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纸质出版:2013
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王丽,谢镒鞠,唐小唪,王正刚,刘道城,张连阳,葛衡江.创伤失血性休克后腹腔高压对心肺基础监测指标的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(20):2159-2163.
Wang Li,Xie Yiju,Tang Xiaofeng,Wang Zhenggang,Liu Daocheng,Zhang Lianyang,Ge Hengjiang.Effect of intra-abdominal hypertension after traumatic hemorrhagic shock on porcine respiratory and circulatory parameters[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(20):2159-2163.
王丽,谢镒鞠,唐小唪,王正刚,刘道城,张连阳,葛衡江.创伤失血性休克后腹腔高压对心肺基础监测指标的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(20):2159-2163. DOI:
Wang Li,Xie Yiju,Tang Xiaofeng,Wang Zhenggang,Liu Daocheng,Zhang Lianyang,Ge Hengjiang.Effect of intra-abdominal hypertension after traumatic hemorrhagic shock on porcine respiratory and circulatory parameters[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(20):2159-2163. DOI:
目的 本研究旨在通过失血性休克复苏后腹腔高压症(intra-abdominal hypertension,IAH)动物模型的建立观察腹腔内压力变化特点以及心肺监测指标的变化。 方法 健康成年小型实验猪经股动脉插管放血致平均动脉压(mean arterial pressure
MAP)约为50 mmHg,持续1 h,同时部分阻断门静脉,建立失血性休克模型。成功建立IAH模型8只,按抛硬币法随机分为治疗组和对照组
每组4只。动态监测呼吸、循环指标。治疗组采用腹腔减张缝合技术治疗。分别于实验动物放血前、放血后1 h、IAH后及IAH治疗后12 h测量、对比膀胱压(vesical pressure
VP)。 结果 随着腹腔内压力逐步增加,两组动物膀胱压均升高 [(12±2)vs (27±8)cmH
2
O,(12±2) vs (30±7) mmHg
P0.01
]
;经腹腔减压处理后,治疗组膀胱压降低[(27±8)vs (12±2)cmH
2
O,
P
0.01
]
,治疗组和对照组膀胱压之间也有显著差异[(30±7)vs(12±2)cmH
2
O,
P
0.01
]
。随着失血性休克的逐步形成,平均动脉压下降[(115±9 ) vs (62±13) mmHg,
P
0.01
]
,心率升高[(118±17)vs (55±4)/min,
P
0.01
]
。腹腔高压后与放血前呼吸频率增加[(59±9)vs ( 32±13) /min,
P
0.01
]
。治疗后,治疗组呼吸频率明显低于对照组[(33±4) vs (53±18) /min,
P
0.01
]
。休克后动脉血中乳酸含量明显增高[(1.9±0.8)vs (0.9±0.5)mmoL/L,
P
0.01
]
,治疗12 h后乳酸含量下降[(1.0±0.4) vs (1.9±0.8)mmoL/L,
P
0.01
]
。 结论 模型成功模拟创伤失血性休克复苏后腹腔高压症的形成。随着IAH形成,腹腔内压明显增高。腹腔减压术可以显著降低腹腔内压,改善呼吸频率,降低乳酸含量。
Objective To establish an animal model of intra-abdominal hypertension (IAH) followed by hemorrhagic shock and in
vestigate the features of the intra-abdominal pressure changes and the alteration of cardiorespiratory monitoring indicators. Methods Healthy adult experimental pigs were employed for bloodletting from the femoral artery till mean arterial pressure (MAP) to 50 mmHg for 1 h to reproduce hemorrhagic shock model. IAH model was successfully reproduced in 8 pigs by partial occlusion of portal vein. The pigs were randomly divided into treatment group (n=4) and control group (n=4). Intra-abdominal volume increment (IAVI) treatment was used to the rats of treatment group. Vesical pressure (VP) was observed before bleeding
in 1 h after bleeding
2 h after IAH and 12 h after IAVI treatment. Results With the gradual increase of intra-abdominal pressure
vesical pressure was increased in both groups (12±2 vs 27±8 cmH
2
O
P
0.01). After IAVI treatment
the pressure was reduced (27±8 vs 12±2 cmH
2
O
P
0.01)
and also had significant difference with that in the control (30±7 vs 12±2 cmH
2
O
P0.01). With the gradual formation of hemorrhagic shock
MAP was deceased from 115±9 to 62±13 mmHg (
P
0.01)
heart rate was increased from 55±4 to 118±17 beats/min (
P
0.01). Respiratory rate was significantly elevated with the increase of abdominal hypertension (59±9 vs 32±13 times/min
P
0.01). After treatment
the respiratory rate was significantly lower in the treatment group than the control group (33±4 vs 53±18 times/min,
P
0.01). Serum level of lactic acid after shock was significantly increased (1.9±0.8 vs 0.9±0.5 mmoL/L
P
0.01)
and was decreased after 12 hours’ treatment (1.0±0.4 vs 1.9±0.8 mmoL/L
P
0.01). Conclusion Our model is a good simulation of IAH secondary to traumatic hemorrhagic shock. With IAH formation
intra-abdominal hypertension is significantly increased. Abdominal decompression significantly reduces the pressure
improves breathing frequency
and lowers serum level of lactic acid.
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