机械通气对百草枯中毒家猪急性肺损伤的影响
发布时间:2018-08-17 13:34
【摘要】:第一部分:百草枯中毒致家猪急性肺损伤模型的建立 目的: 建立百草枯(paraquat,PQ)致家猪急性肺损伤模型,为进一步研究肺保护性通气策略治疗百草枯中毒提供条件。 方法: 将10头健康雌性家猪随机分为对照组(n=4)和实验组(n=6)。实验组家猪给予20%PQ溶液20ml腹腔注射,对照组给予等量生理盐水腹腔注射。使用脉搏指示连续心排血量(PiCCO)监测仪动态监测两组动物心率(HR)、平均动脉压(MAP)、血管外肺水指数(ELWI)、肺血管通透性指数(PVPI),记录动脉血pH值、氧分压(PaO2)、二氧化碳分压(PaCO2)、氧合指数(PaO2/FiO2)、气道峰压(PIP)及气道平台压(Pplat)变化,直到氧合指数≤300mmHg。 结果: 实验组有5头猪成功建立急性肺损伤模型,平均造模成功时间为(4.5±0.2)h。实验组从造模开始2.5h后HR、MAP、ELWI、PVPI、PIP和Pplat呈逐渐上升趋势,造模成功时实验组与对照组相比差异有统计学意义(均P0.05)。造模开始后实验组pH值、PaO2及氧合指数呈逐渐下降趋势,而PaCO2逐渐上升,造模成功时实验组与对照组相比差异有统计学意义(均P0.05)。肺组织病理结果显示造模成功时肺组织出现明显的损伤性改变。 结论: 本方法可以建立稳定的百草枯致急性肺损伤模型,为进一步动物实验研究提供条件。 第二部分:脉搏指示连续心排血量监测下不同潮气量机械通气对百草枯中毒家猪急性肺损伤的影响 目的: 研究脉搏指示连续心排血量(PiCCO)监测下不同潮气量(VT)联合呼气末正压(PEEP)机械通气对百草枯中毒家猪急性肺损伤/急性呼吸窘迫综合症(ALI/ARDS)的影响。 方法: 用20%百草枯原液20ml腹腔注射制备家猪急性百草枯中毒后ALI/ARDS模型,造模成功后随机分为三组,每组各6只。接呼吸机辅助呼吸,潮气量分别为小VT组(6ml/kg)、中VT组(10ml/kg)和大VT组(15ml/kg),PEEP均设为10cmH2O。采用PiCCO监测造模前(基础值)、造模成功(t0)及机械通气后2h(t2)、4h(t4)及6h(t6)时的心率(HR)、平均动脉压(MAP)、血管外肺水指数(ELWI)和肺血管通透性指数(PVPI),记录各时点的动脉血pH值、氧分压(PaO2)、二氧化碳分压(PaCO2)以及气道峰压(PIP)及气道平台压(Pplat)等指标,计算氧合指数(PaO2/FiO2);同时在造模前、造模成功时及机械通气后6h分别进行肺组织穿刺进行苏木精-伊红(HE)染色法观察肺组织病理变化。 结果: 家猪在注射百草枯后(4.5±0.8)h达到ALI/ARDS。造模成功时各组HR和MAP均较基础值明显上升,差异有统计学意义(均P0.05);机械通气后各组HR和MAP均逐渐下降,与同组t0相比差异均有统计学意义(均P0.05)。造模成功时各组pH值、PaO2及氧合指数与基础值相比均明显下降,而PaCO2明显上升,差异均有统计学意义(均P0.05);机械通气后各组pH值呈逐渐下降趋势,通气后6h小VT组下降最为明显;通气后2h各组PaO2及氧合指数均明显上升,其中小VT组上升最为明显,之后均逐渐下降,通气后6h小VT组PaO2及氧合指数明显高于其余两组;机械通气后各组PaCO2均呈逐渐上升趋势,以小VT组上升最为明显。造模成功时各组ELWI和PVPI与基础值相比均明显上升,差异均有统计学意义(均P0.05);机械通气后2h各组ELWI均明显上升,之后小VT组及中VT组ELWI逐渐下降,通气后6h小VT组下降更为明显;通气后各组PVPI无明显变化。机械通气后小VT组PIP及Pplat逐渐下降,而中VT组和大VT组则均逐渐上升,通气后6h小VT组PIP及Pplat明显低于其余两组。造模成功时(t0)肺泡组织呈明显损伤性改变,通气6h后(t6)损伤加重,其中以大VT组最为明显,小VT组损伤较轻。 结论: 小潮气量联合呼气末正压机械通气可减轻百草枯中毒急性肺损伤,改善氧合状况。 第三部分:压力控制法与呼气末正压递增法肺复张对百草枯致急性肺损伤家猪血流动力学的影响 目的: 探讨压力控制(PC)法与呼气末正压(PEEP)递增法肺复张(RMs)对百草枯(PQ)致急性肺损伤家猪血流动力学的影响。 方法: 10头健康雌性家猪给予20%PQ溶液20ml腹腔注射建立百草枯中毒急性肺损伤/急性呼吸窘迫综合症(ALI/ARDS)模型。建模成功后将所有动物随机分为压力控制法肺复张组(RM1)和PEEP递增法肺复张组(RM2),每组各5头。比较两组间正常值(基础值)、建模成功时(t0)、RMs后5min(t5)、15min(t15)和30min(t30)时的心率(HR)、平均动脉压(MAP)、心功能指数(CI)、氧分压(PaO2)、二氧化碳分压(PaCO2)、氧合指数(PaO2/FiO2)变化。同时在造模前、t0及t30时刻分别进行肺组织穿刺进行苏木精-伊红(HE)染色并观察肺组织病理变化。 结果: 造模成功时HR与MAP与基础值相比均明显上升,而CI明显降低(均P0.05),RMs后HR与MAP呈逐渐下降趋势,,在RMs后5minRM1组HR与MAP明显低于RM2组(均P0.05),RMs后30min两组间HR与MAP差异无统计学意义(均P0.05);CI在RMs后呈先下降后上升的趋势,RMs复张后5min时RM1组明显高于RM2组(P0.05),RMs后30min两组间差异无统计学意义(P0.05);造模成功时两组PaO2和氧合指数均明显下降,而PaCO2明显上升(与基础值相比均P0.05);RMs后两组PaO2、PaCO2和氧合指数均呈上升趋势,两组间差异无统计学意义(均P0.05)。RMs后30min两组动物的肺组织均表现出多样的病理学改变,主要表现为肺泡上皮细胞脱落、肺泡间隔进一步增宽及肺泡过度膨胀,部分可见肺泡间隔断裂。 结论: 压力控制法与呼气末正压递增法肺复张均可以明显改善百草枯中毒家猪ALI/ARDS时的氧合状况,而且压力控制法对血流动力学的影响较小。
[Abstract]:Part one: establishment of acute lung injury model induced by paraquat poisoning in pigs *
Objective:
