AIMTo investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema.

METHODSThe levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method.

RESULTSAfter heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour.

CONCLUSIONThe inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

Animals ; Endothelin-1 ; metabolism ; Lung ; metabolism ; Male ; Pulmonary Alveoli ; metabolism ; Pulmonary Edema ; etiology ; metabolism ; Rats ; Rats, Wistar

Animals ; Biogenic Polyamines ; metabolism ; Biological Transport ; Humans ; Paraquat ; poisoning ; Pulmonary Edema ; metabolism

Hypothermia during lung preservation decreases metabolic processes. After the rabbit lung was flushed with modified Euro-Collins solution, heart-lung block was harvested and the left lung was assessed after ligation of the right pulmonary artery and right main-stem bronchus. Heart-lung block was immersed in the same solution for 6 hours. The modified Euro-Collins solution and storage temperature of group 1( 10 cases ) was 4 degrees C, group 2( 10 cases ) was 10 degrees C. On completion of the storage period, the left lung was ventilated and reperfused with blood which used a cross-circulating paracorporeal rabbit as a " biologic deoxygenator " for 60 minutes. Pulmonary artery pressure, airway pressure, difference in oxygen tension between inflow and outflow perfusate and degree of pulmonary edema were assessed at 10-minute intervals while the left lung was ventilated at 0.8 of the inspired oxygen fraction. The mean pulmonary venous oxygen tensions at 10 and 60 minutes after reperfusion were 209.52 +/- 42.46 and 103.48 +/- 15.96 mmHg in group I versus 247.78 +/- 36.19 and 147.91 +/- 11.07 mmHg in group II( p = 0.049, <0.0001 ). The mean alveolar-arterial oxygen differences at 20 and 60 minutes after reperfusion were 357.95 +/- 12.84 and 437.31 +/- 14.26 mmHg in group I versus 310.88 +/- 33.47 and 390.93 +/- 15.86 mmHg in group II( p = 0.0092, <0.0001 ). The mean pulmonary arterial pressures at 10 and 60 minutes after reperfusion were 40.56 +/- 18.66 and 87.22 +/- 17.22 mmHg in group I versus 31.22 +/- 6.84 and 65.78 +/- 11.02 mmHg in group II( p = 0.048, 0.0062 ). The mean pulmonary vascular resistances at 10 and 60 minutes after reperfusion were 2.69 +/- 0.85 and 4.36 +/- 0.86 mmHg/ml/min in group I versus 1.99 +/- 0.39 and 3.29 +/- 0.55 mmHg/ml/min in group II( p = 0.0323, 0.0062 ). There were no difference between groups in peak airway pressure, lung compliance and degree of pulmonary edema. In conclusion that preservation of lung at 10 degrees C was superior to preservation at 4 degrees C.
Arterial Pressure ; Bronchi ; Hypothermia ; Ligation ; Lung Compliance ; Lung Transplantation ; Lung* ; Metabolism ; Organ Preservation ; Oxygen ; Pulmonary Artery ; Pulmonary Edema ; Reperfusion

Female ; Humans ; Incidence ; Infant ; Male ; Oxygen ; metabolism ; Prospective Studies ; Pulmonary Edema ; diagnosis ; epidemiology ; Respiration ; Respiration, Artificial

Laparoscopy is a surgical procedure used both for diagnosis and for various treatments. A rare but sometimes fatal complication of laparoscopy is pulmonary embolism with CO2 resulting in pulmonary edema. During laparoscopic gynecological surgery in a 29-year-old woman who had previously undergone lower abdominal surgery, the end-tidal CO2 suddenly increased from 40mmHg to 85mmHg and then decreased to 13mmHg with hemodynamic deterioration. These events are characteristic of a CO2 embolism. When this occurred, CO2 insufflation was immediately stopped and the patient was resuscitated. The patient's condition gradually improved with aggressive treatment, but the clinical course was complicated by bilateral pulmonary edema. This case of pulmonary edema was soon resolved with supportive management. The formation of a CO2 embolism during laparoscopy must be suspected whenever there is a sudden change in the end-tidal CO2. In addition, the possibility of pulmonary edema should be considered when a CO2 embolism occurs.
Adult ; Carbon Dioxide/*metabolism ; *Cystectomy ; Female ; Humans ; *Laparoscopy ; Ovarian Cysts/*surgery ; Pulmonary Edema/*complications/metabolism/radiography ; Pulmonary Embolism/*complications/metabolism/radiography

OBJECTIVETo investigate the effects of methylprednisolone pretreatment on pulmonary lung permeability index and the content of the pulmonary surfactant dipalmitoylphosphatidylcholine (DPPC) in a rabbit model of reexpansion pulmonary edema.

