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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of crystalloid (75 ml/kg of Ringer's lactate) or colloid (6% dextran-70, 6% hydroxyethyl starch, or 25 ml/kg of 5% human serum albumin) fluid infusions or no treatment (control) on the calculated lung capillary (Pc)-plasma oncotic pressure (pi c) gradient and pulmonary edema. Two sets of mongrel dogs were studied: uninjured (n = 25; 14 to 22 kg) and pulmonary fibrin-microembolized (n = 25; 15 to 23 kg). In both sets of experiments, left atrial pressure was controlled (15 mm Hg) throughout the 4-h plus experimental period. In the uninjured set, the Pc-pi c gradient averaged +1.0 and -0.2 mm Hg in the hydroxyethyl starch and dextran groups, +0.7 and +2.3 mm Hg in the human serum albumin and control groups, and +6.2 mm Hg in the Ringer's lactate group. In the fibrin-microembolized group, this gradient averaged 2.6, 2.4, 3.0, 5.3, and 9.5, respectively. The extravascular lung water to bloodless dry lung wet weight ratios in the no-fluid treatment group of the uninjured and microembolism groups with increased pressure (3.8 +/- 0.3 to 4.1 +/- 0.4 [SEM]; NS) are consistent with interstitial or perivascular edema. There were, however, no significant differences noted between the respective control groups or any fluid treatment group in either set of experiments. These data support the view that infusion of either colloid or crystalloid solutions in normal or pulmonary fibrin-microembolized lungs does not produce sufficient change in the Pc-pi c gradient to elevate edemagenesis when pulmonary capillary pressure is limited to 22 mm Hg in dogs.
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PMID:Effects of colloid or crystalloid solutions on edemagenesis in normal and thrombomicroembolized lungs. 367 64

Adult respiratory distress syndrome has been reported after endoscopic variceal sclerotherapy with sodium morrhuate. It has been proposed that sclerosant entering the pulmonary circulation during intravariceal injections may cause pulmonary hypertension and capillary injury. The purpose of this study was to determine whether variceal sclerotherapy with sodium morrhuate causes capillary injury or pulmonary edema in humans. We studied the effect of sclerotherapy on gas exchange and pulmonary and systemic hemodynamics in 8 patients who required endoscopic variceal sclerotherapy for treatment of variceal hemorrhage. The pulmonary vascular resistance index increased from 246 +/- 67 dyn X s X cm-5/m2 (mean +/- SEM) at baseline to a high of 303 +/- 85 dyn X s X cm-5/m2 60 min after sclerotherapy (normal range 250-500 dyn X s X cm-5/m2). Pulmonary artery pressure remained stable while cardiac index decreased by 12% over the same period. There were also small increases in systemic vascular resistance index and systemic arterial pressure after sclerotherapy. Although there was no change in arterial oxygen tension, the alveolar-arterial oxygen difference improved after sclerotherapy. These results indicate that variceal sclerotherapy with sodium morrhuate is associated with clinically insignificant changes in pulmonary and systemic hemodynamics. We did not detect evidence of acute lung injury after sclerotherapy.
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PMID:Effect of endoscopic variceal sclerotherapy on gas exchange and hemodynamics in humans. 387 11

Prolonged exposure to 100% O2 at 1 atm is known to result in a progressive increase of the alveolar epithelial permeability to lipid-insoluble molecules. To investigate whether the damage to the capillary endothelium precedes or follows this event, conscious, unanesthetized rabbits were exposed to 100% O2 from 24 to 66 hr, and (a) the filtration coefficient (Kf) of the pulmonary capillary endothelium in isolated, perfused lungs and (b) the arterial and carbon dioxide gas tensions and right and left heart vascular pressures were measured in intact animals. The mean value of the filtration coefficient (+/- SEM) in air-breathing animals was 0.036 +/- 0.002 ml/(min x Torr x g dry lung). After 48 and 66 hr in 100% O2, it increased by 58 and 114% from its baseline value, respectively. At the later period the lung wet/dry weight of the isolated, but not the intact lungs, increased also from 5.42 +/- .2 to 7.3 +/- .3 (means +/- 1 SEM) due to the combination of a higher capillary conductance and the lack of lymph flow in this preparation. All other variables remained normal throughout the exposure. Thus, in contrast to previous morphological findings, these results indicate that the oxygen damage to the capillary endothelium is progressive and occurs concurrently with the increase of the alveolar permeability to solute but before the appearance of pulmonary edema and the compromise of gas exchange.
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PMID:Effects of 100% oxygen breathing on the capillary filtration coefficient in rabbit lungs. 398 87