To establish a model of acute lung injury induced by paraquat (PQ) in pigs, and provide conditions for further study of lung protective ventilation strategy in the treatment of paraquat poisoning.
Method:
Ten healthy female pigs were randomly divided into control group (n=4) and experimental group (n=6). Pigs in experimental group were given 20% PQ solution intraperitoneally, and control group was given the same amount of normal saline intraperitoneally. Pulmonary vascular permeability index (PVPI), arterial blood pH, partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), oxygenation index (PaO2/FiO2), peak airway pressure (PIP) and airway plateau pressure (Pplat) were recorded until the oxygenation index was less than 300 mmHg.
Result:
In the experimental group, 5 pigs were successfully established * an acute lung injury model, and the average time for establishing the model was (4.5 + 0.2) h.. After the start of 2.5h, the HR, MAP, ELWI, PVPI, PIP and Pplat in the experimental group showed a gradual upward trend. When the model was successful, the difference between the experimental group and the control group was statistically significant (P0.05). PaCO2 increased gradually, and the difference between the experimental group and the control group was statistically significant (all P 0.05). The pathological results of lung tissue showed that the lung tissue showed obvious damage changes after successful modeling.
Conclusion:
This method can establish a stable paraquat-induced acute lung injury model and provide conditions for further animal experimental study.
Part 2: Effect of mechanical ventilation with different tidal volume on acute lung injury in pigs poisoned by Paraquat
Objective:
To study the effects of different tidal volume (VT) combined with positive end-expiratory pressure (PEEP) mechanical ventilation on acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in pigs poisoned by paraquat.
Method:
ALI/ARDS model of pigs after acute paraquat poisoning was established by intraperitoneal injection of 20% paraquat solution 20 ml. Six pigs in each group were randomly divided into three groups. Heart rate (HR), mean arterial pressure (MAP), extravascular lung water index (ELWI) and pulmonary vascular permeability index (PVPI) were recorded at 2 h (t2), 4 h (t4) and 6 h (t6) after mechanical ventilation. The arterial pH, partial oxygen pressure (PaO2), partial carbon dioxide pressure (PaCO2), peak airway pressure (PIP) and plateau pressure (Pplateau) were recorded at each time point. (PaO2/FiO2) puncture and hematoxylin-eosin (HE) staining were used to observe the pathological changes of lung tissue before and 6 hours after mechanical ventilation.
