The authors evaluated high resolution computed tomographic (HRCT) findings of the isolated rabbit lungs with paraquat poisoning, and the findings were correlated with pathologic specimens. The purposes of this study are 1) to obtain the HRCT findings of the normal rabbit lung, 2) to find out if pulmonary pathology can be induced in rabbits by paraquat, and 3) to correlate the HRCT findings to those of pathology. Thirty rabbits were divided into three groups: group I included four control rabbits; group II included 16 rabbits given paraquat intraperitoneally(IP group); and group III included 10 rabbits given paraquat intravenously(IV group). The rabbits were sacrificed seven, 10 and 14 days after injection of various amount of paraquat, and then the lungs were isolated for HRCT and pathologic studies. Gross and microscopic findings of the three groups of control and paraquat-injected rabbit lungs were correlated with HRCT findings. Pulmonary congestion, mild thickening of alveolar walls and septae, and multifocal micro-atelectasis were the main pathologic findings of the lungs in both groups of the rabbits. Pulmonary hemorrhage was noted in five (31%) of 16 rabbits of IP group and three (30%) of 10 IV group. Pulmonary edema was seen in one rabbit (6%) of IP and four (40%) of IV group. Typical pulmonary fibrosis was seen in one rabbit of IP (6%) and IV (10%) group, respectively. There was no correlation between the amount of paraquat and frequency of the pulmonary pathology. Pulmonary fibrosis was seen at least one week after the paraquat injection. On HRCT, pulmonary hemorrhage and edema appeared as diffuse air-space consolidation and pulmonary fibrosis as linear or band-like opacities. However, minimal changes such as mild congestion.
Edema ; Estrogens, Conjugated (USP) ; Hemorrhage ; Lung* ; Paraquat ; Pathology ; Poisoning ; Pulmonary Edema ; Pulmonary Fibrosis ; Rabbits

Humans ; Lung ; ultrastructure ; Paraquat ; toxicity ; Pulmonary Edema ; pathology ; Research Report

Aged ; Anthracosis ; complications ; pathology ; Cardiomyopathy, Hypertrophic ; pathology ; Edema ; Humans ; Male ; Middle Aged ; Myocardium ; pathology ; Pulmonary Heart Disease ; etiology ; pathology

Enterovirus A, Human ; Enterovirus Infections ; pathology ; Female ; Hemorrhage ; etiology ; virology ; Humans ; Infant ; Male ; Pulmonary Edema ; etiology ; virology

BACKGROUNDp120 catenin (p120ctn) is an adheren junction protein that regulates barrier function, but its role has not been explored in alveolar edema induced by ventilation. We measured stretch-induced cell gap formation in MLE 12 cells due to the loss of p120. We hypothesized that alveolar permeability was increased by high lung inflation associated with alveolar epithelia cell tight junctions being destroyed, which resulted from the loss of p120.

METHODSCultured MLE12 cells were subjected to being stretched or un-stretched (control) and some cells were pretreated with pp2 (c-src inhibitor). After the end of stretching for 0, 1, 2, and 4 hours, the cells were lysed, and p120 expression and c-src activation was determined by Western blotting analysis. In vivo, SD rats were taken to different tidal volumes (Vt 7 ml/kg or 40 ml/kg, PEEP = 0, respiratory rate 30-40 betas/min) for 0, 1, 2, and 4 hour and some were pretreated with pp2, and alveolar edema was calculated.

RESULTSIt was found that p120 expression was reduced and c-src activation increased in a time-dependent and strain-dependent manner due to cyclic-stretch of the alveolar epithelial cells. These changes could be reversed by inhibition of c-src. We obtained similar changes in rats when they were subjected to large tidal volumes and the alveolar edema increased more than in rats in the low Vt group. Pretreated the rats with inhibition of c-src had less pulmonary edema induced by the high tidal volume ventilation.

CONCLUSIONSCyclic stretch MLE 12 cells induced the loss of p120 and may be the same reason by high tidal volume ventilation in rats can aggravate alveolar edema. Maintenance of p120 expression may be a novel therapeutic strategy for the prevention and treatment of ventilation induced lung injury (VILI).

Animals ; Blotting, Western ; Catenins ; physiology ; Cells, Cultured ; Mice ; Pulmonary Alveoli ; pathology ; Pulmonary Edema ; pathology ; Rats ; Rats, Sprague-Dawley ; Tidal Volume ; Ventilator-Induced Lung Injury ; pathology

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

OBJECTIVETo study the clinicopathologic features of fatal enterovirus 71 (EV71) infection.

METHODSAutopsy was performed in 5 neonates died of EV71 infection. Tissue samples from major organs were collected, formalin-fixed and examined under light microscopy. Immunohistochemical study was carried out in selected examples.

RESULTSFour of the 5 cases showed predominant changes in central nervous system, with encephalitis and encephalomyelitis identified mainly in brainstem and upper cervical spinal cord. Histologic findings included neuronal degeneration and necrosis, neuronophagia, perivascular cuffing and diffuse or nodular hyperplasia of macrophages/microglia. Cerebral edema, brain herniation and aseptic meningitis were also noted. The lungs showed mainly pulmonary congestion, neurogenic pulmonary edema and focal hemorrhage. There were minimal changes in the intestinal epithelium. The intestinal lymphoid tissue however was hyperplastic and associated with apoptosis of follicular center cells. The remaining case had cerebral edema and mild meningitis. The lung alveolar septa were thickened with lymphocytic infiltrates. Some alveolar cells were hyperplastic and associated with diffuse hyaline membrane formation. No specific abnormalities were identified in gastrointestinal tract. In all the 5 cases studied, there was enlargement of lung hilar and mesenteric lymph nodes, coupled with apoptosis of follicular center cells. In general, no significant pathologic changes were demonstrated in heart, liver and kidneys.

