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At least 343 records · Page 19Linked to original sources
PubMed2000

Alveolar epithelial barrier. Role in lung fluid balance in clinical lung injury.

Several studies have established that transport of sodium from the air spaces to the lung interstitium is a primary mechanism driving alveolar fluid clearance, although further work is needed to determine the role of chloride in vectorial fluid transport across the alveolar epithelium. Although there are significant differences among species in the basal rates of sodium and fluid transport, the basic mechanism seems to depend on sodium uptake by channels on the apical membrane of alveolar type II cells, followed by extrusion of sodium on the basolateral surface by Na,K-ATPase. This process can be upregulated by several catecholamine-dependent and independent mechanisms. The identification of water channels expressed in lung, together with the high water permeabilities, suggest a potential role for channel-mediated water movement between the air space and capillary compartments, although definitive evidence will depend on the results of transgenic mouse knock-out studies. The application of this new knowledge regarding salt and water transport in alveolar epithelium in relation to pathologic conditions has been successful in clinically relevant experimental studies, as well as in a few clinical studies. The studies of exogenous and endogenous catecholamine regulation of alveolar fluid clearance are a good example of how new insights into the basic mechanisms of alveolar sodium and fluid transport can be translated to clinically relevant experimental studies. Exogenous catecholamines can increase the rate of alveolar fluid clearance in several species, including the human lung, and it is also apparent that release of endogenous catecholamines can upregulate alveolar fluid clearance in animals with septic or hypovolemic shock. It is possible that therapy with beta-adrenergic agonists might be useful to accelerate the resolution of alveolar edema in some patients. In some patients, the extent of injury to the alveolar epithelial barrier may be too severe for beta-adrenergic agonists to enhance the resolution of alveolar edema, although some experimental studies indicate that alveolar fluid clearance can be augmented in the presence of moderately severe lung injury. A longer-term upregulation of alveolar epithelial fluid transport might be achieved by strategies that accelerate the proliferation of alveolar type II cells repopulating the injured epithelium in clinical lung injury. More clinical research is needed to evaluate the strategies that can upregulate alveolar epithelial fluid transport with both short-term therapy (i.e., beta-agonists) and more sustained, longer-term effects of epithelial mitogens such as keratinocyte growth factor. These approaches may be useful in reducing mortality in the acute respiratory distress syndrome.

Animals↗
PubMed1986

Superoxide dismutase prevents the thrombin-induced increase in lung vascular permeability: role of superoxide in mediating the alterations in lung fluid balance.

We investigated the effects of superoxide dismutase (SOD) and SOD linked to Ficoll (mol. wt = 400,000) on the changes in pulmonary transvascular fluid and protein exchange following pulmonary microembolism induced with alpha-thrombin. Studies were made in chronically prepared unanesthetized sheep with lung lymph fistulas. Control thrombin challenged sheep (n = 5) were compared to animals infused with SOD (the SOD-thrombin group, n = 5) or animals infused with SOD linked to high molecular weight Ficoll (the Ficoll-SOD-thrombin group, n = 6). The Ficoll-SOD-thrombin animals were also compared to animals infused with Ficoll alone (the Ficoll-thrombin group, n = 4). In the control-thrombin group, thrombin induced sustained increases in the pulmonary transvascular protein clearance (pulmonary lymph flow X lymph/plasma protein concentration ratio) and pulmonary vascular resistance (PVR). In the SOD-thrombin group, thrombin initially increased both pulmonary transvascular protein clearance and PVR; however, the later increases in protein clearance and PVR were blunted. The pulmonary reflection coefficients for total protein (sigma), a measure of vascular permeability to protein, decreased from a value of 0.70 +/- 0.03 in normal sheep to 0.60 +/- 0.01 following thrombin challenge (p less than 0.05) indicating an increase in lung vascular permeability. The sigma value in the SOD-treated animals was 0.70 +/- 0.02, indicating a protective effect of SOD. The infusion of the Ficoll-SOD complex also attenuated the increases in pulmonary transvascular protein clearance and PVR after thrombin. However, the infusion of Ficoll alone induced a similar protection. The lymph from the SOD-thrombin and Ficoll-SOD-thrombin groups prevented the reduction of ferricytochrome C by xanthine/xanthine oxidase, whereas, the lymph from the Ficoll-thrombin animals did not have this effect, indicating SOD activity was present in the animals receiving the enzyme but not in the group infused with Ficoll alone. Differences in the degree of intravascular coagulation could not explain the response to Ficoll since the decreases in fibrinogen concentration following the thrombin were similar in all the groups. Since Ficoll and related dextrans may modify neutrophil function, in particular neutrophil adherence to the endothelium, we examined the effects of Ficoll on neutrophil adherence. The results indicated that when Ficoll was added to the endothelial medium Ficoll reduced the increase adherence of neutrophils to the endothelial cell monolayer. Therefore, Ficoll as a carrier for SOD may provide a direct protection in models of lung vascular injury that are dependent on neutrophils.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Transcapillary fluid balance in subcutaneous tissue of patients undergoing aortocoronary bypass with extracorporeal circulation.

