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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The consequences of near-lethal smoke inhalation in dogs were studied for a 72-hour period following injury. Progressive hypoxemia and decrease in compliance developed. Severe respiratory distress and frank pulmonary edema were not encountered. Respiratory insufficiecy was related more to alterations in ventilation perfusion ratios than to alveolar destruction. These data were related to clinical observations made by others. No deterioration of lung function was seen with crystalloid overload imposed upon smoke inhalation. The presence of bacterial infection in dogs surviving beyond 24 hours appears pathogenically significant.
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PMID:The pathophysiology of smoke inhalation injury. 24 81

We report the case of a previously healthy 56-year-old male who suddenly developed severe chest pain and pulmonary edema. Cardiac catheterization and angiography revealed an aneurysm of the noncoronary sinus of Valsalva which had ruptured into the left atrium. This was confirmed at operation and it was noted that there were no signs of bacterial infection or rheumatic valve disease. We therefore concluded that the aneurysm was of congential origin. A successful repair of the defect was carried out and the patient made a satisfactory recovery. There are only 3 other reported cases of rupture of a congenital sinus of Valsalva aneurysm into the left atrium, and in only one case did the aneurysm originate from the noncoronary sinus and this patient had associated rheumatic aortic and mitral valve disease. We have received the classification of sinus of Valsalva aneurysms, the associated congenital and acquired defects and the presenting features of unruptured and ruptured aneurysms.
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PMID:Ruptured sinus of Valsalva aneurysm with aortic-left atrial fistula. 118 73

We analyzed data on renal allograft recipients over a 27-year period in order to investigate the frequency, etiology, and outcome of pericarditis developing during the first two months following renal transplantation. Of the 1497 patients receiving renal transplants between 1963 and 1990, 34 patients developed 36 episodes of pericarditis and/or pericardial effusions, for an overall incidence of 2.4%. Pericarditis was attributed to uremia in 14 episodes, cytomegalovirus infection in three, both uremia and CMV infection in four, nonspecific bacterial infection in three, and tuberculosis and minoxidil therapy in one episode each. No etiologic diagnosis could be established in 10 episodes. No statistically significant differences were found between pericarditis and case-matched control patients considering demographic features, the number of immediately functioning grafts, the duration of posttransplant acute renal failure, the number of supportive dialysis days, pre- and postoperative CMV status of the patients, and pretransplant BUN and serum creatinine levels. There were more uremic-related complications (pulmonary edema, gastrointestinal bleeding, central nervous system symptoms) in the pericarditis group. Five allografts in the pericarditis group never functioned, versus only one in the control group. Three patients with pericarditis developed pericardial tamponade. Early diagnosis, close follow-up, and in the case of cardiac tamponade early invasive treatment, should improve the prognosis of this potentially life-threatening complication.
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PMID:Pericarditis following renal transplantation. 164 5

Healthy adult baboons exposed to 100% oxygen for 5 to 7 days maintained on continuous mechanical ventilation develop severe bilateral noncardiogenic pulmonary edema that resembles in many aspects the human adult respiratory distress syndrome (ARDS). In the present study, we evaluated the effects of hyperoxia for 5 to 6 days in 8 baboons to compare changes in abnormalities in bronchoalveolar lavage fluid (BALF) biochemical markers, hemodynamic measurements, and pulmonary function tests in order to find early predictors of lung injury. All animals had bilateral alveolar infiltrates, severe hypoxemia, and progressive deterioration of pulmonary function tests. Diffuse alveolar damage and mild-moderate pneumonias were found and were associated with low-grade bacterial infection. Total lung capacity, diffusing capacity for carbon monoxide, pulmonary static compliance, and oxygenation were significantly impaired after Day 5; BALF proteins, elastase, and total polymorphonuclear leukocytes increased significantly at least 24 h before (Day 4) any abnormalities in chest radiographs, pulmonary function tests, and hemodynamic measurements were detected. We conclude that exposure to 100% oxygen in this model causes marked gas exchange, hemodynamic, biochemical, cytologic, radiographic, and pathologic changes similar to those noted in patients with ARDS. Bronchoalveolar lavage abnormalities precede hemodynamic and gas exchange abnormalities.
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PMID:One hundred percent oxygen lung injury in adult baboons. 363 38

