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

Patients who are victims of near drowning in fresh water or salt water very frequently have acute edema of the lung which occurs either immediately, or after a free interval of variable duration. The mechanism of this edema is explained, in near drowning in salt water, by the hyperosmolarity of the alveolar fluid leading to a seeping of plasma from the capillaries in the alveoli. In the case of near drowning in fresh water, it is on the contrary the inhaled liquid which passes into the circulation, therby leading to immediate hypervolemia, but this overload is only transitory and is not responsible for the pulmonary edema which occurs later is not accompanied by a rise in pulmonary capillary pressure. It is therefore a lesional edema as is certified by the anatomopathological modifications found in the lungs of drowned patients. Therapeutic management must therefore take into consideration this physiopathology of acute edema of the lung in the drowned.
 ...
PMID:[Pulmonary edemas of drownings]. 0 52

It has been shown that bile injected intratracheally in rabbits produces severe pulmonary edema, atelectasis, and focal hemorrhages. The authors investigated the effect of a number of solutions, including physiological concentration of bile, hydrochloric acid pH 1.0, bile salt diluted to 1%, and bile at 100% concentrations. Whenever the bile concentration exceeded 3%, none of the test animals survived. It is not possible to apply directly the results of an experimental animal study to humans. However, the severity of the pulmonary changes produced force the conclusion that bile is a potentially dangerous aspirate in humans.
 ...
PMID:Bile aspiration: an experimental study in rabbits. 23 62

The effects of hemodynamic resuscitation with protein-containing or balanced salt solution were studied prospectively in 29 patients undergoing abdominal aortic surgery. Blood loss was replaced with packed red cells and extracellular volume with either Ringer's Lactate (RL) or 5% albumin in Ringer's lactate (ALB). Fluids were given to maintain the pulmonary capillary wedge pressure (PCWP) equal to or within 5 torr above preoperative (PO) levels, the cardiac output (CO) equal to or greater than preoperative values, and the urine output at least 50 ml/hr. Serum colloid osmotic pressure (COP), CO, PCWP, the gradient between COP and PCWP (COP-PCWP), and intrapulmonary shunt (Qs/Qt) were measured PO, intraoperatively (IO), and daily for 3 days. The measured variables were similar PO in both groups. Operation time, estimated blood loss, and transfusions were similar. Total fluids received for resuscitation (day of operation) was 11.3 +/- 0.8 liters (RL) and 6.2 +/- 0.4 liters (ALB). Fluid balance at the end of resuscitation was 8.4 +/- 0.8 liters (RL) and 3.4 +/- 0.5 liters (ALB). Maximum decrease in COP was 40% (P less than 0.001) in the RL group and was insignificant in the ALB group. The COP-PCWP decreased from 11 +/- 1 to 2 +/- 1 in RL (P less than 0.001) and insignificantly in ALB. Qs/Qt increased slightly in both groups following operation but was not different between groups. Fluid balance, total fluid infused, sodium balance, total sodium infused, COP, or COP-PCWP did not significantly correlate with Qs/Qt. Two patients in the ALB group experienced pulmonary edema associated with normal COPs and elevated PCWPs. There were no cases of pulmonary edema associated with low COPs and normal PCWPs in the crystalloid group. These data seriously question the necessity to maintain COP by using protein-containing solutions during acute hemodynamic resuscitation. When titrated to physiological end points, even large volumes of balanced salt solutions are tolerated well.
 ...
PMID:Crystalloid vs. colloid resuscitation: is one better? A randomized clinical study. 41 54

The effects of d,l-alpha-tocopheryl nicotinate (EN) on model hypertension in rats were studied in comparison with d,l-alpha-tocopheryl acetate (EA). The progress of hypertension in young SHR during the 9th to 15th weeks after birth was markedly accelerated by replacing their driking water with 1% saline. The highly-developed hypertension in old SHR (9 months of age) was further advanced by salt-loading. Oral administration of 20 or 100 mg/kg of EN or 88 mg/kg of EA, once a day, delayed the progress of hypertension in young SHR and reduced advanced hypertension in old SHR. An antihypertensive effect of tocopheryl esters was also found in DOCA-salt hypertensive rats. The treatment with EN or EA definitely reduced the incidence of pathological changes accompanying model hypertension such as suppressed weight gain, pulmonary edema, myocardial fibrosis, cerebral hemorrhage and protected the animals from death. In antihypertensive effect, EN was about 5 times more active than EA in molecular base, and the effects of EN protecting from pathological changes associated with model hypertension were more definite than those of EA. The treatment with EN or EA reduced water and sodium retention in the DOCA-salt hypertensive animals. This fact may suggest the implication of a mechanism through electrolyte metabolism in the antihypertensive action of these tocopheryl esters.
 ...
PMID:Antihypertensive action of d,l-alpha-tocopheryl nicotinate in rats. 50 48

The oxygen consumption of rat bronchioles suspended in a physiological salt solution containing plasma proteins was measured with the Cartesian diver microrespirometer. The oxygen consumption of the bronchiolar tissue 100-300 and 300-400 micrometer in diam was significantly (P greater than 0.01) reduced as the protein concentration of the suspending solution was increased from the low to the high extreme of the normal plasma physiological range and as the diffusion distance through the suspending medium was increased from 25 to 50 micrometer. The reduction in the bronchiolar oxygen consumption was significantly (P greater than 0.01) reversed by using 95% oxygen-5% nitrogen instead of air as the diffusing gas in the Cartesian diver. Measurements of the oxygen diffusivity in the protein solutions using a diaphragm diffusion cell showed a large decrease in the diffusivity as the plasma protein concentration was increased over the same concentration range used in the oxygen consumption studies. These results suggest that the reduction in oxygen consumption was secondary to a decrease in oxygen diffusion and may provide at least a partial explanation for the diffusion abnormalities which exist in noncardiogenic pulmonary edema in which there is an increase in microvascular membrane permeability to proteins.
 ...
PMID:Inhibition of rat bronchiolar oxygen consumption by plasma proteins. 64 66

