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

We have used an isolated rat lung model to compare the quality of preservation of different flush techniques with each other and with topical cooling alone. Lung injury was assessed by recording lung weights after reperfusion after 4 and 6 hours of ischemia. The flush solutions studied were intracellular (Collins-Sacks), traditional extracellular, extracellular with low potassium plus dextran, and extracellular containing blood, mannitol, albumin, and prostacyclin (Wallwork's solution). Flushing with Wallwork's solution before both 4 and 6 hours of ischemia gave superior protection from lung edema after reperfusion over all the other methods.
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PMID:Extracellular flush solution that contains blood, mannitol, albumin, and prostacyclin protects rat lungs from six hours of ischemia. 175 65

Transient impairment of the transplanted lung in early postoperative period is one of difficult problems in lung transplantation. It is likely that reperfusion injury of the warm ischemic lung is contributory. The purpose of this study is to evaluate the effects of superoxide dismutase (SOD) on reperfusion injury of warm ischemic lung. Thirty mongrel dogs were divided into four groups. In group I (n = 6), the left lung with complete hilar stripping was placed in warm ischemic state under deflation for 1 hour. In group II (n = 9), the left lung with complete hilar stripping was kept in warm ischemic condition under inflation. Group III (n = 6) animals with same manipulation as group I received superoxide dismutase (SOD 20 mg/kg) before reperfusion. Group IV (n = 9) animals underwent same manipulation as group II and received SOD (20 mg/kg) before reperfusion. Before warm ischemia, immediately after reperfusion, and 1 and 2 hours, blood gases, left pulmonary vascular resistance were measured under the occlusion of right pulmonary artery. Extra vascular lung water content (EVLW) was measured at autopsy and lung was processed for histology. In group II, III and IV, blood gases and EVLW showed significantly better values than group I. In group I and III, left pulmonary vascular resistance increased prominently after reperfusion, however did not change in group II and IV. From these results, we concluded that inflated lung reduced the extent of pulmonary edema after reperfusion and SOD was effective in preventing warm ischemic damage even in deflated lung.
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PMID:[Experimental studies on the effects of superoxide dismutase on warm ischemic-reperfusion injury of the lung]. 177 76

Common intracranial complications following head injury are meningitis, usually associated with a basilar skull fracture or open-depressed skull fracture; delayed hematoma; hydrocephalus; and vascular injuries. Prophylactic antibiotics are not recommended for the management of basilar skull fractures. The best means of preventing infection from open-depressed skull fractures is operative debridement and thorough irrigation, though recent evidence suggests that select cases can be safely managed without operation. Serial CT scans should be obtained in severely head-injured patients to identify delayed hematomas. CT and MRI scans obtained several weeks or months after severe head injury frequently reveal enlarged ventricles, though only a small percentage of these patients have clinical hydrocephalus. Those that do, often benefit from a shunt. Vascular injuries frequently are not detected until ischemic symptoms develop hours or days after the injury. Recommended treatment for intimal tears or dissection is full anticoagulation, but in those with cerebral contusions or other intracranial lesions, this may present an unacceptable risk for intracranial hemorrhage. Pulmonary infections frequently occur following head injury, and can be associated with admission to the ICU and intubation. A large percentage of these infections are caused by enteric gram-negative organisms, and aggressive treatment with appropriate antibiotics is necessary. Aspiration of gastric contents is common in head-injured patients and is frequently complicated by bacterial superinfection. The routine use of antacids and H2 blocking agents leads to bacterial colonization of the stomach with anaerobes and gram-negative aerobes. Thus, empiric therapy for aspiration pneumonia should include clindamycin. Sinusitis is a frequent cause of fever and leukocytosis in patients with nasotracheal or nasogastric tubes in place for several days and often subsides spontaneously with removal of the tubes. Pulmonary edema is often caused by excessive fluid administration during resuscitation of these patients, and can be avoided by monitoring central venous pressures. Pulmonary edema may also be caused by ARDS, excessive catecholamine release, or primary cardiac failure. Most of these patients will benefit from early intubation and PEEP. Pulmonary emboli most often originate from deep venous thrombi, and there is increasing evidence that prophylaxis with low-dose heparin and pulsating boots can significantly reduce the incidence of both complications. Erosive gastritis is found in the majority of severely head-injured patients and may be due to ischemia of the gastric mucosa as well as gastric hyperacidity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Complications of head injury and their therapy. 182 50