Acute myocardial infarction induces an inflammatory reaction. We related conventional inflammatory parameters including C-reactive protein, erythrocyte sedimentation rate, white blood cell count and axillary temperature to plasma concentrations of procalcitonin in patients with acute myocardial infarction. In a prospective-descriptive study, we evaluated 54 patients with acute myocardial infarction. During a time period of 8 days following myocardial infarction, C-reactive protein, erythrocyte sedimentation rate, white blood cell count and axillary temperature as well as the plasma concentrations of procalcitonin were measured. Maximal procalcitonin remained normal (below 0.5 microgram/L) in patients with uncomplicated acute myocardial infarction. This contrasted with results obtained from patients additionally afflicted by pulmonary edema and cardiogenic shock, in whom maximal procalcitonin increased up to 5.24 micrograms/L. Resuscitation after cardiac arrest and/or concomitant bacterial infection increased procalcitonin to a maximal value of 134 micrograms/L, which was independent of the severity of left heart failure. Conventional inflammatory parameters were all significantly increased even in the absence of cardiac and non-cardiac complications of acute myocardial infarction. In conclusion, procalcitonin increases in patients with acute myocardial infarction only if associated with severe left heart failure, resuscitation after cardiac arrest or in the presence of bacterial infections. Thus, procalcitonin may help to elucidate the etiology of systemic inflammatory response during the early course of acute myocardial infarction.
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PMID:Procalcitonin in patients with acute myocardial infarction. 1223 10

A 75-year-old previously healthy man presented for elective resection of rectal cancer under general anesthesia. Six days before the operation, he had a high-grade fever, and elevated leukocyte count and C-reactive protein concentration, but this was resolved by an intravenous antibiotic. His condition was well controlled before the operation. Soon after the operation started, severe hypoxemia emerged, with low arterial pressure. Fiberoptic bronchoscopy demonstrated a massive amount of plasma-like edema fluid; the total amount of suctioned fluid was approximately 800 ml at the end of the surgery. This acute pulmonary edema appeared to be due to increased permeability rather than pulmonary congestion as indicated by chest radiography, pulmonary artery occlusion pressure, echocardiogram, and the protein-rich edema fluid. Elevated concentrations of the proinflammatory cytokines, interleukin (IL)-6 and IL-8, in both plasma and the pulmonary edema fluid, suggested a possible role of systemic and pulmonary inflammation in the development of this acute pulmonary capillary leak. According to the "two-hit" hypothesis, the bacterial infection preceding the operation may have primed the immune cells, and the following surgical stress may have then triggered rapid progression of acute respiratory distress syndrome. We should keep in mind that, especially following sepsis, sudden massive pulmonary capillary leak can occur during elective surgery, even though the patient's condition is well controlled.
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PMID:Acute pulmonary capillary leak syndrome during elective surgery under general anesthesia. 1830 21

Chronic obstructive lung diseases are characterized by the inability to prevent bacterial infection and a gradual loss of lung function caused by recurrent inflammatory responses. In the past decade, numerous studies have demonstrated the importance of nucleotide-mediated bacterial clearance. Their interaction with P2 receptors on airway epithelia provides a rapid 'on-and-off' signal stimulating mucus secretion, cilia beating activity and surface hydration. On the other hand, abnormally high ATP levels resulting from damaged epithelia and bacterial lysis may cause lung edema and exacerbate inflammatory responses. Airway ATP concentrations are regulated by ecto nucleoside triphosphate diphosphohydrolases (E-NTPDases) which are expressed on the mucosal surface and catalyze the sequential dephosphorylation of nucleoside triphosphates to nucleoside monophosphates (ATP --> ADP --> AMP). The common bacterial product, Pseudomonas aeruginosa lipopolysaccharide (LPS), induces an acute reduction in azide-sensitive E-NTPDase activities, followed by a sustained increase in activity as well as NTPDase 1 and NTPDase 3 expression. Accordingly, chronic lung diseases, including cystic fibrosis (CF) and primary ciliary dyskinesia, are characterized by higher rates of nucleotide elimination, azide-sensitive E-NTPDase activities and expression. This review integrates the biphasic regulation of airway E-NTPDases with the function of purine signaling in lung diseases. During acute insults, a transient reduction in E-NTPDase activities may be beneficial to stimulate ATP-mediated bacterial clearance. In chronic lung diseases, elevating E-NTPDase activities may represent an attempt to prevent P2 receptor desensitization and nucleotide-mediated lung damage.
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PMID:E-NTPDases in human airways: Regulation and relevance for chronic lung diseases. 1840 79

