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

We measured steady-state lung lymph flow, lymph protein flow, and simultaneous pulmonary vascular pressures in 12 1-wk-old unanesthetized lambs and compared these measurements to those of previous studies, performed under similar conditions, on nine awake adult sheep. The purpose of these experiments was to compare newborn and adult sheep with respect to transvascular filtration of fluid and microvascular permeability to plasma proteins. We prepared the lambs surgically to isolate and collect lung lymph and measure average pulmonary arterial and left atrial pressures, allowing at least 2 days for the lambs to recover from surgery before studies began. Lambs had higher pulmonary arterial and left atrial pressures, lower lymph and plasma protein concentrations, and 57% more lymph flow per gram of dry bloodless lung than sheep; the difference in protein flow between lambs and sheep was not significant. Protein concentration in lymph relative to that in plasma was significantly lower in lambs than in sheep; but the ratio of albumin concentration to globulin concentration in both lymph and plasma was almost identical in the two groups of animals. Extravascular lung water per gram of dry bloodless lung was greater in lambs (4.82+/-0.11 g) than in sheep (4.45+/-0.08 g), but there was no histologic evidence of pulmonary edema in either group of animals. These findings suggest that lambs have more transvascular filtration of fluid per unit lung mass than sheep, but that microvascular sites for protein exchange do not differ appreciably in lambs and sheep. To test this conclusion, we measured steady-state lymph flow in three lambs before and after raising pulmonary microvascular pressure by rapid intravenous infusion of saline. Lymph flow increased as a function of the net transvascular driving pressure (hydraulic pressure gradient-protein osmotic pressure gradient). This response was almost identical to that of four sheep with pulmonary microvascular pressure augmented by inflation of a balloon in the left atrium. In eight lambs we measured the time for intravenously injected (125)I-albumin to equilibrate in lymph at half the specific activity of plasma: the protein tag equilibrated faster than in sheep. This difference could be explained partly by the higher pulmonary arterial and left atrial pressures of lambs than sheep, and possibly by the presence of more microvascular sites for protein exchange relative to the volume of distribution of protein in the lung of the younger animals.
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PMID:Lung fluid dynamics in awake newborn lambs. 90 54

To see whether antihistamines could prevent and reverse histamine-induced pulmonary edema and increased lung vascular permeability, we compared the effects of a 4-h intravenous infusion of 4 mug/kg per min histamine phosphate on pulmonary hemodynamics, lung lymph flow, lymph and plasma protein content, arterial blood gases, hematocrit, and lung water with the effects of an identical histamine infusion given during an infusion of diphenhydramine or metiamide on the same variables in unanesthetized sheep. Histamine caused lymph flow to increase from 6.0+/-0.5 to 27.0+/-5.5 (SEM) ml/h (P less than 0.05), lymph; plasma globulin concentration ratio to increase from 0.62+/-0.01 to 0.67+/-0.02 (P less than 0.05), left atrial pressure to fall from 1+/-1 to -3+/-1 cm H2O (P less than 0.05), and lung lymph clearance of eight protein fractions ranging from 36 to 96 A molecular radius to increase significantly. Histamine also caused increases in lung water, pulmonary vascular resistance, arterial PCO2, pH, and hematocrit, and decreases in cardiac output and arterial PO2. Diphenhydramine (3 mg/kg before histamine followed by 1.5 mg/kg per h intravenous infusion) completely prevented the histamine effect on hematocrit, lung lymph flow, lymph protein clearance, and lung water content, and reduced histamine effects on arterial blood gases and pH. 6 mg/kg diphenhydramine given at the peak histamine response caused lymph flow and lymph: plasma protein concentration ratios to fall. Metiamide (10 mg/kg per h) did not affect the histamine lymph response. We conclude that diphenhydramine can prevent histamine-induced pulmonary edema and can prevent and reverse increased lung vascular permeability caused by histamine, and that histamine effects on lung vascular permeability are H1 actions.
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PMID:Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability. 95 73