Colloid osmotic pressure in plasma (COPpl) from a cubital vein and in interstitial fluid (COPif) in the subcutaneous tissue at heart level, and interstitial fluid pressure (Pif) at the same level, were measured in 18 healthy subjects and in 28 patients requiring aortocoronary bypass. Interstitial fluid was collected via subcutaneously implanted double nylon wicks and Pif was measured with the 'wick-in-needle' technique. Measurements were made preoperatively and 1 1/2 to 8 hours (mean 4 hours) after termination of extracorporeal circulation. Pif rose to 2.3 mmHg above the pre-bypass level. COPpl concomitantly fell from 22.2 to 14.4 and COPif from 12.4 to 10.1 mmHg. These changes were statistically significant. Although the relatively large COPpl drop resulted in a net rise of 3.2 mmHg in filtration pressure, the incidence of pulmonary complications was low and no subcutaneous edema was discernible. The fall in COPif and rise in Pif may be regarded as important edema-preventing mechanisms.

Adult↗
PubMedDate not supplied

Fluid balance in severe pre-eclampsia.

Women with severe pre-eclampsia are at high risk of pulmonary oedema, especially 12-24 hours postdelivery. Effective vasodilatation with fluid restriction and early diuretic therapy are the cornerstones of preventative therapy.

Delivery, Obstetric↗
PubMedDate not supplied

Cochlear fluid balance. A clinical/research overview.

Stria edema, and in some cases atrophy, follows osmotic agents, loop-inhibiting diuretics, acoustic trauma, and rupture of Reissner's membrane. All have in common an imbalance of fluid and electrolytes in the cochlear duct. The glycerol test causes temporary improvement in hearing in Menière's disease. Glycerol causes stria edema and collapse of Reissner's membrane in the chinchilla. Stria edema, as well as stria atrophy, are found in Menière's disease. Metabolic manipulation of the stria might be that the best approach in the search for successful treatment of Menière's disease.

Adenylyl Cyclase Inhibitors↗
PubMed1994

The effects of twenty-four hours of reduced uterine blood flow on fetal fluid balance in sheep.

OBJECTIVE: Our aim was to determine the effects of a sustained reduction in uteroplacental perfusion, leading to fetal hypoxia, on determinants of amniotic fluid volume in sheep. STUDY DESIGN: Surgery was performed on five pregnant ewes 110 to 116 days after mating. At 127.3 +/- 2.2 days uterine blood flow was reduced for 24 hours, which reduced fetal SaO2 from 61.9% +/- 1.2% to 24.9% +/- 0.8%. RESULTS: Fetal urine production was increased from a control value of 193.0 +/- 24.0 ml/kg per 24 hours to 279.3 +/- 30.0 ml/kg per 24 hours during periods of reduced uterine blood flow and remained above control values for up to 48 hours after the reduced uterine blood flow period. A substantial loss of fetal water and electrolytes occurred through urine, which was associated with changes in the composition of fetal plasma and fetal tracheal, fetal swallowed, and amniotic fluids. Fetal swallowing was reduced throughout the reduced uterine blood flow period from a control value of 200.8 +/- 56.0 ml/kg per 24 hours to 32.7 +/- 8.4 ml/kg per 24 hours and returned to control levels after the cessation of the reduced uterine blood flow. CONCLUSION: We conclude that 24 hours of reduced uterine blood flow causes major changes in fetal renal function and fetal swallowing that, in spite of an expected reduction in lung liquid production, would increase the flow of fluid and electrolytes from the fetus into the amniotic sac.

Amniotic Fluid↗