不同液体容量复苏对失血性休克犬血管外肺水的影响

目的 评价不同液体容量复苏对失血性休克犬血管外肺水的影响。方法 杂种犬32只,雌雄不拘,随机分为4组：NS组、HES组、HS组和HHS组,每组8只,股动脉放血建立失血性休克模型后,各组分别静脉输注容积相当于3倍失血量的生理盐水、失血量等容积的6%羟乙基淀粉130/0．4溶液、7．5%氯化钠溶液6 ml/kg及7．5%氯化钠-6%羟乙基淀粉130/0．4溶液6 ml/kg行容量复苏。经右颈内静脉持续监测中心静脉压、右股动脉置入PiCCO导管监测平均动脉压、心脏指数、每搏输出量、体循环阻力指数、血管外肺水指数及全心舒张末期容量指数,记录放血之前（基础值）、失血性休克模型成功即刻、容量复苏开始后5、30、60、120及180min的上述指标。结果 （1）各组在失血性休克的早期复苏中均可改善血液动力学,HES组、HHS组、HS组和NS组血液动力学改善持续时间依次缩短;（2）复苏早期HS组与HHS组血管外肺水无增加,NS组明显增加,而HES组下降。结论 （1） 7．5%氯化钠溶液与7．5%氯化钠-6%羟乙基淀粉130/0．4溶液小容量液体复苏可有效恢复犬失血性休克早期血液动力学的稳定,且不增加休克后血管外肺水,7．5%氯化钠-6%羟乙基淀粉130/0．4溶液效果较好;（2）6%羟乙基淀粉130/0．4溶液用于犬失血性休克早期复苏不仅可以改善血液动力学,而且能防止复苏后肺水肿。     

Effect of pulmonary artery pressure on extravascular lung water in an experimental model of acute lung injury

BACKGROUND: Lung edema can be influenced by hemodynamic changes in pulmonary circulation. The aim of this study was to evaluate, in an experimental model of acute lung injury, the effect on extravascular lung water (EVLW) of an increase in pulmonary artery pressure (Ppa) without changes in cardiac output and wedge pressure. METHODS: Lung edema was produced by an intravenous oleic acid infusion in mixed-breed pigs weighing 25-31 kg, which, after 20 min, were randomly assigned to a control group (100% FiO(2)) (n = 6) or a high Ppa group (21% FiO(2)) (n = 7). An increase in pulmonary artery pressure of at least 40% over baseline was produced in the high Ppa group by alveolar hypoxia. Hemodynamic, ventilatory and gas exchange parameters were collected at regular intervals. Pulmonary, wedge and capillary pressures were measured with a pulmonary artery catheter and the occlusion technique. EVLW was calculated gravimetrically. RESULTS: At 240 min, both gravimetric-measured EVLW and mean pulmonary artery pressures were significantly higher (P < 0.05) in high Ppa animals vs. controls (12.06 +/- 4.21 vs. 7.98 +/- 2.46 ml/kg and 39.0 +/- 1.3 vs. 26.6 +/- 4.7 mmHg, respectively). Cardiac output (6.8 +/- 2.5 vs. 7.3 +/- 1.3) and pulmonary wedge pressures (9.2 +/- 1.7 vs. 9.4 +/- 2.8 mmHg) were similar. A difference was detected in pulmonary capillary pressures [17.0 +/- 3.3 (high Ppa) vs. 13.8 +/- 2.7 mmHg (controls)] but did not reach statistical significance. CONCLUSIONS: In this model, an increase in pulmonary artery pressure by alveolar hypoxia produces an increase in extravascular lung water, probably related to changes in pulmonary capillary pressures.     

Pulmonary function, extravascular lung water and chest radiography in a porcine model of adult respiratory distress syndrome

To study the pathophysiology and the value of chest radiography in the diagnosis of early adult respiratory distress syndrome spontaneously air-breathing pigs under ketamine anaesthesia were investigated. Five control animals received physiological saline and showed no notable changes in physiological or radiological data. Eleven animals were infused i.v. with E. coli endotoxin over 6 h. The pulmonary dysfunction in the endotoxin animals was characterized by an early increase in venous admixture with hypoxaemia and a peak increase in pulmonary vascular resistance at 0.5 h after start of endotoxin infusion. Subsequently there was a tendency towards a restitution to baseline physiology, but from 3 h onwards a "second wave" of pulmonary dysfunction developed in addition to an increase in extravascular lung water. No significant correlation (r = 0.44) existed between the increase in extravascular lung water and venous admixture. The increase in calculated pulmonary microvascular pressure correlated significantly (r = 0.77) with the increase in extravascular lung water. Radiographic signs of pulmonary oedema were sparse. Thus, only three of 11 animals displayed increased density on chest radiography indicative of pulmonary oedema.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

