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

Acute edematous lung injury is associated with a marked increase in the number of granulocytes in the alveoli and microvasculature of the lung. Phorbol myristate acetate (PMA) causes granulocytes to adhere, aggregate, and release oxygen radicals and granular enzymes. We found that intravenously injected PMA caused a protein-rich edema in lungs of control rabbits but not in granulocytopenic rabbits pretreated with nitrogen mustard. Specifically, control rabbits treated with PMA had higher lung weight to body weight ratios (6.4 +/- 1.0 X 10(-3)) and lung lavage albumin concentrations (190 +/- 44 mg/dl) than granulocytopenic rabbits pretreated with nitrogen mustard and then given PMA (4.74 +/- 0.23 X 10(-3) and 9.9 +/- 3.8 mg/dl, respectively). To further clarify the role of granulocytes in the production of edema, additional experiments were conducted in an isolated perfused rabbit lung. Addition of purified granulocytes and PMA to the balanced salt perfusate caused lung edema, whereas neither granulocytes nor PMA alone caused edema. Specifically, increases in lung weights (42 +/- 9.2 g) and albumin concentrations (1,182 +/- mg/dl) in lung lavages from isolated lungs exposed to granulocytes and PMA were greater than increases in lung weights or albumin concentrations in lung lavages from isolated lungs exposed to granulocytes alone (2.0 +/- 0.4 g and 15 +/- 0.6 mg/dl), or to PMA alone (6.0 +/- 0.6 g and 81 +/- 34 mg/dl). To determine the contribution of oxygen radicals to the pathogenesis of the edema, chronic granulomatous disease granulocytes, which are deficient in oxygen radical production, were added to the isolated lung perfusate. Chronic granulomatous disease granulocytes and PMA did not cause edema in isolated lungs (delta lung weight 1.0 +/- 0.2 g and lavage albumin 12 +/- 5.0 mg/dl) whereas granulocytes from normal human subjects and PMA did (delta lung weight 43 +/- 5.2 g and lavage albumin 1,120 +/- 54 mg/dl). These data suggest that oxygen radicals released from stimulated granulocytes contribute to the pathogenesis of acute edematous lung injury.
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PMID:Granulocytes mediate acute edematous lung injury in rabbits and in isolated rabbit lungs perfused with phorbol myristate acetate: role of oxygen radicals. 707 14

Plasma oncotic pressure (POP), albumin and total protein were measured in 14 patients with thermal injuries varying extent from 16 to 90% of the body surface. The patients were treated with large amounts of balanced salt solutions in the initial phase. There was an abrupt, pronounced decrease in POP to about 51% of the normal during the first 24 h. Despite the low POP values (minimum 0.78 kPa) and marked peripheral oedema, no patient had overt pulmonary oedema. Clinical and roentgenological evidence of pulmonary dysfunction during the initial period was only seen in conjunction with lung burn or aspiration pneumonitis. Oedema-preventing mechanism and inability to detect interstitial pulmonary oedema are discussed as possible explanations. There was no significant correlation between decrease in POP and mortality, but low POP values seemed to persist longer in the patients who died.
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PMID:Plasma oncotic pressure and plasma protein concentration in patients following thermal injury. 746 16

At least theoretically, ACE-inhibitors may influence each of the factors involved in the regulation of salt and water metabolism. Angiotensin II exerts an antidiuretic and antinatriuretic action on the kidney through influences on the glomerular filtration coefficient, glomerular filtration rate, mesangial tone, filtration fraction, proximal and distal tubule. Angiotensin II and renin also regulate the input of water and salt through an unequivocal dipsogenic effect. In congestive heart failure angiotensin II participates in the preservation of the glomerular filtration rate through its vasoconstrictor properties on the systemic vessels (maintenance of the perfusion and filtration pressure) as well as on the efferent arteriole (maintenance of the filtration pressure). ACE-inhibition weakens or abolishes these influences. However, two favorable mechanisms may also come into action: rise of cardiac output and improvement in renal blood flow; widening of the filtration surface and increment of the filtration coefficient. The efficacy of these factors depends on renal function, age, functional recovery of the heart, treatment with diuretics, duration of treatment with ACE-inhibitors, duration of action of the ACe-inhibitor used, blockade of the facilitating action on the adrenergic vasoconstriction, formation of vasodilating prostaglandins, reduced degradation of kinins. All these effects may account for the variable and often contradictory clinical results, in particular as concerns the relationship between ACE-inhibition and use of diuretics in congestive heart failure. This also explains the variability of efficacy (from the development of pulmonary edema and requirement of diuretics to diuretic withdrawal and clinical improvement) of the ACE-inhibitors as monotherapy in mild to moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ACE-inhibitors and water metabolism in heart failure]. 763 56

We measured effluent nitric oxide levels using a chemiluminescence method from leukotoxin (Lx, a linoleate epoxide) injured isolated rat lungs perfused with physiological salt solution. Nitric oxide production from Lx-injured lung promptly increased and lasted for 20 min. Pretreatment with NG-monomethyl-L-arginine (LNMMA) significantly suppressed Lx-induced production of nitric oxide. Effluent from control lungs showed trace levels of nitric oxide. The wet to dry lung weight (WLW/DLW) after termination of the experiments was significantly elevated in Lx-treated lungs compared with that of LNMMA pretreated lungs or control lungs. There was a correlation between nitric oxide levels (at 10 min) and lung edema (WLW/DLW). Thus, nitric oxide plays a role in the pathogenesis of Lx-induced lung injury.
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PMID:Increased nitric oxide biosynthesis in leukotoxin,9,10-epoxy-12-octadecenoate injured lung. 774 32

