探索机械通气下猪腹腔间隔室综合征(ACS)心功能损伤变化及可能机制。

健康成年实验猪10头，按随机数字表法分为实验组(6头)和对照组(4头)。实验组在机械通气情况下采用水囊叠加加压法复制腹腔高压液体动物模型，对照组在麻醉后沿腹部切口置入空瘪的加压水囊后即关腹。机械通气设定：容量控制通气(VCV)模式，潮气量(VT)10 mL/kg，呼吸频率16次/min，吸入氧浓度(FiO₂)40%，呼气末正压(PEEP)5 cmH₂O。通过加压管向加压水囊注入0.9%氯化钠注射液(每注入50 mL测压1次)，直至腹腔压力达到30 mmHg，记录并绘制腹腔压力-增容量曲线，抽出部分注液调整腹腔压力维持在25 mmHg，连续观察4 h，并分别在建模前及压力维持后每小时由耳缘静脉抽血5 mL，行心肌酶谱检查。建模并维持腹腔压力4 h后过量丙泊酚静脉推注处死实验动物，完整切取心脏，用10%甲醛溶液固定24 h后常规石蜡包埋，冠状位连续切片(切片厚度4 μm)，经苏木精-伊红(HE)染色后在生物光学显微镜下(×200)观察其心肌的病理变化。

腹腔高压液体(猪)动物模型的腹腔内压力与腹腔增容量呈正相关，腹腔压力-腹腔增容量曲线为线性函数，函数方程为：Y=0.1074X－206.045(r²=0.8396，P<0.05)。与建模前对比，在建模后1 h，乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)和a-羟丁酸脱氢酶(α-HBDH)均升高(P均<0.05)，而建模后2~4 h各指标差异均无统计学意义。机械通气下，ACS使心肌纤维嗜酸性变，心肌纤维部分萎缩，部分肥大，横纹消失，局部可见玻璃样变性，可见细胞核聚集。

机械通气改变了ACS腹腔压力-容积曲线的形态，机械通气下ACS发展仍伴随心肌细胞损伤和心肌酶谱改变。

To explore the changes of cardiac function and its mechanism in the animal model of abdominal compartment syndrome (ACS) under mechanical ventilation.

Ten healthy adult pigs was randomly divided into experimental group (N=6) and control group (N=4) according to the random number method. In the experimental group; the abdominal hypertensive liquid animal model was reproduced by water sac superimposed pressure under mechanical ventilation; in the control group, the abdomen was closed immediately after the empty pressurized water sac was placed along the abdominal incision after anesthesia. Mechanical ventilation was set in volume controlled ventilation (VCV) mode with tidal volume (VT) 10 mL/kg, respiratory frequency 16 times/min, inhaled oxygen concentration (Fi02) 40%, and positive end-expiratory pressure (PEEP) 5 cm H₂O (1 cmH₂O= 0.098 kPa). 0.9% sodium chloride was injected into the pressurized water sac through a pressurized tube (once every 50 mL pressure measurement) until the intraperitoneal pressure reached 30 mmHg (1 mmHg = 0.133 kPa). The pressure-volume curve was recorded and drawn. The intraperitoneal pressure was maintained at 25 mmHg after partial injection. The intraperitoneal pressure was continuously observed for 4 hours before and after the establishment of the model, respectively. After maintenance, 5 ml of venous blood was drawn from ear vein every hour, and myocardial enzymogram was performed. After modeling and maintaining abdominal pressure for 4 hours, the animals were killed by intravenous injection of propofol. The hearts were cut intact. The hearts were fixed in 10% formaldehyde solution for 24 hours and embedded in paraffin. Coronal sections were made continuously (4 microns thick). The hearts were stained with hematoxylin-eosin (HE) and the pathological changes of myocardium were observed under bio-optical microscope (x 200).

The intraabdominal pressure of abdominal hypertension liquid (pig) animal model was positively correlated with abdominal volume increasing, and the abdominal pressure abdominal volume curve was a linear function. The function equation was Y=0.1074X-206.045 (r²=0.8396, P<0.05). Compared with before modeling, lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB) and α-hydroxybutyrate dehydrogenase (alpha-HBDH) increased 1 h after modeling (all P<0.05), but there was no significant difference in each index between 2 and 4 h after modeling. Under mechanical ventilation, ACS resulted in eosinophilic degeneration, atrophy, hypertrophy, disappearance of transverse lines, vitreous degeneration and nuclear aggregation in myocardial fibers.

Mechanical ventilation changes the shape of pressure-volume curve of ACS. The development of ACS under mechanical ventilation is accompanied by myocardial cell injury and myocardial enzymogram changes.