Sepsis is a common problem in feline patients and is associated with substantial morbidity and mortality. There has been little research investigating the physiologic response to bacterial infection in cats, in part because appropriate models have not been developed. The objective of this study was to characterize the response to low-dose LPS infusion in conscious, healthy cats. Measures of systemic inflammation, hemodynamic stability, coagulation, metabolic function, and organ damage were compared between placebo and low-dose LPS infusion (2mcg/kg/hx4h, IV) in cats, with each cat serving as its own control. Markers of systemic inflammation including temperature, plasma TNF activity, IL-6, CXCL-8 and IL-10 concentrations were significantly increased and white blood cell counts were significantly decreased after LPS infusion. A biphasic hypotensive response was observed after initiation of LPS infusion without concurrent tachycardia. Additionally, LPS administration significantly increased blood glucose, lactate and creatinine concentrations. Patchy alveolar congestion, multifocal acute alveolar epithelial necrosis, and mild pulmonary edema were noted in the lungs along with acute centrilobular hepatocellular necrosis, and mild lymphocyte apoptosis in the spleen and/or intestinal Peyer's patches. No biologically significant alterations in coagulation parameters developed after LPS infusion. Low-dose LPS infusion in cats induced systemic inflammation, hemodynamic derangement, metabolic alterations and mild organ damage. Low-dose endotoxin infusion is a viable pre-clinical model to study naturally developing sepsis in cats.
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PMID:Systemic response to low-dose endotoxin infusion in cats. 1957 10

The high case-fatality rate--especially among young adults--during the 1918-1919 influenza pandemic is incompletely understood. Although late deaths showed bacterial pneumonia, early deaths exhibited extremely "wet," sometimes hemorrhagic lungs. The hypothesis presented herein is that aspirin contributed to the incidence and severity of viral pathology, bacterial infection, and death, because physicians of the day were unaware that the regimens (8.0-31.2 g per day) produce levels associated with hyperventilation and pulmonary edema in 33% and 3% of recipients, respectively. Recently, pulmonary edema was found at autopsy in 46% of 26 salicylate-intoxicated adults. Experimentally, salicylates increase lung fluid and protein levels and impair mucociliary clearance. In 1918, the US Surgeon General, the US Navy, and the Journal of the American Medical Association recommended use of aspirin just before the October death spike. If these recommendations were followed, and if pulmonary edema occurred in 3% of persons, a significant proportion of the deaths may be attributable to aspirin.
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PMID:Salicylates and pandemic influenza mortality, 1918-1919 pharmacology, pathology, and historic evidence. 2023 50

C-reactive protein (CRP) is an acute-phase protein that plays an important defensive role in innate immunity against bacterial infection, but it is also upregulated in many noninfectious diseases. The generic function of this highly conserved molecule in diseases that range from infection, inflammation, trauma, and malignancy is not well understood. In this article, we demonstrate that CRP defends the human body against the toxicity of histones released into the circulation after extensive cell death. In vitro, CRP significantly alleviates histone-induced endothelial cell damage, permeability increase, and platelet aggregation. In vivo, CRP rescues mice challenged with lethal doses of histones by inhibiting endothelial damage, vascular permeability, and coagulation activation, as reflected by significant reductions in lung edema, hemorrhage, and thrombosis. In patients, elevation of CRP significantly increases the capacity to neutralize extracellular histones in the circulation. We have also confirmed that CRP interacts with individual histones in vitro and forms CRP-histone complexes in serum from patients with both elevated CRP and histones. CRP is able to compete with phospholipid-containing liposomes for the binding to histones. This explains how CRP prevents histones from integrating into cell membranes, which would otherwise induce calcium influx as the major mechanism of cytotoxicity caused by extracellular histones. Because histone elevation occurs in the acute phase of numerous critical illnesses associated with extensive cell death, CRP detoxification of circulating histones would be a generic host defense mechanism in humans.
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PMID:Human CRP defends against the toxicity of circulating histones. 2389 99


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