Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At the University of Minnesota, University of Wisconsin (UW), modified Euro-Collins (MEC), and Marshall (M) solutions were compared as agents for pulmonary preservation in an isolated rabbit lung model. Normal saline (NS) was used as a control. The heart-lung blocks of donor rabbits were flushed with, and then preserved in, one of the solutions at 4 degrees C. Five rabbits were studied in each group. After 8 h of cold ischemia, the left lung was ventilated and reperfused with fresh venous blood from donor rabbits for 30 min. Pulmonary function was assessed by serial measurements of oxygen (O2) and carbon dioxide (CO2) tensions in blood obtained from the left atrial appendage. The ratios of wet/dry (W/D) weight of the lungs were calculated to assess the extent of pulmonary edema. After 8 h of preservation followed by 30 min of reperfusion, O2 tension was significantly higher with UW (178.36 + 1.72 mmHg). The calculated P values were UW vs NS, < 0.0001; UW vs MEC, 0.154; and UW vs M, 0.0001. CO2 tension with UW was also lower than the other solutions: UW, 35.8 +/- 0.698 mmHg; NS, 48.5 +/- 0.745 mmHg; MEC, 40.69 +/- 0.749 mmHg; and M, 44.68 +/- 0.697 mmHg. The calculated P value was UW vs NS, 0.0001; UW vs MEC, 0.0003; and UW vs M, 0.0001 using repeated-measures analysis of covariance. The W/D ratio was lower with UW as well; UW, 6.82 +/- 0.19; NS, 8.01 +/- 0.23; MEC, 7.28 +/- 0.10; and M, 7.34 +/- 0.17. The P value was < 0.001 using post-hoc tests. In this model, UW solution preserved the lungs better than the other three solutions tested and therefore warrants further clinical application.
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PMID:Comparative study of solutions for pulmonary preservation using an isolated rabbit lung model. 965 94

Percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI) achieves high patency rates. Conversely, it has been shown that after thrombolysis, early reocclusion of the infarct-related artery (IRA) is associated with substantial morbidity and mortality. The aim of this retrospective study was to study the incidence, prognostic implications, and clinical risk factors for in-hospital reocclusion of the IRA after successful emergency PTCA for AMI. We studied 399 consecutive patients (aged 59+/-14 years, 52% with anterior wall infarction) admitted <6 hours after AMI onset, of whom 374 (94%) were successfully treated with primary (n = 297) or rescue (n = 77) PTCA, with a stenting rate of 8%. Predischarge angiography was performed in 306 (82%). Early reocclusion of the IRA occurred in 28 patients (9%) and was silent in 6 (2%). The reocclusion rate was 10% for primary PTCA and 8% for rescue PTCA (p = NS). Twenty-two of 28 patients (6%) underwent repeat emergency coronary angiography because of early recurrent ischemia and most (n = 18) were treated with emergency PTCA. Early recurrent ischemia occurred mostly (86%) within 5 days of AMI onset. There was a higher prevalence of on-site hemorrhage (18% vs 5%, p = 0.007), blood transfusion (11% vs 2%, p = 0.01), pulmonary edema (21% vs 4%, p <0.01), and in-hospital death (21% vs 1%, p = 0.0001) in patients with predischarge reocclusion. On multivariate analysis, cardiogenic shock on admission and absence of dyslipidemia were strong and independent predictors (p = 0.01) of IRA reocclusion. In conclusion, early reocclusion after emergency PTCA occurred in 9% of the patients and was associated with substantial morbidity and mortality. This warrants attempts to decrease its incidence, e.g., with more frequent use of stents.
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PMID:Incidence, consequences, and risk factors of early reocclusion after primary and/or rescue percutaneous transluminal coronary angioplasty for acute myocardial infarction. 973 78