Seventy-nine patients with ischemic mitral regurgitation were followed up for a period of 20 +/- 8 months. The risk of death increased with age and cardiac failure at the time of inclusion. The risk of cardiac events increased with these factors and also with raised serum creatinine and decreased echocardiographic fractional shortening. The global 2 year survival was 72.8% and survival without a further cardiac event was 48.7%. Surgery and angioplasty increased global survival and freedom from cardiac events of patients with severe regurgitation (74.9% and 68.8% versus 59.4% and 46.1% for medical therapy alone). The functional improvement was also greater in patients undergoing surgery or angioplasty (80% of patients in NYHA Stage I versus 53.8% in the medical group). Angioplasty was only performed in cases of paroxysmal mitral regurgitation by reversible papillary muscle ischemia. Surgery (coronary bypass usually associated with mitral valve replacement) was associated with better results than medical therapy alone in permanent mitral regurgitation by papillary muscle dysfunction or rupture. Despite a high immediate mortality, this option should be considered rapidly in cases of severe ischemic mitral regurgitation with pulmonary oedema.
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PMID:[Prognosis of ischemic mitral valve insufficiency]. 192 8

The pulmonary reimplantation response (PRR) is a form of membrane permeability pulmonary edema occurring in lung transplants. The severity of the PRR reflects the quality and duration of lung graft preservation. Free radicals formed during ischemia with reperfusion in the autotransplanted dog lung may play a role in producing PRR. We hypothesized that the addition of reduced glutathione (GSH) to the preservative solution could decrease PRR if hydroperoxides are being formed. Six dogs underwent left lung autotransplantation after the lung was flushed with Euro-Collins solution (EC). These dogs demonstrated radiographic and histopathologic evidence of bilateral pulmonary edema, greatest in the transplanted left lung. They also had increases in lung wet to dry weight (W/D) ratios in both lungs (left, 12.0 +/- 0.9; right, 10.1 +/- 0.8) as compared with a group of five unmanipulated control animals (left, 6.0 +/- 0.5; right, 7.0 +/- 0.4). Malondialdehyde (MDA) concentrations were significantly increased in the transplanted left lungs (14 +/- 4) from this group as compared with the controls (5 +/- 7). Five additional dogs underwent left lung autotransplantation with GSH added to the EC cryopreservation fluid. These animals did not develop histologic or radiographic evidence of pulmonary edema, and W/D ratios as well as MDA concentrations were not different from those in controls. To evaluate the effect of ischemia alone on changes in lung GSH concentrations, ten additional dogs underwent left pneumonectomy. Left lungs were cryopreserved in EC + GSH. In five of the animals, the right lung was removed and preserved in EC alone. In the other five animals, the right lung remained in vivo for 3 h and was then removed. Lung GSH concentrations were doubled after 3 h of ischemia when incubated in EC + GSH compared to in vivo controls and to EC-treated lungs. These data suggest that GSH added to the preservation fluid prevents PRR following transplantation and that lung GSH concentrations actually increase during preservation prior to reimplantation and reperfusion if the lung graft is exposed to GSH in the preservation fluid.
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PMID:Glutathione decreases the pulmonary reimplantation response in canine lung autotransplants. 195 16

We have previously demonstrated that reperfusion of a rabbit lung in vivo after 24 h of unilateral pulmonary artery occlusion results in edema, transient leukopenia, and intravascular leukocyte aggregation. We hypothesized that complement was activated by reperfusion and that this in turn contributed to lung injury. In the preliminary phase of the study, we found that ischemia followed by reperfusion resulted in a drop in C3 to 15 +/- 10% (mean +/- SEM) of the prereperfusion value as compared with no change in a group of control animals that had undergone an identical thoracotomy but without pulmonary artery occlusion and reperfusion (p less than 0.05). We then studied three groups of animals to determine if complement depletion with cobra venom factor (CVF) prior to ischemia and reperfusion would prevent the injury. Rabbits treated with CVF but without occlusion and reperfusion did not develop significant lung edema, with left and right lung wet/dry ratios of 5.32 +/- 0.11 and 5.26 +/- 0.12, respectively. For rabbits that were not treated with CVF but underwent ischemia and reperfusion, the comparable numbers were 6.15 +/- 0.36 and 5.19 +/- 0.32 (p less than 0.05 for right versus left). For CVF-treated rabbits that underwent ischemia and reperfusion, the right/left difference persisted (6.77 +/- 0.48 versus 5.35 +/- 0.14, p less than 0.01). Immunocytochemistry documented C3 deposition in non-CVF rabbits that underwent ischemia and reperfusion but not in CVF-treated rabbits. We conclude that ischemia/reperfusion of the lung results in complement activation, but it is not a complement-dependent injury.
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PMID:Complement activation is a secondary rather than a causative factor in rabbit pulmonary artery ischemia/reperfusion injury. 199 Sep 58