This is a prospective study on 24 patients with chronic renal failure. Thirteen of them had evidence of acute uraemic encephalopathy. Of those 9 patients were found to have dilutional hyponatraemia, two patients severe salt and water depletion and one patient septicaemia. Hyponatraemia was associated with pulmonary oedema in 3 patients. Correction of salt and water disturbances and treatment of heart failure improved cerebral functions in 10 (77%) patients. It is therefore concluded that dilutional hyponatraemia probably leading to cerebral oedema is a reversibe major factor in the development of acute uraemic encephalopathy. This, if left uncorrected, may prove fatal especially in tropical countries.
 ...
PMID:Acute uraemic encephalopathy in tropical countries. 70 18

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.
 ...
PMID:Use of artificial circulation in resuscitation of drowned dogs. 105 96

The first phase of accidental drowning begins with asphyxia, due to either laryngospasm (10-15 percent of cases) or water aspiration. The second phase is characterized by water and electrolyte changes in the blood. The physiopathological modifications caused by drowning in fresh water differ from those of drowning in sea water. The hypotonic fresh water quickly diffuses in the bloodstream. The consequences are, in many cases, hypervolemia with pulmonary edema, hemolysis, hyperkalemia with risk of ventricular fibrillation, diminution of hemoglobin, and a relative decrease in plasma concentration of Na, Cl, Ca, and albumin. Further, inactivation and washing out of the anti-atelectasis factor from the alveoli by fresh water facilitate the formation of atelectasis. In cases of accidental drowing in sea water the osmotic gradient is in inverse: the electrolytes of aspirated salt water diffuse in the circulation, whereas the blood serum and the plasma albumin pass into the alveoli. Acute pulmonary edema often follows these pathological changes. Hypovolemia with circulatory collapse, hemoconcentration with rise in hemoglobin, hematocrit, sodium, potassium and albumin, and, finally, an elevated risk of thromboembolism due to increased blood viscosity, represent further complications. On the other hand, ventricular fibrillation is rare, hemolysis is absent and atelectasis usually does not occur.
 ...
PMID:[Physiopathology of accidental drowning]. 112 62

Endothelin-1 (ET-1) is a potent vasoactive peptide that has been reported to cause lung edema. This study tested if the edemagenic effect of ET-1 is due to preferential venoconstriction and, if so, whether the site of resistance is similar with salt solution (PSS) and more physiologic blood perfusate. ET-1 caused concentration-dependent contraction of pulmonary arterial and venous rings, with an EC50 of 1.3 nM in artery and 0.6 nM in vein (p less than 0.05). In PSS-perfused lungs, 5 nM ET-1 caused a 7.0 +/- 0.8 torr pressor response that was associated with a 5.0 +/- 0.3 torr increase in microvascular pressure and a 530 +/- 20 mg increase in lung weight within 10 min. In contrast, KCl-treated lungs had an equivalent pressor response (7.4 +/- 1.1 torr), yet the microvascular pressure increased by only 2.5 +/- 0.4 torr (p less than 0.05 from ET-1) and the lung weight was unchanged. Meclofenamate did not prevent the effect of ET-1 on microvascular pressure or lung weight. In blood-perfused lungs, ET-1 caused a 7.3 +/- 0.1 torr pressor response but only a 2.0 +/- 0.5 torr increase in microvascular pressure and no increase in lung weight. ET-1 had no effect on permeability either of cultured endothelial cell monolayers or in the pulmonary microvasculature in vivo. We conclude that the edemagenic effect of ET-1 in PSS-perfused lungs is mediated through venoconstriction and an increase in microvascular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Endothelin-1 increases the pulmonary microvascular pressure and causes pulmonary edema in salt solution but not blood-perfused rat lungs. 128 Jul 24

Alveolar type II epithelial cells in adult mammalian lungs actively transport salt and water, secrete surfactant, and differentiate into type I cells under normal conditions and following lung injury. It has become increasingly apparent that, like all epithelial cells, alveolar pneumocytes have evolved specialized ion transport mechanisms by which they regulate their intracellular pH (pHi). pHi is an important biological parameter in all living cells whose regulation is necessary for normal cellular homeostasis. pHi, and the ion transport mechanisms by which it is regulated, may contribute to many cellular processes, including transcellular transport, cell volume and osmolarity regulation, and intracellular transport, cell volume and osmolarity regulation, and intracellular electrolyte composition. Moreover, changes in pHi may serve as intracellular signals for biological processes such as cell growth, proliferation, and differentiation. We review herein the general principles of pHi regulation in epithelia and describe the mechanisms and effects of pHi regulation in alveolar pneumocytes. Many of the critical issues in current pulmonary research involve processes that pHi is most likely to affect, including maintenance of alveolar epithelial barrier integrity, development and maintenance of epithelial polarity, epithelial proliferation and differentiation, and regulation of transepithelial transport with respect to alveolar fluid balance in normal individuals and in those with excess alveolar fluid (i.e., pulmonary edema). Investigations into the regulation of pHi in alveolar pneumocytes and the regulatory effects of pHi in turn on other cellular processes are likely to yield information important to the understanding of lung biology and pulmonary disease.
 ...
PMID:Regulation of intracellular pH in alveolar epithelial cells. 131 Feb 24


1 2 3 4 5 6 7 8 Next >>