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

The role of intracranial hypertension in the genesis of neurogenic pulmonary edema was studied in 25 sheep; cardiopulmonary hemodynamics (aortic, pulmonary arterial, and left atrial pressures and cardiac output) and fluid and protein movement across the pulmonary capillary bed (efferent pulmonary lymph flow and lymph/plasma protein ratio) were monitored. Only when intracranial pressure was raised to equal the baseline mean systemic pressure (75 to 120 Torr) did we observe the expected Cushing response of increased aortic pressure, or any alteration in pulmonary hemodynamics or fluid movement. When pulmonary changes did occur, they included an increase in pulmonary arterial pressure of between 5 and 15 Torr without any notable rise in left atrial pressure, and a sustained doubling of the pulmonary lymph flow with no dilution of the lymph/plasma protein ratio. In 3 additional animals cerebral ischemia alone produced an elevation in systemic pressure (74 Torr over baseline) without change in pulmonary arterial pressure, left atrial pressure, or pulmonary lymph flow. Thus, intracranial hypertension and ischemia both affect systemic pressure, but only the elevated intracranial pressure is followed by changes in the pulmonary circuit. We suggest that these changes in pulmonary vascular pressure, independent of changes in left atrial pressure, produce increased pulmonary transcapillary fluid flux that may result in neurogenic pulmonary edema.
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PMID:Pulmonary lymphatic flow alterations during intracranial hypertension in sheep. 670 58

Knowledge of the interrelation of the central nervous system-respiratory axis is crucial to the management of patients with head injuries with or without concomitant pulmonary-thoracic problems. Damage to the central nervous system (CNS) can result in unexplained hypoxemia, noncardiac pulmonary edema, altered patterns of respiration, and an increased risk of aspiration. The damaged thorax and lung can contribute to brain ischemia and rises in intracranial pressure. The treatment of one end of the CNS-respiratory axis is not without effect on the other end of the continuum. Corticosteroids, diuretics, mannitol, iatrogenic hyperventilation, barbiturates, and vasopressors are used in the management of patients with head trauma, but may have an impact on oxygenation and ventilation. When positive end expiratory pressure is used in the management of a pulmonary process, it should be optimized and used with caution while monitoring for its effect on intracranial pressure. Pulmonary toilet, while remaining a necessity, must be performed in a manner so as to minimize potential negative effects on the brain. Hyperoxia and hypothermia should be avoided. Mechanical ventilation should be used as dictated by the desired PaCO2 and not as a mandatory adjunct to endotracheal intubation.
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PMID:Pulmonary effects of head trauma. 679 86

The natural history of acute cardiogenic pulmonary edema was studied in a group of patients who did not have acute myocardial infarction, cardiomyopathy, or valvular heart disease. Most of these patients had coronary artery disease. Cardiac catheterization in selected patients showed depressed contractility in some with segmental abnormalities. In the group older than 70 years, this carried a 70 percent two-year mortality rate. It is important to approach patients with this syndrome vigorously, both diagnostically and therapeutically. Acute, reversible segmental ischemia may be responsible for this syndrome and may respond to measures designed to prevent recurrent ischemia.
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PMID:Acute pulmonary edema due to ischemic heart disease without accompanying myocardial infarction. Natural history and clinical profile. 688 Nov 86

To evaluate the viability of the lung for transplantation, we observed in dogs the ultrastructural alterations after temporary ischemia with cooling and after subsequent reestablishment of ventilation and pulmonary circulation. Initial alterations were vacuolization and condensation in the alveolar lining of the epithelial cells. At this stage, gross lung edema did not occur after the subsequent reestablishment of ventilation and pulmonary circulation. According to the prolongation of the ischemia, edematous changes extended over the alveolar structure. In cases of gross lung edema after the reestablishment of pulmonary circulation, alterations such as swollen endothelial cytoplasm and coarse interstitium appeared in the lung before recirculation, in addition to changes in the pneumocytes. Our observations clearly show the importance of changes in the endothelium as a cause of gross lung edema, hence such should be considered when evaluating the viability of a donor lung.
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PMID:Viability of canine lung after temporary ischemia under cooling. An electron microscopy study. 703 79