CONCLUSIONSIn fatal EV71 infection, the major pathologic changes lie in the central nervous system. The pulmonary lesions are mainly secondary in nature. The usual cause of death is cerebral edema complicated by brain herniation and pulmonary edema. It is also noteworthy that some cases show only lung damages, without classic neurologic changes.

Autopsy ; Brain Edema ; etiology ; pathology ; Brain Stem ; pathology ; Child, Preschool ; Encephalitis, Viral ; etiology ; pathology ; Encephalomyelitis ; etiology ; pathology ; Enterovirus A, Human ; isolation & purification ; Enterovirus Infections ; complications ; pathology ; virology ; Female ; Humans ; Infant ; Male ; Pulmonary Edema ; etiology ; pathology ; Spinal Cord ; pathology

To report a non-fatal case of reperfusion pulmonary edema (RPE) after the removal of a hepatocellular carcinoma embolus, which had caused an acute obstruction of the tricuspid valve and pulmonary vasculature during a hepatic lobectomy. Pulmonary embolism caused by hepatocellular carcinoma embolus is extremely rare, and, in the present case, it was associated with unusual clinical features. A 69-year-old ASA II woman with hepatocellular carcinoma was presented for an elective left hepatic lobectomy. During the surgery, the tumor embolus was dislodged from the interior of the lumen of the inferior vena cava (IVC), which then drifted into the tricuspid valve area and pulmonary vasculature. The patient showed the specific signs of acute pulmonary embolism, such as a reduction in end-tidal carbon dioxide, an increase in central venous pressure, and a decrease in arterial pressure. The patient exhibited the symptoms for about 10 minutes. After this period, however, cardiovascular variables became relatively stable, even during a mechanical obstruction due to cross-clamping the pulmonary artery for embolectomy. After several hours of pulmonary embolectomy, the patient experienced an episode of RPE. The ventilatory supports for the treatment of RPE were successful, and the patient recovered without any complications. The patient's case in the present study demonstrates that pulmonary embolism may occur as a result of a hepatocellular carcinoma extending into the IVC during operative management. The anesthesiologist should be careful of the possibilities of RPE after removal of the tumor embolus.
Vena Cava, Inferior ; Tomography, X-Ray Computed ; Time Factors ; Reperfusion ; Radiography, Thoracic ; Pulmonary Embolism/diagnosis/radiography ; Pulmonary Edema ; Liver Neoplasms/*pathology ; Liver/pathology ; Humans ; Female ; Edema ; Cardiovascular System ; Carcinoma, Hepatocellular/*pathology ; Aged

Betulinic acid, a pentacyclic triterpene isolated from Jujube tree (Zizyphus jujuba Mill), has been known for a wide range of biological and medicinal properties such as antibacterial, antimalarial, anti-inflammatory, antihelmintic, antinociceptive, and anticancer activities. In the study, we investigated the antiviral activity on influenza A/PR/8 virus infected A549 human lung adenocarcinoma epithelial cell line and C57BL/6 mice. Betulinic acid showed the anti-influenza viral activity at a concentration of 50 muM without a significant cytotoxicity in influenza A/PR/8 virus infected A549 cells. Also, betulinic acid significantly attenuated pulmonary pathology including increased necrosis, numbers of inflammatory cells and pulmonary edema induced by influenza A/PR/8 virus infection compared with vehicle- or oseltamivir-treated mice in vivo model. The down-regulation of IFN-gamma level, which is critical for innate and adaptive immunity in viral infection, after treating of betulinic acid in mouse lung. Based on the obtained results, it is suggested that betulinic acid can be the potential therapeutic agent for virus infection via anti-inflammatory activity.
Adaptive Immunity ; Adenocarcinoma ; Animals ; Down-Regulation ; Epithelial Cells ; Humans ; Inflammation ; Influenza, Human* ; Lung ; Mice ; Necrosis ; Pathology ; Pulmonary Edema ; Trees ; Ziziphus*

BACKGROUNDAlthough acute congestive heart failure (CHF) patients typically present with abnormal auscultatory findings on lung examination, lung sounds are not normally subjected to rigorous analysis. The goals of this study were to use a computerized analytic acoustic tool to evaluate lung sound patterns in CHF patients during acute exacerbation and after clinical improvement and to compare CHF profiles with those of normal individuals.

METHODSLung sounds throughout the respiratory cycle was captured using a computerized acoustic-based imaging technique. Thirty-two consecutive CHF patients were imaged at the time of presentation to the emergency department and after clinical improvement. Digital images were created, geographical area of the images and lung sound patterns were quantitatively analyzed.

RESULTSThe geographical areas of the vibration energy image of acute CHF patients without and with radiographically evident pulmonary edema were (67.9 +/- 4.7) and (60.3 +/- 3.5) kilo-pixels, respectively (P < 0.05). In CHF patients without and with radiographically evident pulmonary edema (REPE), after clinical improvement the geographical area of vibration energy image of lung sound increased to (74.5 +/- 4.4) and (73.9 +/- 3.9) kilo-pixels (P < 0.05), respectively. Vibration energy decreased in CHF patients with REPE following clinical improvement by an average of (85 +/- 19)% (P < 0.01).

CONCLUSIONSWith clinical improvement of acute CHF exacerbations, there was more homogenous distribution of lung vibration energy, as demonstrated by the increased geographical area of the vibration energy image. Lung sound analysis may be useful to track in acute CHF exacerbations.

Adult ; Aged ; Diagnosis, Computer-Assisted ; Female ; Heart Failure ; complications ; Humans ; Male ; Middle Aged ; Pulmonary Edema ; etiology ; pathology ; Respiratory Sounds ; physiology