METHODSTwenty-one male New Zealand white rabbits were randomly divided into control group, reexpansion, and reexpansion+methylprednisolone pretreatment groups. The rabbit model of reexpansion pulmonary edema was established using Sakaos method. A bolus dosage of methylprednisolone (3 mg/kg) in reexpansion+methylprednisolone group group or 2.0 ml/kg normal saline in the other two groups was administered intravenously 20 min before reexpansion pulmonary edema. Bronchoalveolar lavage fluid (BALF) and arterial blood samples were collected for measurement of the total protein (TP) and DPPC contents 4 h after reexpansion, and the pulmonary permeability index was calculated.

RESULTSThe pulmonary permeability index in methylprednisolone pretreatment group was significantly lower than that in the reexpansion group (0.007∓0.002 vs 0.177∓0.004, P<0.05). Methylprednisolone pretreatment significantly increased DPPC concentration in the BALF as compared with saline treatment in the reexpansion group (61.815∓28.307 vs 101.955∓24.544 µg/ml, P<0.05).

CONCLUSIONMethylprednisolone pretreatment can increase pulmonary surfactant content and improve pulmonary permeability in the rabbit model of reexpansion pulmonary edema.

1,2-Dipalmitoylphosphatidylcholine ; analysis ; Animals ; Bronchoalveolar Lavage Fluid ; Capillary Permeability ; drug effects ; Male ; Methylprednisolone ; pharmacology ; Permeability ; Pulmonary Edema ; metabolism ; physiopathology ; Pulmonary Surfactants ; metabolism ; Rabbits

OBJECTIVE: To investigate the expression changes of aquaporins 1 (AQP1) in contused lung tissue of rats and its relationship with pulmonary edema. METHODS: SD rats were randomly divided into experimental and control groups. The pulmonary contusion models were then prepared. The expression and distribution of AQP1 in lung tissue of the rats were detected by immunohistochemistry. RESULTS: The lung tissue showed edema, hemorrhage, inflammatory cell infiltration 1 h, 3 h after pulmonary contusion, and the inflammatory response aggravated after 5 h. AQP1 expression at 1 h, 3 h and 5 h in the contusion group were significantly higher than that of the control group (P < 0.01). The expression of AQP1 continued to increase with time and aggravation of edema compared to the control group. AQP1 was mainly distributed in the capillary endothelial cells and interstitial cells of the bronchial and alveolar walls. Although there were no observed changes in AQP1 expression location in contused lung tissue, the intergrated optical density(IOD) showed significant statistical difference (P < 0.01). CONCLUSION There might exist an dysregulation of AQPs gene expression in contused lung tissue, leading to a large number of abnormal transmembrane water transportation and abnormal water accumulation, which may be one of the reasons for pulmonary edema in contused lung tissue.
Animals ; Aquaporin 1/metabolism* ; Contusions/metabolism* ; Female ; Forensic Pathology ; Lung Injury/metabolism* ; Male ; Pulmonary Edema/metabolism* ; Random Allocation ; Rats ; Rats, Sprague-Dawley

BACKGROUNDThe dialysis disequilibrium syndrome is characterized by neurologic deterioration and cerebral edema which occurs after hemodialysis. The purpose of this study was to investigate the pathogenesis of acute cerebral and pulmonary edema induced by hemodialysis.

METHODSWe evaluated the effects of hemodialysis on the biochemical and hemodynamic parameters of the plasma and cerebrospinal fluid, including the intracranial pressure, dry/wet ratio, and pulmonary edema index, and we also examined the pathological changes of the brain and lung tissue in dogs suffering from uremia.