A reproducible noninvasive monkey model for global brain ischemia with exact insult (no flow x 16 min) to the brain, with survival and with standardized preischemic, ischemic and postischemic variables is described. This model allowed us to demonstrate for the first time: 1) that a substantial part of brain damage early postischemia is reversible and amenable especially to barbiturate treatment; 2) that the postischemic brain shows increased vulnerability for additional insults. Optimal postischemic intensive monitoring and immobilization for 24-48 hours is important for improved outcome; 3) that immediate postischemic reperfusion pressure (MAP 110-150 mm Hg) significantly improves the outcome; 4) that heparinisation during ischemia has no protective effect and 5) that postischemic heparinisation and intravenous hemodilution does not ameliorate the outcome. The protective effect of trimetaphan against neurogenic pulmonary edema can be explained by the prevention of pulmonary hypertension but its protective effect on the development of secondary cerebral edema has to be elucidated.
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PMID:[Pathogenesis and treatment of anoxic encephalopathy. Definition and importance of experimental animal models (author's transl)]. 746 71

Serum endothelin levels increase during sepsis, ischemia, reperfusion, pulmonary operations, and systemic hypertension after surgery. Despite extensive study, the site and extent of action of endothelin on the pulmonary microcirculation are not well established. To assess the effect of endothelin on the pulmonary vasculature, especially the veins, the circulation of the lung was cast with methyl methacrylate 10 minutes after endothelin-1 was given intravenously to rats. Endothelin-1, at concentrations of 0.1, 1.0, and 10.0 micrograms/kg of body weight, increased the mean systemic arterial blood pressure 8%, 7%, and 17% (p < 0.01) and mean pulmonary arterial blood pressure 15%, 28%, and 53%, respectively (p < 0.01). The proportional increases in the pulmonary pressures were greater than those of the systemic pressures (p < 0.01). Scanning electron microscopy of cast blood vessels showed more contraction of the veins than the arteries. For doses of 0, 0.1, 1.0, and 10.0 micrograms/kg, the respective focal contraction of small veins was 6.7% (+/- 4.4), 15.4% (+/- 9.1), 23.3% (+/- 10.1), and 14.4% (+/- 9.0) of the vessel diameter (p < 0.01). In addition, the diameter of capillaries increased (p < 0.01) and the capillary interspaces decreased (p < 0.01) after endothelin administration, but not in a linear dose-dependent manner. The dose of endothelin correlated with the change in the mean systemic (r = 0.82, p < 0.01) and the mean pulmonary (r = 0.80, p < 0.01) blood pressures. The mean pulmonary pressure change correlated with the focal venous contraction on the casts (r = 0.35, p < 0.01), capillary diameter (r = 0.64, p < 0.01), and capillary interspace distance (r = -0.34, p < 0.01). The venous contraction was related to the capillary diameter (r = 0.26, p < 0.01). The most notable effect of endothelin-1 in rat pulmonary microcirculation is focal constriction of small veins. Because this effect may lead to pulmonary edema, endothelin antagonists may be of benefit in a variety of clinical situations.
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PMID:Endothelin-1 focally constricts pulmonary veins in rats. 760 38

This study examines the relationship between hypovolemia and remote organ injury following intestinal reperfusion. Sprague-Dawley rats underwent intestinal ischemia (120 min) and reperfusion (90 min, IIR) or sham operation (CTL). The animals received normal saline (NS) at 0, 30, or 40 ml/kg/h intravenously. Lung and intestinal injury was quantitated using an edema index, and liver injury was assessed by measuring bile flow rates. The infusion of 40 ml/kg/h of NS attenuated the intestinal edema index of IIR animals nearly 50% (p < .05). Despite this improvement, this parameter remained nearly 10-fold greater than that of CTL (p < .05). The lung edema index was 70% greater in IIR animals receiving 30 and 40 ml/kg/h of NS than those not receiving NS. The infusion of 40 ml/kg/h of NS restored bile flow rates in IIR animals to that of CTL. These data suggest that hypovolemia may contribute to the intestinal and hepatic injury in this model. The lung injury is independent of hypovolemia.
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PMID:The effects of hypovolemia on multiple organ injury following intestinal reperfusion. 773 69