Result:
The HR and MAP of each group were significantly higher than those of the baseline (all P 0.05). After mechanical ventilation, the HR and MAP of each group were gradually decreased, and the difference was statistically significant (all P 0.05). The pH value, PaO2 and oxygenation index and baseline of each group were significantly higher than those of the same group (all P 0.05). Compared with the baseline values, PaCO2 increased significantly, and the difference was statistically significant (all P 0.05); After mechanical ventilation, the pH value of each group showed a gradual downward trend, especially in the small VT group at 6 hours after ventilation; PaO2 and oxygenation index of each group increased significantly at 2 hours after ventilation, especially in the small VT group, and gradually decreased after 6 hours after ventilation. PaO2 and oxygenation index in T group were significantly higher than those in the other two groups; PaCO2 in each group increased gradually after mechanical ventilation, especially in small VT group. After ventilation, the levels of PIP and Pplat in small VT group decreased gradually, while those in medium VT group and large VT group increased gradually. The levels of PIP and Pplat in small VT group were significantly lower than those in the other two groups at 6 hours after ventilation. After 6h ventilation (T6), the injury was aggravated, especially in the large VT group, and in the small VT group.
Conclusion:
Small tidal volume combined with positive end-expiratory pressure mechanical ventilation can alleviate acute lung injury caused by paraquat poisoning and improve oxygenation.
Part III: Effects of pressure control and positive end-expiratory pressure increment on hemodynamics in pigs with paraquat-induced acute lung injury
Objective:
To investigate the effects of pressure control (PC) and positive end-expiratory pressure (PEEP) incremental lung relaxation (RMs) on hemodynamics in pigs with acute lung injury induced by paraquat (PQ).
Method:
10 healthy female pigs were given 20% PQ solution 20 ml intraperitoneal injection to establish acute lung injury/acute respiratory distress syndrome (ALI/ARDS) model of paraquat poisoning. Heart rate (HR), mean arterial pressure (MAP), cardiac function index (CI), partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaO2), and oxygenation index (PaO2/FiO2) were measured at 5 min (t5), 15 min (t15) and 30 min (t30) after RMs. Change.
Result:
HR and MAP in RM1 group were significantly lower than those in RM2 group (all P 0.05). HR and MAP in RMs group were significantly lower than those in RM2 group (all P 0.05). HR and MAP in RM1 group were significantly lower than those in RM2 group (all P 0.05). There was no significant difference in HR and MAP between the two groups 30 minutes after RMs (all P 0.05). RM1 group was significantly higher than RM2 group at n time (P 0.05), and there was no significant difference between the two groups at 30 minutes after RMs (P 0.05); PaO2 and oxygenation index were significantly decreased, while PaCO2 was significantly increased (P 0.05 compared with the baseline); PaO2, PaCO2 and oxygenation index were increased in both groups after RMs, and there was no significant difference between the two groups (P 0.05). The alveolar epithelial cells were exfoliated, the alveolar septum was widened and the alveolar septum was overstretched, and some of the alveolar septum was broken.
Conclusion:
Both pressure control and positive end-expiratory pressure incremental lung relaxation could significantly improve oxygenation in paraquat poisoned pigs with ALI/ARDS, and the effect of pressure control on hemodynamics was less.
【学位授予单位】:郑州大学
【学位级别】:硕士
【学位授予年份】:2014
【分类号】:R595.4
本文编号:2187796
[Abstract]:Part one: establishment of acute lung injury model induced by paraquat poisoning in pigs *
Objective:
To establish a model of acute lung injury induced by paraquat (PQ) in pigs, and provide conditions for further study of lung protective ventilation strategy in the treatment of paraquat poisoning.
Method:
Ten healthy female pigs were randomly divided into control group (n=4) and experimental group (n=6). Pigs in experimental group were given 20% PQ solution intraperitoneally, and control group was given the same amount of normal saline intraperitoneally. Pulmonary vascular permeability index (PVPI), arterial blood pH, partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), oxygenation index (PaO2/FiO2), peak airway pressure (PIP) and airway plateau pressure (Pplat) were recorded until the oxygenation index was less than 300 mmHg.
Result:
In the experimental group, 5 pigs were successfully established * an acute lung injury model, and the average time for establishing the model was (4.5 + 0.2) h.. After the start of 2.5h, the HR, MAP, ELWI, PVPI, PIP and Pplat in the experimental group showed a gradual upward trend. When the model was successful, the difference between the experimental group and the control group was statistically significant (P0.05). PaCO2 increased gradually, and the difference between the experimental group and the control group was statistically significant (all P 0.05). The pathological results of lung tissue showed that the lung tissue showed obvious damage changes after successful modeling.
Conclusion:
This method can establish a stable paraquat-induced acute lung injury model and provide conditions for further animal experimental study.