The pathophysiology of elevated intracranial pressure (ICP) is assessed from a three cerebral compartment model and from brain compliance. The mechanisms leading to elevated ICP (expanding process, cerebral edema, brain swelling, hydrocephalus) and their consequences (brain herniation, ischemia-anoxia phenomenon, Cushing reaction and neurogenic pulmonary edema) are overviewed. The causes of elevated ICP in children are reported with emphasis on traumatology. Diagnostic procedures include clinical assessment, fundoscopy, cerebral computerized tomography scan and specific problems of cerebrospinal fluid investigation. Methods and results of intracranial pressure monitoring are reported. The treatment of elevated ICP is based upon clinical follow-up and monitoring of ICP. General therapeutic rules consist of adequate position, suppression of any neck, skull and abdominal compression, stimuli limitation and fluid restriction. Specific treatments include mechanical ventilation, sedation and analgesia, barbiturates, anticonvulsant drugs, mannitol, corticosteroids, hypothermia, enteral nutrition, and antibiotics.
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PMID:[Intracranial hypertension in the infant: from its physiopathology to its therapeutic management]. 975 78

Pulmonary edema develops when pulmonary blood flow is interrupted, then restored. Because the lung is not always hypoxic when ischemic, mechanisms of pulmonary ischemia-reperfusion injury are likely to differ from systemic organs, where reactive oxygen species generated during reperfusion mediate organ dysfunction. We previously showed that pulmonary vascular permeability of isolated ferret lungs increased prior to reperfusion, if ventilation was maintained while blood flow was impaired. To determine whether reactive oxygen metabolites generated during ischemia mediated ischemic injury, we measured tissue levels of F2-isoprostanes as an index of lipid peroxidation, 30 min after administration of glucose (5 mM)-glucose oxidase (GOX, 0.1 U/ml), or after short (45 min) or long (180 min) ventilated ischemia, in isolated ferret lungs. Osmotic reflection coefficient for albumin (sigma alb), an estimate of vascular protein permeability, was measured in the same lungs. Tissue F2-isoprostanes increased 375% after exposure to glucose-GOX in association with a 42% decrease in sigma alb, and administration of catalase (CAT, 100,000 U) and superoxide dismutase (SOD, 25,000 U) completely attenuated this lipid peroxidation. In contrast, tissue F2-isoprostanes increased only 60% following 45 min of ischemia, then did not increase additionally. sigma alb was not altered by 45 min of ischemia, but decreased 72% following 180 min of ischemia. CAT+SOD did not alter F2-isoprostane formation during ischemia, but partially attenuated vascular injury. These results suggest that tissue levels of F2-isoprostanes reflect lung lipid peroxidation, but that F2-isoprostane generation does not directly increase vascular permeability following ventilated pulmonary ischemia.
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PMID:F2-isoprostane generation in isolated ferret lungs after oxidant injury or ventilated ischemia. 980 Oct 71

To expand the cadaveric lung donor pool, protecting the endothelium and alveoli from warm ischemia and reperfusion injury is important. The effects of initial low flow reperfusion and surfactant administration were studied in non-heart-beating donor lungs. The rat heart-lung bloc was excised immediately (group 1) or 30 min (groups 2-4) after euthanasia (n = 6 in each group). The graft was ventilated and reperfused (50 ml/min) immediately after excision for 1 h in groups 1 and 2. In groups 3 and 4, the reperfusion flow rate was increased gradually to 50 ml/min, while ensuring that the pulmonary arterial pressure did not exceed 40 mmHg. Then the graft was reperfused for 1 h. Surfactant was introduced into the airway in group 4 before reperfusion. Airway pressure (AWP) and pulmonary arterial pressure were monitored during reperfusion. After reperfusion, the wet/dry weight ratio (W/D) of the right lung was calculated, and histologic examination using trypan blue staining of the left lung was performed. In group 2, lung failure appeared in all animals during reperfusion. In group 3, although all lungs were reperfused for 1 h, AWP and W/D were higher than in group 1. In group 4, AWP and W/D were lower than in group 3. Histologic examination showed that surfactant administration had attenuated the alveolar cell death. To avoid damage caused by high pulmonary arterial pressure associated with graft reperfusion, iniital low flow reperfusion was beneficial in cadaveric lungs. Surfactant administration before reperfusion was effective in preventing pulmonary edema.
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PMID:Effects of initial low flow reperfusion and surfactant administration on the viability of perfused cadaveric rat lungs. 983 32

