rats in each group. All the rats were subjected to 30% total body surface area (TBSA) full-thickness scald. Rats in HS and NS groups were infused with hydrogen-rich saline or normal saline with one half of the total fluid replacement volume as calculated according to the Parkland formula (4 spectively. The general condition of rats during the experiment was observed. The systolic pressure of rats was measured at PSH 6 and 24. All rats were sacrificed at PSH 24 to collect lung tissue for detecting superoxide dismutase (SOD) inhibition ratio and malondialdehyde (MDA) level. Data were processed with t test.Results All rats survived through the experiment. The systolic pressure of rats in HS group and NS group was respectively (87 ±4) mm Hg (1 mm Hg=0. 133 kPa) and (86 ±5) mm Hg at PSH 6, and the values were close ( t = 0.213, P = 0. 834); however the systolic pressure at 24 h was higher in HS group than in NS group [(124±7) mmHgvs. (115 ±6) mmHg, t =2.958,P =0.008]. SOD inhibition ratio of lung tissue in HS group [(0.465 ±0.014)%] was higher than that in NS group [(0.358 ±0.021)%, t =11. 767, P =0. 000]. MDA level of lung tissue in HS group [(922 ± 196) pmol/mg] was lower than that in NS group [(1118 ±212) pmol/mg, t = -2. 142, P =0.046]. Conclusions Delayed resuscitation for scalded rats with hydrogen-rich saline is helpful in the recovery of systolic pressure, and it can ameliorate lung tissue injury caused by reperfusion through enhancing the effect of antioxidase.