目的 了解口服补液对烧伤休克犬肺组织含水量和血管通透性的影响.方法 雄性Beagle犬18只,行颈动、静脉置管后24 h造成50%TBSAⅢ度烧伤.伤后随机分为不补液组、口服补液组和静脉补液组,每组6只.伤后第1个24 h不补液组不作任何治疗,口服补液组和静脉补液组分别经胃管或静脉输注葡萄糖-电解质溶液;伤后24 h起3组犬均给予静脉补液.统计各组犬伤后72 h内的死亡率.测定3组犬伤前、伤后30 min和4、8、24、48、72 h非麻孵状态下的平均动脉压(MAP)、呼吸频率(RR)、PaO2、血管外肺水指数(ELWI)和肺血管通透性指数(PVPI),于伤后72 h或犬濒死前测定肺组织含水率.结果 不补液组6只犬均在伤后9～22 h死亡,口服补液组中3只犬伤后25～47 h死亡,静脉补液组犬无一死亡.不补液组伤后8 h RR为(44.0±5.0)次/min、ELWI(10.3±0.6)mL/kg、PVPI 6.6±0.6,比伤前大幅增加;PaO2和MAP均明显低于伤前(P<0.05).口服补液组伤后8 h RR为(33.0±4.0)次/min、ELWI(8.9±0.3)mL/kg、PVPI 5.7±0.4,显著低于不补液组(P<0.05),但高于静脉补液组[(26.0±3.0)次/min、(8.2±0.3)mL/kg、4.2±0.4,P<0.05];口服补液组PaO2和MAP均高于不补液组(P<0.05).两补液组肺组织含水率相近(P>0.05),均低于不补液组(P<0.05).结论 早期口服补液对烧伤犬肺的保护作用虽不如静脉补液,但与不补液相比能显著改善休克期肺血管通透性,减轻肺水肿,减少肺脏并发症.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

口服补液对烧伤休克犬肺组织含水量和血管通透性的影响

Objective To investigate the effect of oral fluid resuscitation on pulmonary vascular per-meability and lung water content in burn dogs during shock stage. Methods Eighteen male Beagle dogs with catheterization of carotid artery and jugular vein for 24 hours were subjected to 50% TBSA full-thickness burn, then they were divided into non-fluid resuscitation(NR), oral fluid resuscitation (OR), intravenous fluid resuscitation (IR) groups, with 6 dogs in each group. Dogs in OR and IR groups were given glucose-electrolyte solution (GES) by gastric tube or intravenous infusion according to Parkland formula within 24 hours after burn, while those in NR group were not given any treatment. Dogs in each group were then given intravenous fluid for further resuscitation after 24 post burn hours(PBH). Deaths were recorded within 72 hours after burn. Mean arterial pressure(MAP) , respiratory rate (RR) , PaO2, extravascular lung water in-dex (ELWI) and pulmonary vascular permeability index (PYPI) were determined before burn and at 30 mins and 4, 8, 24, 48, 72 PBH with the aid of PICCO. Dogs were sacrificed to collect lung tissue for deter-mination of water content at 72 PBH or just before death. Results All dogs died during 9-22 PBH in NR group, 3 dogs died during 25-47 PBH in OR group, and all dogs survived within 72 PBH in IR groups. Com-pared with those before burn, RR (44.0±5.0) times/min, ELWI (10.3±0.6) mL/kg and PVPI (6.6± 0.6) were markedly increased in NR group at 8 PBH, but PaO2 and MAP were obviously decreased (P<0.05). In OR group, RR (33.0±4.0) times/min, ELWI (8.9±0.3) mL/kg and PVPI (5.7±0.4) were significantly lower than those of NR group (P<0.05) , but higher than those of IR group [ RR (26.0± 3.0) times/min, ELWI (8.2±0.3) mL/kg, PVPI (4.2±0.4), P <0.05] at 8 PBH. PaO2 and MAP in OR group were higher than that in NR group (P<0.05). Lung water content showed no statistically signifi-cant difference between OR ang IR groups (P>0.05), which were lower than that in NR group ( P < 0.05). Conclusions Although the protective effect of oral fluid resuscitation with GES on the lung of burn dog at shock stage was inferior to intravenous fluid, it still can decrease pulmonary vascular permeabili-ty, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.     