Part 2: Effect of mechanical ventilation with different tidal volume on acute lung injury in pigs poisoned by Paraquat
Objective:
To study the effects of different tidal volume (VT) combined with positive end-expiratory pressure (PEEP) mechanical ventilation on acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in pigs poisoned by paraquat.
Method:
ALI/ARDS model of pigs after acute paraquat poisoning was established by intraperitoneal injection of 20% paraquat solution 20 ml. Six pigs in each group were randomly divided into three groups. Heart rate (HR), mean arterial pressure (MAP), extravascular lung water index (ELWI) and pulmonary vascular permeability index (PVPI) were recorded at 2 h (t2), 4 h (t4) and 6 h (t6) after mechanical ventilation. The arterial pH, partial oxygen pressure (PaO2), partial carbon dioxide pressure (PaCO2), peak airway pressure (PIP) and plateau pressure (Pplateau) were recorded at each time point. (PaO2/FiO2) puncture and hematoxylin-eosin (HE) staining were used to observe the pathological changes of lung tissue before and 6 hours after mechanical ventilation.
Result:
The HR and MAP of each group were significantly higher than those of the baseline (all P 0.05). After mechanical ventilation, the HR and MAP of each group were gradually decreased, and the difference was statistically significant (all P 0.05). The pH value, PaO2 and oxygenation index and baseline of each group were significantly higher than those of the same group (all P 0.05). Compared with the baseline values, PaCO2 increased significantly, and the difference was statistically significant (all P 0.05); After mechanical ventilation, the pH value of each group showed a gradual downward trend, especially in the small VT group at 6 hours after ventilation; PaO2 and oxygenation index of each group increased significantly at 2 hours after ventilation, especially in the small VT group, and gradually decreased after 6 hours after ventilation. PaO2 and oxygenation index in T group were significantly higher than those in the other two groups; PaCO2 in each group increased gradually after mechanical ventilation, especially in small VT group. After ventilation, the levels of PIP and Pplat in small VT group decreased gradually, while those in medium VT group and large VT group increased gradually. The levels of PIP and Pplat in small VT group were significantly lower than those in the other two groups at 6 hours after ventilation. After 6h ventilation (T6), the injury was aggravated, especially in the large VT group, and in the small VT group.
Conclusion:
Small tidal volume combined with positive end-expiratory pressure mechanical ventilation can alleviate acute lung injury caused by paraquat poisoning and improve oxygenation.
Part III: Effects of pressure control and positive end-expiratory pressure increment on hemodynamics in pigs with paraquat-induced acute lung injury
Objective:
To investigate the effects of pressure control (PC) and positive end-expiratory pressure (PEEP) incremental lung relaxation (RMs) on hemodynamics in pigs with acute lung injury induced by paraquat (PQ).
Method:
10 healthy female pigs were given 20% PQ solution 20 ml intraperitoneal injection to establish acute lung injury/acute respiratory distress syndrome (ALI/ARDS) model of paraquat poisoning. Heart rate (HR), mean arterial pressure (MAP), cardiac function index (CI), partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaO2), and oxygenation index (PaO2/FiO2) were measured at 5 min (t5), 15 min (t15) and 30 min (t30) after RMs. Change.
Result:
HR and MAP in RM1 group were significantly lower than those in RM2 group (all P 0.05). HR and MAP in RMs group were significantly lower than those in RM2 group (all P 0.05). HR and MAP in RM1 group were significantly lower than those in RM2 group (all P 0.05). There was no significant difference in HR and MAP between the two groups 30 minutes after RMs (all P 0.05). RM1 group was significantly higher than RM2 group at n time (P 0.05), and there was no significant difference between the two groups at 30 minutes after RMs (P 0.05); PaO2 and oxygenation index were significantly decreased, while PaCO2 was significantly increased (P 0.05 compared with the baseline); PaO2, PaCO2 and oxygenation index were increased in both groups after RMs, and there was no significant difference between the two groups (P 0.05). The alveolar epithelial cells were exfoliated, the alveolar septum was widened and the alveolar septum was overstretched, and some of the alveolar septum was broken.
Conclusion:
Both pressure control and positive end-expiratory pressure incremental lung relaxation could significantly improve oxygenation in paraquat poisoned pigs with ALI/ARDS, and the effect of pressure control on hemodynamics was less.
【学位授予单位】:郑州大学
【学位级别】:硕士
【学位授予年份】:2014
【分类号】:R595.4
【参考文献】
相关期刊论文 前1条
1 YIN Yu;GUO Xiang;ZHANG Shou Lin;SUN Cheng Ye;;Analysis of Paraquat Intoxication Epidemic (2002-2011) within China[J];Biomedical and Environmental Sciences;2013年06期
本文编号:2187796
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