The mechanism by which hydralazine increases venous admixture (QVA/QT) in the setting of lung injury was investigated in a canine model of noncardiogenic pulmonary edema. Permeability pulmonary edema was produced by administration of oleic acid, 0.08 ml/kg given intravenously to 9 mongrel dogs. After stabilization of lung injury, hydralazine was administered intravenously in a loading dose of 1 mg/kg and followed by a constant infusion at 0.05 mg/kg/h. To control for the effect of increased cardiac output (QT) on QVA/QT, a balloon catheter was placed in the inferior vena cava, and stepwise inflation of the balloon was used to impede venous return and maintain QT at predrug levels. Prior to inflation of the balloon catheter, administration of hydralazine produced a 51% decrease in total systemic resistance (TSR) and a 23% decrease in mean arterial pressure (Pa). In contrast, pulmonary vascular resistance (PVR) showed no significant change, and mean pulmonary artery pressure (Ppa) increased 47%. Cardiac output increased from 3.4 +/- 0.3 to 5.5 +/- 0.4 L/min (mean +/- SEM; p less than 0.01) after administration of hydralazine, and QVA/QT increased from 23 +/- 7 to 35 +/- 5% (p less than 0.05). Mean arterial oxygen tension (PaO2) showed no significant change. Inflation of the balloon in the inferior vena cava after hydralazine administration reduced QT to 3.1 +/- 0.4 L/min and QVA/QT to 28 +/- 4%. Neither of these values differed significantly from the prehydralazine levels. Similarly, values for Ppa and PVR after hydralazine administration plus balloon inflation did not differ significantly from predrug levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of hydralazine on cardiac output and venous admixture in experimental lung injury. 649 64

Physiologic effects of colloidal (5% albumin, 6% hydroxyethylstarch, 6% dextran-70) and crystalloidal (Ringer's lactate) fluids were examined in rats (six in each fluid group) after infusion of an LD99 of rattlesnake venom, previously shown to produce shock secondary to increased vascular permeability. Venom infusion (iv, 2.0 mg/kg, 30 min) was followed by fluid infusion (iv, 30 min) in quantities sufficient to reverse venom-induced hemoconcentration. Venom infusion decreased mean arterial pressure, increased blood lactate, and increased hematocrit in all animals (p less than .01). Fluid infusion reversed these changes, although six times the volume of crystalloid was required to produce hemodilution comparable to the colloidal fluids (120 ml/kg Ringer's lactate, 20 ml/kg colloids). Although no significant changes in the respiratory parameters were noted after administration of the three colloids, Ringer's lactate produced decreases in PaC2 (107 +/- 6 torr, mean +/- SEM to 72 +/- 7, p less than .05), increases in PaCO2 (30 +/- 4 torr to 55 +/- 5, P less than .001), decreases in plasma colloid osmotic pressure (14.2 +/- 0.8 torr to 6.6 +/- 0.9, p less than .001) at the end of fluid infusion. These changes were associated with significantly increased wet-dry lung ratios (p less than .001) in identically prepared animals, sacrificed after fluid infusion. In spite of the development of pulmonary edema in the crystalloid-treated animals, survival was similar for each group (6/6 for albumin and dextran, 5/6 for hydroxyethylstarch and Ringer's lactate). We thus conclude that both colloidal and crystalloidal fluid resuscitation leads to survival in permeability shock. Resuscitation with crystalloidal fluid, however, requires significantly greater volumes and is associated with the development of pulmonary edema.
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PMID:Increased pulmonary edema with crystalloid compared to colloid resuscitation of shock associated with increased vascular permeability. 671 2

Because of their multiple medical problems, patients with the adult respiratory distress syndrome (ARDS) often develop anemia. In order to determine the effects of a low hemoglobin concentration on gas exchange in such patients, the authors studied the effects of isovolemic hemodilution in the dog oleic acid model of ARDS. Twelve splenectomized dogs with oleic acid-induced pulmonary edema and a consequent venous admixture of 31% +/- 5% (mean +/- SEM) (FIO2 = 0.21) underwent two-stage isovolemic hemodilution with Hetastarch followed by retransfusion of the withdrawn red cells. This resulted in hemoglobin levels at each stage of 12.7 +/- 0.7 g/100 ml, 9.1 +/- 0.6 g/100 ml, 6.5 +/- 0.5 g/100 ml, and 10.1 +/- 0.5 g/100 ml (mean +/- SEM). Oxygen transport fell from 363 +/- 25 ml/kg/min to 219 +/- 17 ml/kg/min (p less than 0.001) at maximum hemodilution during air ventilation and from 383 +/- 79 ml/kg/min to 292 +/- 91 ml/kg/min (p less than 0.001) during oxygen ventilation. Since oxygen consumption remained constant throughout the hemoglobin range studied, decreased hemoglobin resulted in declines in P-VO2. Hemodilution with Hetastarch did not affect intrapulmonary shunt or venous admixture despite the significant increase in cardiac output associated with hemodilution.
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PMID:The effects of hemodilution during pulmonary edema in dogs. 685 99