Effect of zinc pretreatment on pulmonary endothelial cells in vitro and pulmonary function in a porcine model of endotoxemia

BACKGROUND: During endotoxemia, the systemic inflammatory response often leads to severe pulmonary damages. Destruction of endothelial cells, interstitial edema, and interstitial alveolitis depress pulmonary circulation and raise extravascular lung water and intrapulmonary shunt. As protective effects of zinc are described in vitro as well as in vivo, this study investigates its impact on septic porcine pulmonary endothelial monolayers as well as on the pulmonary function of endotoxemic pigs. MATERIALS AND METHODS: Cell culture: Endothelial cells were incubated with ascending doses of zinc and pooled with septic plasma. Cellular damage, metabolism, and proliferation were measured by vital stain, XTT-assay, and BrDU-ELISA. HSP70 was visualized by immunohistochemistry. Animal study: We used an established porcine model. Twenty-four hours before endotoxemia (intravenous infusion of 1.0 microg/kg Escherichia coli endotoxin WO111:B4), each animal received an intravenous pretreatment. Group I (n = 3): saline pretreatment, group II (n = 5): zinc pretreatment (5 mg/kg elementary zinc). Monitoring included blood gas analysis and the thermal dye dilution technique. RESULTS: In vitro, zinc leads to significantly altered rates of viable cells, metabolism, and proliferation with the strongest cell-protective effect at moderate concentrations of 1 microg/ml Zn2+. This correlates with a qualitatively increased expression of HSP70. In vivo, the zinc pretreatment before LPS-induced endotoxemia grossly improves all measured hemodynamic and pulmonary parameters. CONCLUSION: Zinc pretreatment of endotoxemia decreases cellular damages in vitro and improved pulmonary function in vivo. This could be mediated by the heat shock response. Further studies, particularly concerning the dose-effect relationship and the underlying mode of action, are mandatory.     

Lung fluid balance evaluated by the rate of change of extravascular lung water content

Lung fluid balance was studied in 27 mongrel dogs by measuring changes in extravascular lung water content (EVLW). The expression delta EVLWi, which is the difference in EVLWi per kilo bodyweight per hour between two measurement occasions, was used as an estimate of the rate of change of EVLW. EVLW was measured by a double-indicator dilution technique (EVLWi) using iced glucose and indocyanine green. In addition, EVLW was determined at the end of each experiment with gravimetric technique (EVLWg), which enabled the calculation of a regression equation between EVLWi and EVLWg. Delta EVLWi was calculated repeatedly during an 8-h period of mechanical ventilation (MV) with no application of a positive end-expiratory pressure (n = 5), during an 8-h period with a positive end-expiratory pressure (PEEP) of 10 cmH2O (1.0 kPa) (n = 5), during the development of oleic acid (OA)-induced pulmonary oedema (n = 7), and hydrostatic pulmonary oedema (left atrial balloon inflation) (n = 9). An increase of EVLW was seen during PEEP 8 h (mean 35%) and after induction of OA and hydrostatic oedema (mean 300%), but no change was found during MV without PEEP. The regression equation was EVLWi = 5.5 + 0.97 x EVLWg (P = 0.001, r = 0.90). OA-induced oedema caused a mean maximum delta EVLWi of 5.1 ml/kg/h, indicating capillary leakage which, however, was self-limiting within 2 h after OA injection. In hydrostatic oedema there was a maximum delta EVLWi of 16.0 ml/kg/h. Delta EVLWi was negative after deflation of the left atrial balloon, indicating reabsorption of oedema.     

Ringer's solution but not hydroxyethyl starch or modified fluid gelatin enhances platelet microvesicle formation in a porcine model of septic shock