Diastolic function in coronary artery disease is modified to a variable extent. There are distinct abnormalities produced during acute ischemia, and following myocardial infarction. The pathophysiology of diastolic abnormalities in these two syndromes is reviewed. During acute ischemia filling pressures of the left ventricle are increased. Pulmonary edema may be produced. Silent ischemia causes less of an increase in filling pressures. The diastolic pressure-volume relation is shifted in an upward manner with a variable contribution from altered myocardial relaxation, increased muscle stiffness, acute pericardial restriction, ventricular interaction, and acute chamber dilatation. The impairment of myocardial relaxation plays a central role and has been quantified in multiple clinical and experimental studies. Filling of the left ventricle during ischemia is altered due to the factors which shift the pressure-volume relation. The acute increase in left atrial pressure may increase filling rates somewhat surprisingly, given the reduced left ventricular compliance. Myocardial fibrosis following infarction may elevate filling pressures, but the degree of elevation is closely tied to the intravascular volume status. Shifts in the diastolic pressure-volume relation reflect a loss of chamber compliance due to an increase in muscle stiffness. Increased amounts of extracellular matrix, specifically collagen, produce this permanent increase in muscle stiffness which is central to the diastolic abnormalities in chronic coronary artery disease.
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PMID:Diastolic function in coronary artery disease. 202 80

Washed human platelets prevent edema formation in isolated rabbit lungs infused with xanthine oxidase, an enzyme that injures endothelial membranes by generating extracellular oxidants. We hypothesized that platelets would similarly preserve membrane permeability in isolated lungs exposed to ischemia-reperfusion injury, a model that perturbs endothelial cells by the generation of intracellular oxidants. Isolated perfused rabbit lungs (IPL) were exposed to warm ischemia-reperfusion to cause lung edema. The infusion of washed human platelets (1.05 +/- 0.02 x 10(10) cells) prevented edema formation as measured by lung weight gain, wet-to-dry lung weight ratios, histological edema, and preservation of paraendothelial cell tight junctions. Inhibition of the platelet glutathione redox cycle with 1,3-bis(2-chloroethyl)-1-nitrosourea, dehydroepiandrosterone, or 1-chloro-2,4-dinitrobenzene interfered with platelet protective effects. In contrast, inhibition of platelet catalase with aminotriazole and H2O2 had no effect on platelet protection. Lung tissue malonyldialdehyde concentrations were similar in isolated lungs exposed to ischemia-reperfusion with or without the infusion of platelets. These results indicate that platelet attenuation of ischemia-reperfusion lung edema depends on platelet glutathione redox cycle antioxidants but not platelet catalase.
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PMID:Washed human platelets prevent ischemia-reperfusion edema in isolated rabbit lungs. 203 73

Ischaemia is a common clinical event leading to local and remote injury. Evidence indicates that tissue damage is largely caused by activated neutrophils which accumulate when the tissue is reperfused. If the area of ischaemic tissue is large, neutrophils also sequester in the lungs, inducing non-cardiogenic pulmonary oedema. Ischaemia reperfusion injury is initiated by production of reactive oxygen species which initially appear responsible for the generation of chemotactic activity for neutrophils. Later, once adherent to endothelium, neutrophils mediate damage by secretion of additional reactive oxygen species as well as proteolytic enzymes, in particular elastase. Therapeutic options for limiting ischaemia reperfusion injury include inhibition of oxygen radical formation, pharmacological prevention of neutrophil activation and chemotaxis, and also the use of monoclonal antibodies which prevent neutrophil-endothelial adhesion, a prerequisite for injury.
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PMID:Pathophysiology of ischaemia reperfusion injury: central role of the neutrophil. 207 Feb 26

Diastolic heart failure is characterized by increased resistance to diastolic filling of one or both cardiac ventricles. Although some degree of diastolic failure exists in most patients presenting clinically with heart failure, a substantial subset of patients have relatively pure diastolic heart failure with normal systolic function. Diastolic heart failure can be due to structural abnormalities that increase resistance to ventricular inflow, and these structural abnormalities can be extramyocardial (e.g., constrictive pericarditis and mitral stenosis) or intramyocardial (e.g., fibrosis and amyloidosis). In addition to structural abnormalities, physiological derangement of myocardial inactivation and relaxation can contribute importantly to diastolic dysfunction in patients with heart failure. There is mounting evidence that advanced myocardial hypertrophy is associated with increased resistance to ventricular diastolic inflow due to both structural alteration (increased wall thickness and altered collagen matrix) and impaired diastolic relaxation of the hypertrophied myocardium. Physiological mechanisms for impaired relaxation in advanced hypertrophy remain controversial but can include disordered function of myocardial sarcoplasmic reticulum, subendocardial ischemia, and altered adenylate cyclase function. Diastolic dysfunction can play an important role in the genesis of flash pulmonary edema seen in patients with ischemic heart disease because myocardial ischemia is associated with a decline in relaxation rate, increased resistance to early diastolic filling, and in some cases, a striking upward shift in the left ventricular diastolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic dysfunction and congestive heart failure. 213 51


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