To study the mechanisms responsible for ischemia-reperfusion lung injury, we developed an anesthetized rabbit model in which the effects of lung deflation, lung inflation, alveolar gas composition, hypothermia, and neutrophils on reperfusion pulmonary edema could be studied. Rabbits were anesthetized and ventilated, and the left pulmonary hilum was clamped for either 2 or 4 h. Next, the left lung was reperfused and ventilated with 100% oxygen. As indexes of lung injury, we measured arterial oxygenation, extravascular lung water, and the influx of a vascular protein (131I-labeled albumin) into the extravascular space of the lungs. The principal results were that 1) all rabbits with the deflation of the lung during ischemia for 4 h died of fulminant pulmonary edema within 1 h of reperfusion; 2) inflation of the ischemic lung with either 100% oxygen, air, or 100% nitrogen prevented the reperfusion lung injury; 3) hypothermia at 6-8 degreesC also prevented the reperfusion lung injury; 4) although circulating neutrophils declined during reperfusion lung injury, there was no increase in interleukin-8 levels in the plasma or the pulmonary edema fluid, and, furthermore, neutrophil depletion did not prevent the reperfusion injury; and 5) ultrastructural studies demonstrated injury to both the lung endothelium and the alveolar epithelium after reperfusion in deflated lungs, whereas the inflated lungs had no detectable injury. In summary, ischemia-reperfusion injury to the rabbit lung can be prevented by either hypothermia or lung inflation with either air, oxygen, or nitrogen.
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PMID:Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection. 988 66

The effects of long-term preoperative administration of low-dose erythromycin (EM) were experimentally examined in relation to the treatment of reperfusion disorders following pulmonary thermal ischemia. EM was administered at a dose of 100 mg/day for 1 month to adult mongrel dogs with an average weight of about 12 kg (EM group). A control group that did not receive EM was also enrolled. Using a pulmonary autograft model, collapse-thermal ischemia of the lungs was performed on each animal for 60 minutes. In the early stage of reperfusion, the following measurements were assessed: gas-exchange potency in the left lung, hemodynamics, water content, adhesion of neutrophils to vascular endothelium, and concentration of blood eicosanoids. The results for the 2 groups were then compared. In the control group, the blood level of leukotriene B4 (LTB4) increased shortly after reperfusion, neutrophils migrated toward the vascular endothelium and adhered to it, and pulmonary edema developed after 1 hour. However in the EM group, the blood level of thromboxane B2 was significantly suppressed before and after hilar stripping, and the increase in the blood LTB4 level and the migration of neutrophils shortly after reperfusion in thermal ischemia were suppressed. Eventually alleviation of pulmonary edema was indicated and significantly improved gas exchange was maintained. In conclusion, pulmonary injury during detachment of the hilum of the lung, as well as warm ischemia-reperfusion pulmonary injury, may be alleviated by preoperative administration of low-dose EM on a long-term basis.
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PMID:[Effects of long-term preoperative administration of low-dose erythromycin on warm ischemia-reperfusion pulmonary injury]. 991 77

In lung transplantation, the safety period of the ischemic time of the graft is within 6 hours. Because of the problem of donor shortage, it is essential to extend the safety period of the preservation time of the donor lung. However, the longer the preservation time is, the more severe is the resulting ischemia-reperfusion injury. This study was designed to evaluate the efficacy of initial controlled perfusion pressure in the reduction of ischemia-reperfusion injury in a 24-hour preserved lung. Japanese white rabbit lungs were flushed with a low-potassium dextran solution (4C, 500 ml) after injection of prostaglandin E1 (20 microgram, bolus via PA) and submersed in the same solution for 24 hours at 4C. After preservation, the left lung was reperfused using an extracorporeal lung perfusion model which comprised of a closed circuit combined with a membrane deoxygenator. Assessment of lung function included gas analysis of influent and effluent blood and mean pulmonary artery perfusion pressure. Then the lung wet/dry weight ratio was calculated. In group I of the control group (n=6), the left lung was reperfused immediately following flushing (without preservation) at a flow rate of 50 ml/min for 60 minutes. In groups II and III, grafts were stored for 24 hours. In group II, grafts (n=6) were reperfused at a flow rate of 50 ml/min for 60 minutes. In group III (n =6), the flow rate was controlled by maintaining the perfusion pressure below 30 mmHg during the initial 5 minutes and was increased to 50 ml/min for the subsequent 60 minutes. In group II, the mean pulmonary artery pressure during perfusion increased rapidly, and oxygenation deteriorated. All grafts developed pulmonary edema within 12 minutes after reperfusion. Examination of the specimen revealed that the peripheral lung was not perfused. In group III, the mean pulmonary artery perfusion pressure was maintained below 30 mmHg, and oxygenation was preserved sufficiently throughout the experiment (delta PO2 > 100 mmHg) with no significant difference from control values. In conclusion, ischemia-reperfusion injury of the 24-hour preserved lung was attenuated prominently by controlling initial perfusion pressure for 5 minutes.
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PMID:Efficacy of initial controlled perfusion pressure for ischemia-reperfusion injury in a 24-hour preserved lung. 1007 64