17 parameters of vital activity (VA) were scanned in 35 female and 12 male dependent geriatric patients (mean age 81). These included mental testing, Barthel score, lung function, urinanalysis, creatinine clearance, Hb, albumin, globulin and electrolytes, skin-folds, locomotion, presence of IHD, hemodynamic state, continence, infections, WBC and lymphocyte count, pressure sores and dysphagia, 4 main templates of VA deterioration identified were: IHD, hemisyndrome (due to CVA), vegetative state (post-CVA) and senile dementia (SDAT). The IHD template was characterized by marked variations in VA, ending in death due to cardiac complications (pulmonary edema, ischemia, etc.). In the 3 other templates VA gradually deteriorated. Gradual declining VA allowed assessment of individual mortality prognosis. Assessment was by approximation of the computed exponent of the extrapolated VA curves; the longer the observation, the fewer the mistakes in assessment. Epidemiologic prognosis data of 48 dependent patients is described; mean age was about 81 years. Hospitalization mean was 853.5 +/- 601 days and for patients with dementia, 1158.6 +/- 622.7 days.
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PMID:[Assessment of vital activity in geriatric patients]. 781 43

Acute lung injury as a remote sequela of severe lower torso ischemia-reperfusion has been demonstrated experimentally, in a process involving leukosequestration and generation of the arachidonate derivatives thromboxane and leukotriene B4. However, contemporary clinical reports have been limited to development of transient, subclinical "reperfusion pulmonary edema" several hours after declamping in patients undergoing elective abdominal aortic aneurysm repair. This report refocuses attention on the clinical syndrome of severe, acute deterioration in pulmonary function occurring several hours after restoration of perfusion to an ischemic lower torso in two patients. The lung injury is characterized by progressive hypoxemia, pulmonary hypertension, decreased lung compliance, and non-hydrostatic pulmonary edema, consistent with adult respiratory distress syndrome (ARDS). This report reinforces the concept that humoral mediators generated at reflow may induce end-organ injury at a site remote from the focus of ischemia-reperfusion, and that the lung is a target organ.
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PMID:Pulmonary failure following lower torso ischemia: clinical evidence for a remote effect of reperfusion injury. 789 94

This study addresses the hypothesis that endotoxin (LPS) is an important proximal mediator of remote organ dysfunction following intestinal reperfusion. Sprague-Dawley rats underwent intestinal ischemia for 120 min followed by 60 min of reperfusion (IIR). Animals underwent pretreatment with polymyxin B (PMB, 200 micrograms, sc) or the induction of tolerance to LPS prior to assignment to the IIR or sham group. Controls received equal volumes of normal saline. Lung and intestinal injury was quantitated using an edema index. Bile flow was quantitated by measuring the volume of bile produced per 15 min. The intestinal edema index of IIR animals pretreated with PMB was nearly 50% less than that of saline-treated animals sustaining the same injury (P < 0.05). The induction of LPS tolerance reduced the edema index of IIR animals by 28% compared to the saline-treated IIR group (P < 0.05). Neither treatment reduced this parameter to that of sham-operated controls (P < 0.05). The lung edema index of animals pretreated with PMB was 50% of that of saline-treated IIR animals (P < 0.05). This remained significantly greater than that of sham-operated controls (P < 0.05). LPS tolerance did not affect the lung edema index of animals sustaining IIR. Bile flow rates following IIR were not significantly affected by PMB or LPS tolerance. These data do not support the hypothesis that LPS is an important proximal mediator of the remote organ injury associated with IIR. However, they do suggest that LPS may be one of many mediators responsible for this injury.
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PMID:Endotoxemia and remote organ injury following intestinal reperfusion. 801 13


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