The relationship between right duct lymph flow and extravascular lung water was studied in 3 normal dogs and 15 dogs with pulmonary edema induced by alpha-naphthylthiourea (ANTU). Right duct lymph was collected in a pouch created by ligating jugular, subclavian, and brachiocephalic veins. Extravascular lung water was measured in vivo by double indicator dilution and post-mortem by weighting lungs before and after drying. Cardiac output, pulmonary artery and pulmonary artery wedge pressures, and the concentration of protein and electrolytes in plasma and right duct lymph were determined. Eight lungs were examined by light and electron microscopy. There was a direct relationship between right duct lymph flow (RDLF in milliters per hour per gram dry lung) and extravascular lung water (Qwl in milliliters per gram dry lung) which was best described by the equation RDLF=0.75-0.26 Qwl+0.03 (Qwl).2 Dogs with severe ANTU-induced edema had extensive lung capillary endothelial destruction but only mild interstitial swelling and no visible damage to type I alveolar epithelial cells. Cardiac output, pulmonary artery and wedge pressures, and protein and electrolyte concentrations did not correlate with either extravascular water or right duct flow. Thus, in ANTU-induced pulmonary edema right duct lymph flow was directly related to extravascular lung water with the highest flows occurring with severe edema. The absence of a rapid increase in lymph flow with small increases in extravascular water may be due to early sequestration of fluid in the alveolar space. Hemodynamic changes did not account for changes in lung water or lymph flow. The pulmonary interstitial factors relating increased extravascular water to lymph drainage remain to be determined.
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PMID:The relationship between right duct lymph flow and extravascular lung water in dogs given alpha-naphthylthiourea. 95 79

Acute water intoxication with deepening coma and uncontrolled epileptiform seizures in a 25-year-old previously fit male schizophrenic was treated with hypertonic (2 N) saline and a 20% mannitol solution. This improved his neurological state but precipitated severe pulmonary oedema. Intravenous frusemide increased his urinary output sufficiently to clear the pulmonary oedema. In acute water intoxication the use of hypertonic solutions may thus precipitate left heart failure by expanding the intra-pulmonary blood volume beyond the capacity of even a healthy left ventricle to compensate. Simple water restriction will produce a slower but perhaps safer improvement.
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PMID:Pulmonary oedema during treatment of acute water intoxication. 98 Oct 97

The effect of lymphatic ligation on relative lung water (g H2O/g dry lung) was studied in dogs. Raising left atrial pressure to 20 mmHg for 2 h in chronically lymphatic-ligated dogs (4 days) caused a significantly greater increase in relative lung water than the same hemodynamic challenge did in sham-operated and acutely lymphatic-ligated dogs. There was no significant difference in relative lung water between the acutely lymphatic-ligated and sham-operated dogs. At normal left atrial pressures, there was no significant difference in relative lung water between the sham-operated and chronically lymphatic-ligated dogs. Since the combined effects of chronic lymphatic ligation and left atrial hypertension is greater than the sum of the individual effects, it appears that chronic lymphatic ligation increases the susceptibility of the lung to hemodynamic edema, we suggest that chronic lymphatic ligation may have produced increases in the interstitial volume and protein mass that are undetectable by our technique. These increases, in turn, could lead to a reduction in tissue safety factors against hemodynamic pulmonary edema.
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PMID:Hemodynamic pulmonary edema in dogs with acute and chronic lymphatic ligation. 99 Jan 16

Aspiration of hydrochloric acid in rabbits resulted in an increased P(A-a)O2 together with increases in both lung water volume and lung extravascular albumin. This finding suggests lung damage following acid aspiration is related to changes in capillary permeability, with pulmonary edema resulting from the movement of albumin and water into the interstitial space. Therapy with albumin and furosemide together reduced the lung water and albumin accumulation and decreased P(A-a)O2. Treatment with albumin or furosemide alone was ineffective. Caution should be exercised in administering albumin alone for therapy of pulmonary edema when plasma protein is not clearly decreased, or when increased pulmonary capillary permeability is suspected.
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PMID:Effects of albumin and/or furosemide therapy on pulmonary edema induced by hydrochloric acid aspiration in rabbits. 99 56

Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.
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PMID:Hypoxemia and lung water in acute myocardial infarction. 99 75

In severe pulmonary oedema, the alveoli fill rapidly with fluid of essentially the same protein composition as free interstitial fluid. The usual explanation is that the normally 'tight' alveolar epithelial intercellular junctions suddenly become freely permeable to proteins. But the pathophysiological basis for such a change is unknown. In seven anaesthetized dogs one lower lobe was filled with iso-osmotic fluid containing 125I-labelled albumin. The calculated alveolus-blood albumin permeability over three hours averaged 0.06 X 10(-7) cm/s. It decreased nearly 50% when the alveolar tracer concentration was tripled for three more hours. At autopsy, large interstitial free fluid cuffs around blood vessels and airways were found. Isolated lung lobes were filled with isosmotic fluid containing tracer albumin at 10 and 20 cmH2O (0.98-1.96 kPa) airway pressure. Free interstitial fluid cuffs developed within 30 and 10 minutes, respectively. The tracer protein concentration in the cuff fluid averaged 0.9 that of the alveolar fluid. It is postulated that the terminal airway epithelium is normally permeable to protein and water. In acute pulmonary oedema alveolar flooding may occur along the same pathway after the loose interstitial tissue space is fluid-filled and its pressure exceeds that in the airway. The anatomical site of the bulk fluid and protein leak has not been identified.
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PMID:Mechanism of alveolar flooding in acute pulmonary oedema. 104 39

Changes in intracellular water content appear to be common abnormalities induced by a wide variety of pathogenic mechanisms. Such changes in cell water produce changes in the water in various subcellular organelles bound by semipermeable membranes. Cell and subcell functions then alter in their turn. In isolated alveolar macrophages (rabbit), intracellular and intramitochondrial oedema reduces mitochondrial O2 utilization. Metabolic control is maintained because lactate production reverses (Pasteur effect). On reconstitution, O2 utilization and lactate production return towards normal, indicating reversibility. Cellular and intramitochondrial dehydration also reduces mitochondrial O2 utilization but metabolic control is lost because lactate production also decreases. Osmotic reconstitution does not reverse the abnormality. Exposure to hypotonic media leads to release of lysosomal enzymes (beta-glucuronidase, EC 3.2.1.31) to the extracellular phase of isolated alveolar macrophages. Some of this release is caused by exocytosis although, at low osmotic concentrations, intralysosomal oedema ultimately ruptures lysosomes, with extensive discharge of enzyme. In turn, lysosomal enzymes may injure more normal cells. Impairment of energy metabolism caused by hypoxia leads to intracellular oedema, because Na+ accumulates in the cells when ATP is no longer available for the sodium pump. Continued studies of the disorders in cell physiology caused by changes in cell and subcell water should provide important new insights into a wide variety of disease states (including pulmonary oedema).
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PMID:Intracellular and subcellular oedema and dehydration. 104 40

The effectiveness of artificial circulation by the method of Bryukhonenko and his colleagues in the resuscitation of dogs that had died from drowning in fresh- or salt-water was studied. Eight out of ten dogs were revived after freshwater drowning 'death' lasting from 10.5 to 21 min, when a variant of the artificial circulation method, dog donor with a venous pump of the artificial heart, was used. Resuscitated dogs remained alive from 3 to 72 h and died from pulmonary oedema. Artificial circulation appeared to be more effective in resuscitation of dogs drowned in saltwater. Their clinical 'death' lasted up to 31.5 min; clinically signs of pulmonary oedema were not observed in any of them, though some signs of oedema were revealed by histological studies. Of the 42 dogs in this series, all the main functions of the central nervous system were restored in 18 with clinical 'death' for up to 25 min. Resuscitation was performed by one of two methods, either the dog donor plus venous pump of the artificial heart, or the method of Bryukhonenko. The effectiveness of artificial circulation for resuscitation of dogs from drowning was demonstrated.
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PMID:Use of artificial circulation in resuscitation of drowned dogs. 105 96


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