Disseminated cholesterol crystal embolism (CCE) is a devastating complication of atherosclerosis that is often considered beyond therapeutic resources. We designed and implemented a treatment protocol based on an analysis of the main causes of death in disseminated CCE with renal involvement. From 1985 to 1996, we applied this protocol in 67 consecutive atherosclerotic patients admitted to our renal intensive care unit for acute renal failure (serum creatinine level, 6 +/- 2.5 mg/dL) accompanied by signs and symptoms of CCE. The other principal clinical features in these patients were cardiac failure with pulmonary edema (61%), gastrointestinal ischemia (33%), cutaneous ischemia (90%), and retinal cholesterol embolism (22%). Disseminated CCE followed one or several precipitating factors, including angiographic procedure(s) (85%), anticoagulant treatment (76%), and cardiovascular surgery (33%). Our treatment schedule systematically addressed the identified causes of death in these patients. (1) To avoid CCE recurrence, any form of anticoagulant treatment was withdrawn, and aortic catheterization and surgery were proscribed. (2) To treat or prevent cardiac failure, a high-dose vasodilator regimen was instituted, including angiotensin-converting enzyme (ACE) inhibitors. In case of cardiac failure refractory to vasodilators, loop diuretics were added and, if necessary, overhydration was corrected by ultrafiltration/hemodialysis (11 patients). (3) To avoid cachexia, severe metabolic disorders were treated by hemodialysis (41 patients), and special attention was given to providing enteral or parenteral nutritional support. Patients with declining general status and laboratory evidence of inflammation, as well as those with new episodes of CCE, were treated with corticosteroids. Statistical analysis found a significant correlation between the requirement for hemodialysis and previous anticoagulation, degree of renal insufficiency, and severity of cardiac failure. Conversely, there was no correlation between requirement for hemodialysis and ACE inhibitor treatment or presence of atherosclerotic renal artery stenosis/thrombosis. The inhospital mortality rate was 16%. There were no clinical or laboratory elements found on admission that were predictive of inhospital mortality. Among survivors, 32% had to remain on maintenance hemodialysis therapy for irreversible chronic renal failure. Including initial hospitalization, the 1-year survival rate was 87%, which compares favorably with reports in the literature indicating a first-year mortality rate of 64% to 81%. Overall follow-up was 19 +/- 20 months, ranging from 1 to 74 months. The 4-year survival rate was 52%. We conclude that an intensive-care, specific-treatment schedule reduces mortality in multivisceral cholesterol embolism.
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PMID:Supportive treatment improves survival in multivisceral cholesterol crystal embolism. 1067 43

We examined variability in ratings of the appropriateness of coronary angiography for 890 clinical scenarios (indications) after an acute myocardial infarction (AMI) from a nine-member multispecialty panel as a function of panel characteristics and the attributes of the clinical indications. We documented a substantial degree of reliability in the ratings. However, key differences among the experts in terms of both their overall propensity to score high and their beliefs regarding the impact of clinical factors on appropriateness were identified. Age, cardiac complications, post-AMI angina, and noninvasive test results were the clinical factors most strongly related to appropriateness ratings for coronary angiography. Further research on the effectiveness of coronary angiography in older patients and in patients with shock, pulmonary edema, and silent ischemia is needed to improve our knowledge about the appropriateness of this procedure in these patients.
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PMID:Understanding variability in physician ratings of the appropriateness of coronary angiography after acute myocardial infarction. 1023 71


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