摘要
目的比较感染性休克与失血性休克早期兔心肌损害情况,为临床早期干预休克引起的心肌损害提供试验证据。方法28只健康中国白兔随机分为:感染性休克组(S组)、感染性休克对照组(Sc药)、失血性休克组(H组)、失血性休克对照组(Hc组)四组,每组7只。分别用CLP法和Wigger’s法复制感染性休克与失血性休克模型,取麻醉后休克前(t0)、休克开始时(t1)、休克后0.5小时(t2)、休克后1小时(t3)及休克后1.5小时(t4)为观察时点。监测各时点兔血流动力学及血清心肌肌钙蛋白I(cTnI)变化情况,两对照组也于相应时点留取标本。于试验结束时测兔心肌组织匀浆丙二醛(MDA)的浓度,比较各时点上述指标变化情况(重点比较两个休克组),并作心肌组织病理切片以观察、比较。结果(1)感染性休克开始时血流动力学指标即已发生显著变化,其后继续变化,但各相邻时点相比差异并非都有统计学意义;失血性休克开始时血流动力学指标无明显变化,休克开始后半小时发生显著变化(P<0.01),其后进行性下降,相邻时间点比较差异有显著性(P<0.05)。(2)感染性休克开始时血清cTnI即已显著升高(P<0.01),其后仍呈进行性升高趋势,相邻时点比较差异无统计学意义(P>0.05);失血性休克开始时血清cTnI无显著变化(P>0.05),休克后半小时cTnI显著升高(P<0.01),其后进行性升高,各时点均较其前一时点显著升高(P<0.05),至试验结束时H组高于S组(P<0.05)。(3)两试验组MDA均较对照组显著升高(P<0.05),H组高于S组(P<0.05)。(4)病理切片:S组心肌及其血管周围有炎症细胞浸润,灶性间质水肿,可见部分心肌细胞空泡变性;H组:从轻度的炎症反应、部分心肌细胞空泡变性,到心肌的灶性坏死,坏死灶周围可见炎症反应。结论感染性休克与失血性休克早期兔均发生心肌损害,感染性休克心肌损害出现时间较早,失血性休克心肌损害出现较迟,但进展较快、损害程度更大。
Objective To compare the myocardial damage in the early stage of septic shock and hemorrhagic shock in rabbits, and provide experimental evidence for early intervening myocardial damage caused by the two type shocks. Methods 28 healthy Chinese white rabbits were randomly divided into the following 4 groups: septic shock group (group S), septic shock control group (group Sc), hemorrhagic shock group (group H) and hemorrhagic shock control group (group Hc), with 7 rabbits in every group . Models of septic shock and hemorrhagic shock were replicated according to CLP method and Wigger' s method respectively. In the course of experiments hemodynamics were monitored. In the two type shock groups, before shock ( t0) , at the beginning of shock ( t1 ) , 0.5 hour after shock ( t2 ) , 1 hour after shock ( t3 ) and 1.5 hours after shock (t4) , serum samples were collected, samples of the two control groups were collected also at the corresponding time points. Levels of troponinI (cTnI) were measured, the animals were killed at the end of the experiments by bloodletting, part of every animal's myocardial tissue was chosed and 10 percent myocardial homogenate was made from it, levels of malondialdehyde (MDA) were measured. The changes of corresponding indicators of every group( with emphasis on the two type shock groups) at each time point were compared. At the end of the experiments pathological sections made from myocardial tissue were observed and compared. Results ( 1 ) At the beginning of shock, hemodynamics of group S changed significantly, then continued changing, but compared with adjacent time points the differences were not significant; and at the beginning of shock there was no significant change in group H and a half hours after shock declined significantly(P 〈 0.01 ), then continued declining, and in adjacent time points, the differences were significant (P〈0.05). (2) At the beginning of shock cTnI of group S was higher than that in group Sc (P〈0. 05), then there was an rising trend, compared with adjacent time points the differences were not significant;in group H at the beginning of shock, cTnI was not higher than that in group Hc, about 0.5 hour after shock it rose significantly (P 〈 0.05), then rose rapidly, the differences of adjacent time points were significant, its peak was higher than that of group S ( P 〈 0.05 ). ( 3 ) In myocardial tissue homogenate, level of MDA in group H was higher than that in group S (P 〈0.05). (4) In the two type shock groups myocardial tissue was infiltrated by inflammatory cells, degeneration can be found in some myocardial cells, focal necroses can be observed in hemorrhagic shock. Conclusion Myocardial damage happens in the early stage of both septic shock and hemorrhagic shock in rabbits. Compared with septic shock, myocardial damage in hemorrhagic shock occurs later, but progresses more rapidly, and the degree of damage is more serious.
出处
《海南医学》
CAS
2009年第12期19-22,共4页
Hainan Medical Journal
关键词
心肌肌钙蛋白I
丙二醛
血流动力学
感染性休克
失血性休克兔
早期
Cardiac troponin I
Malondialdehyde(MDA)
Hemodynamics
Septic shock
Hemorrhagic shock
Rabbit
Early stage