Platelet-activating factor (PAF) is a cell membrane-derived ether lipid that plays an important role in acute lung vascular injury. We recently reported that PAF potentiates protamine-induced lung edema by enhancing pulmonary venoconstriction. As PAF is known to stimulate lung eicosanoid synthesis, we investigated the role of peptidoleukotrienes and other eicosanoids in this priming effect of PAF. Addition of PAF (1.6 nM), followed 10 min later by protamine (50 micrograms/ml), to perfusate of salt solution-perfused rat lungs resulted in marked arterial and venous constrictions and severe lung edema. Lung tissue thromboxane B2, 6-ketoprostaglandin F1 alpha and leukotriene C4 (LTC4) were markedly elevated 20 min after PAF/protamine. Pretreatment of the lungs with AA-861, a specific 5-lipoxygenase inhibitor, blocked PAF/protamine-induced leukotriene synthesis, arterial and venous constrictions, and lung edema. In addition, injection of LTC4 (1 microgram) markedly potentiated protamine-induced arterial and venous constrictions and caused lung edema similar to PAF/protamine. Indomethacin, a specific cyclooxygenase inhibitor, also reduced the vasoconstrictive and edemagenic responses to PAF/protamine. However, the pulmonary edema after LTC4/protamine was not blocked by indomethacin. In separate experiments, infusion of this "priming" dose of PAF into isolated perfused lungs induced LTC4 synthesis and augmented lung thromboxane A2 synthesis after arachidonic acid infusion. We conclude that both cyclooxygenase and lipoxygenase products of arachidonic acid metabolism are involved in PAF-induced potentiation of protamine lung edema.
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PMID:Platelet-activating factor potentiates protamine-induced lung edema. Role of eicosanoids. 811 95

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

In Norway the number of deaths per year from drowning is approximately nine persons per 100,000, most of them men between 25 and 40 years of age. About 60% of these persons can swim, and 50% of the deaths are related to intake of alcohol. About 6% of the drowned are children, most of them boys. In disaster medicine, drowning is associated with accidents at sea, involving large vessels or small boats, or connected to offshore activities. The important pathological events are directly related to asphyxia, hypoxemia, hypercarbia, pulmonary oedema, and circulatory arrest. This paper describes various aspects of drowning and the pathophysiological processes involved, and discusses differences between drowning and near drowning in fresh water and salt water. Although treatment is basically centred on effective cardiopulmonary resuscitation, there are certain differences with regard to further treatment and fluid/electrolyte management. Hypothermia is often a prominent feature, and if cardiopulmonary resuscitation is successful, hypoxic brain damage may be ameliorated by the fall in body temperature.
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PMID:[Drowning--near drowning]. 826 93

This paper summarizes the main findings of 3 publications of our group [2-4] examining fluid balance at high altitude. Of 57 mountaineers ascending from 1170 m to 4559 m within 22 to 77 hours, 24 developed acute mountain sickness (AMS) and 16 developed high altitude pulmonary edema (HAPE). In 14 cases HAPE was preceded by symptoms of AMS. Independently of the amount of fluid intake, which varied from 2 to 4 l/24 h in these studies, subjects developing AMS showed decreased diuresis and natriuresis compared to healthy controls with similar fluid intake. Higher fluid intake resulted in greater urine output but did not prevent AMS. Higher plasma levels of aldosterone at rest and greater exercise-induced rises of plasma aldosterone and vasopressine may explain the increased water and salt retention in subjects with AMS. Whether these hormonal changes are secondary to a more severe hypoxemic stress or present a primary cause of AMS remains to be determined.
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PMID:[Does drinking protect against mountain sickness?]. 846 48

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56

A review summarizing recent findings on the causes of the development, pathogenesis, diagnosis and treatment of acute cardiac failure. It is a condition when the heart is unable to pump blood in amounts needed for the metabolic activity of tissues. It may be the first manifestation of disease or acute deterioration of chronic heart failure. The most frequent causes of acute left-sided failure include acute myocardial infarction, arterial hypertension, valvular defects, myocarditis, toxic damage or metabolic myocardial disorders. In right-sided failure pulmonary embolism, extensive affections of the lungs and pleura, right ventricular infarction and affection of the pericardium predominate. The clinical picture of cardiac failure is due to a combination fo the basic disease, evoking causes, signs of an inadequate minute volume, transudation of fluids into the interstitium and the presence of compensating mechanisms. The diagnosis of cardiac failure is based on an analysis of subjective and objective clinical symptoms and other auxiliary examinations such as X-ray examination of the chest, electrocardiogram, echocardiography, examination of blood gases and other laboratory examinations. In right-sided insufficiency the examination is supplemented by pulmonary scintigraphy, possibly by catheterization of the right heart and pulmonary angiography. As to the differential diagnosis, we must differentiate from acute cardiac failure, asthma bronchiale, spontaneous pneumothorax, dyspnoea in neuroasthenic patients, non-cardiac pulmonary oedema. Treatment of cardiac failure involves lifestyle and dietary provisions, medicamentous treatment which has undergone great changes in recent years. Cardiac failure is controlled by reduction of the cardiac filling pressure and support of the efficiency of the cardiac pump (Inotropy) and control of excessive fluid and salt retention. Decisive for the subsequent development of the disease is diagnosis of the basic cardiac or non-cardiac disease and its aimed treatment. In uncontrolled cardiac failure mechanical support of cardiac activity and transplantation of the heart are options.
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PMID:[Clinical aspects of acute heart failure]. 892 24


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