RESULTSSeventy-two hours after bilateral ureteral ligation, 10 uremic dogs were hemodialyzed for 2 hours, yielding a 73.6% and 60.1% decrease in the plasma urea and creatinine, respectively, a decrease in the plasma osmolality from (359 +/- 18) mOsm/kg H(2)O to (304 +/- 6) mOsm/kg H(2)O (P < 0.01), a decrease in the dry/wet ratio of the lung and brain tissue, and an increase in the hemodynamic parameters (right atrial pressure, right ventricular pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and central venous pressure), intracranial pressure, total pulmonary resistance index, and pulmonary edema index. Moreover, the pathological examination revealed lung and brain edema in the dialyzed dogs. This group was compared to 3 control groups: 6 uremic dogs which were sham dialyzed without dialysate so that no fall in the plasma urea occurred, and 12 uremic and 12 nonuremic animals that were not dialyzed. However, the parameters mentioned above were not significantly changed among these 3 control groups.

CONCLUSIONSThe acute brain and lung edema in our model appeared to be primarily due to a large osmotic gradient between the plasma and the brain and lung. This is the "urea reverse effect" which promoted the osmotically-induced lung and brain swelling.

Acute Disease ; Animals ; Brain ; pathology ; Brain Edema ; etiology ; Dogs ; Intracranial Pressure ; Lung ; pathology ; Pulmonary Edema ; etiology ; Radiography, Thoracic ; Renal Dialysis ; adverse effects ; Urea ; metabolism

BACKGROUNDRapid reexpansion of collapsed lungs leads to reexpansion pulmonary edema (RPE). We aimed to investigate the effect of melatonin in the prevention of RPE formation.

METHODSWe used a Wistar rat model in which the left lung was collapsed by ligating the left bronchus for 48 hours and then reexpanded and ventilated for an additional 2 hours. Thirty minutes before reexpansion, we injected melatonin (10 mg/kg) or vehicle intraperitoneally. We compared the wet/dry ratio, oxygenation index, myeloperoxidase (MPO) activity, nitric oxide (NO), malondialdehyde (MDA) and interleukin 8 (IL-8) levels in the reexpanded lungs between untreated and treated animals.

RESULTSWe found that the wet/dry ratio of the melatonin group was significantly lower than that of the vehicle group, and the oxygenation index was higher in the melatonin group. Compared with the control, melatonin pretreatment significantly decreased the activities of IL-8, NO, MDA levels and MPO in lung tissues. Histopathology of reexpanded lungs showed that the melatonin pretreatment group had less pulmonary edema and less inflammatory cell infiltration.

CONCLUSIONMelatonin decreases pulmonary edema and improves oxygenation after reexpansion by attenuating oxidative stress and inhibiting pro-inflammatory cytokines.

Animals ; Cytokines ; metabolism ; Interleukin-8 ; metabolism ; Lung ; drug effects ; metabolism ; pathology ; Male ; Malondialdehyde ; metabolism ; Melatonin ; therapeutic use ; Nitric Oxide ; metabolism ; Oxidative Stress ; drug effects ; Peroxidase ; metabolism ; Pulmonary Edema ; drug therapy ; metabolism ; pathology ; Rats ; Rats, Wistar

OBJECTIVETo investigate the effect of oral fluid resuscitation on pulmonary vascular permeability and lung water content in burn dogs during shock stage.

METHODSEighteen 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 index (ELWI) and pulmonary vascular permeability index (PVPI) 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 determination of water content at 72 PBH or just before death.

RESULTSAll 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. Compared 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 significant difference between OR ang IR groups (P > 0.05), which were lower than that in NR group (P < 0.05).

CONCLUSIONSAlthough 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 permeability, alleviate pulmonary edema, and reduce pulmonary complication compared with no resuscitation with fluids.

Animals ; Burns ; metabolism ; physiopathology ; therapy ; Capillary Permeability ; Dogs ; Extravascular Lung Water ; Fluid Therapy ; adverse effects ; methods ; Lung ; metabolism ; physiopathology ; Male ; Pulmonary Edema ; etiology ; Shock