Background. Sepsis is associated with volume deficit and clottingsystem activation. Platelet activation in sepsis results inan increased formation of microvesicles, which in turn, havebeen associated with increased mortality. We hypothesized aneffect of different volume replacement solutions on platelet-derivedmicrovesicle formation in septic shock. Methods. Anaesthetized, mechanically ventilated and multi-catheterizedpigs received 1 g kg^–1 body weight faeces into the abdominalcavity to induce sepsis and were observed over 8 h. Five animalsin each group received volume replacement therapy with modifiedfluid gelatin 4% or 8% (MFG4%, MFG8%), 6% hydroxyethylstarch(HES) 200/0.5 or Ringer’s solution (RS) to maintain acentral venous pressure of 12 mm Hg. Flow cytometry was usedfor determination of microvesicles before induction of sepsis(baseline) and after 8 h. Platelets and microvesicles were identifiedwith an anti-platelet monoclonal Ab and a secondary antibody.Microvesicles were determined as the smallest 1–3% positivecells in forward scatter. Intergroup comparisons were performedusing Wilks–Lambda and Ryan–Einot–Gabriel–WelshF-test. Differences within groups were compared using a two-tailedStudent’s t-test. Results. Baseline values were considered as 100%. While microvesicleformation was reduced in HES (73 (SD 19)%), MFG4% (63 (41)%)and MFG8% groups (53 (17)%), an increase in the RS-group (210(121)%) was observed. Eight hours after induction of sepsis,formation of microvesicles was significantly higher in the RSgroup compared to all colloid-treated groups. Conclusion. In this porcine septic shock model the formationof platelet-derived microvesicles was significantly increasedby volume replacement with Ringer’s solution in comparisonto colloid solutions. Br J Anaesth 2004; 92: 716–21     

Influence of positive end-expiratory pressure on extravascular lung water during the formation of experimental hydrostatic pulmonary oedema

The influence of positive end-expiratory pressure (PEEP) on extravascular lung water measured with the double-indicator dilution technique (EVLWi) has been studied during formation of hydrostatic pulmonary oedema in a canine model. The oedema was created by elevating the mean pulmonary artery pressure (PAP) to 30 mmHg (4.0 kPa) by inflation of a left atrial balloon, and a simultaneous intravenous saline infusion of 15 ml.kg-1.h-1. All dogs were ventilated with zero end-expiratory pressure (ZEEP) until the initial EVLWi had increased by 50%. In one group (n = 5) a PEEP of 10 cmH2O (1.0 kPa) was applied and the dogs were studied for a further 4 h and in the other group (n = 5) ZEEP was maintained throughout the study. During the first 2 h after ZEEP/PEEP application EVLWi increased from 13.7 +/- 2.1 to 20.2 +/- 1.2 ml.kg-1 with ZEEP ventilation and from 13.6 +/- 1.2 to 18.6 +/- 1.9 ml.kg-1 with PEEP ventilation. EVLWi remained unchanged during the last 2 h in both groups. The gas exchange improved with PEEP, arterial oxygen tension increased from 30.4 +/- 8.9 kPa to 38.6 +/- 2.5 kPa (P less than 0.01), and the shunt fraction decreased from 6.0 +/- 3.8% to 1.2 +/- 0.8% (P less than 0.001). There were significant differences (P less than 0.01) in both PaO2 and shunt fraction between the ZEEP and PEEP groups throughout the study. In conclusion, positive end-expiratory pressure improves gas exchange but does not protect against increasing extravascular lung water during the creation of hydrostatic pulmonary oedema.     

Graft damage after a single lung transplantation for pulmonary hypertension in a rat model

The hemodynamic effect and degree of damage in grafts of single lung transplants for pulmonary hypertension were studied in rats with monocrotaline-induced pulmonary hypertension. Inbred male Lewis rats (weight 200–230 g) were divided into two groups. Group 1 (control group,n = 16) underwent isogenic left lung transplantation, while group 2 (n = 15) received an intravenous administration of monocrotaline (80 mg/kg i.v.) and underwent isogenic left single lung transplantation 3 weeks later. Hemodynamic evaluations were performed prior to transplantation, at 1h postoperatively, and on days 3 and 7 after transplantation. Mean pulmonary arterial pressure (mPAP) rapidly declined after transplantation in group 2, from 39.3 ± 8.7 mmHg to 18.5 ±3.0 mmHg 1h after transplantation, and remained stable on day 7 after tranaplantation. No significant difference in the mPAP between the two groups was observed after tranaplantation. The extravascular lung water volume (ELWV: dry/wet ratio) in the right lung of group 2 significantly increased on day 3 (0.86 ± 0.02) (P < 0.01), and subsequently decreased to control levels on day 7 (0.83 ± 0.02). There was no significant difference in the ELWV in the grafted lungs between the two groups (0.84 ± 0.03 vs 0.86 ± 0.04), but there was tendency toward an increase in ELWV in group 2 on days 3 and 7. These data thus demonstrated that a hemodynamic improvement was obtained by single lung transplantation; however the degree of graft damage was remarkable in the pulmonary hypertension group.