The pathogenesis of high-altitude pulmonary oedema (HAPE) is disputed. Recent reports show a strong correlation between the occurrence of HAPE and pulmonary artery pressure, and it is known that the oedema is of the high-permeability type. We have, therefore, proposed that HAPE is caused by ultrastructural damage to pulmonary capillaries as a result of stress failure of their walls. However, no satisfactory electron microscopy studies are available in patients with HAPE, and animal models are difficult to find. Madison strain Sprague-Dawley rats show a brisk pulmonary pressure response to acute hypoxia and are susceptible to HAPE. We exposed 13 Madison rats to a pressure of 294 torr for up to 12.5 h, or 4 rats to 236 torr for up to 8 h. Pulmonary arterial or right ventricular systolic pressures measured with a catheter increased from 30.5 +/- 0.5 (SEM) in controls (n = 4) to 48 +/- 2 torr (n = 11). The lungs were fixed for electron microscopy with intravascular glutaraldehyde. Frothy bloodstained fluid was seen in the trachea of three animals. Ultrastructural examination showed evidence of stress failure of pulmonary capillaries, including disruption of the capillary endothelial layer, or all layers of the wall, swelling of the alveolar epithelial layer, red blood cells (RBCs) and oedematous fluid in the alveolar wall interstitium, proteinaceous fluid and RBCs in the alveolar spaces, and fluid-filled protrusions of the endothelium into the capillary lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis of high-altitude pulmonary oedema: direct evidence of stress failure of pulmonary capillaries. 862 Sep 77

Endotoxin sensitivity varies among animal species and appears to correlate with the presence of pulmonary intravascular macrophage (PIM). In rats, which lack PIM, we investigated the hypothesis that chronic cholestatic liver injury leads to induction of PIM and endotoxin sensitivity. Rats were randomized to either common bile duct ligation (BDL) or sham-surgery and studied at 1 wk (acute cholestasis), 2 wk (cholestasis, early cirrhosis), and 4 wk (cholestasis, established cirrhosis) after surgery. Intravascularly injected fluorescent latex microspheres (1 micron diameter) were taken up by large phagocytic cells in lung parenchyma of BDL rats (at 2 and 4 wk), while no uptake was observed in lungs from control rats. Electronmicroscopy revealed accumulation of large, mononuclear, macrophage-like cells containing ingested latex particles within the pulmonary capillaries. Pulmonary intravascular phagocytosis, as reflected in lung uptake of 99mTc microaggregated albumin (Microlite, mean particle diameter = 1 micron), averaged 0.7 +/- 0.1% (mean +/- SEM) of total injected dose in 13 control rats and progressively increased with time after BDL (1 wk, 1.7 +/- 0.2%; 2 wk, 10.0 +/- 3.0%; 4 wk 35.1 +/- 5.9%). Rats with biliary cirrhosis were markedly sensitive to the lethal effects of low dose endotoxin and demonstrated marked lung edema at the time of death. Furthermore, the lung uptake of intravascular 125I-lipopolysaccharide was increased five-fold in cirrhotic rats. We conclude that chronic biliary obstruction leads to the induction of pulmonary intravascular phagocytes and enhances endotoxin sensitivity in rats. Pulmonary intravascular phagocytosis in patients with advanced cirrhosis may account for their increased susceptibility to sepsis-induced adult respiratory distress syndrome.
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PMID:Chronic biliary obstruction induces pulmonary intravascular phagocytosis and endotoxin sensitivity in rats. 796 47

Reduced tolerance to high altitude may be associated with a low ventilatory and an increased pulmonary vascular response to hypoxia. We therefore, examined whether individuals susceptible to acute mountain sickness (AMS) or high altitude pulmonary oedema (HAPE) could be identified by noninvasive measurements of these parameters at low altitude. Ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) at rest and during exercise, as well as hypoxic pulmonary vascular response (HPVR) at rest, were examined in 30 mountaineers whose susceptibility was known from previous identical exposures to high altitude. Isocapnic HVR expressed as difference in minute ventilation related to difference in arterial oxygen saturation (delta V'E/ delta Sa,O2) (L.min-1/%) was significantly lower in subjects susceptible to HAPE (mean +/- SEM 0.8 +/- 0.1; n = 10) compared to nonsusceptible controls (1.5 +/- 0.2; n = 10), but was not significantly different from subjects susceptible to AMS (1.2 +/- 0.2; n = 10). Hypercapnic ventilatory response was not significantly different between the three groups. Discrimination between groups could not be improved by measurements of HVR during exercise (50% maximum oxygen consumption (V'O2,max)), or by assessing ventilation and oxygen saturation during a 15 min steady-state exercise (35% V'O2,max) at fractional inspiratory oxygen (FI,O2) of 0.14. Pulmonary artery pressure (Ppa) estimated by Doppler measurements of tricuspid valve pressure at an FI,O2 of 0.21 and 0.12 (10 min) did not lead to a further discrimination between subjects susceptible to HAPE and AMS with the exception of three subjects susceptible to HAPE who showed an exaggerated HPVR. It is concluded that a low ventilatory response to hypoxia is associated with an increased risk for high altitude pulmonary oedema, whilst susceptibility to acute mountain sickness may be associated with a high or low ventilatory response to hypoxia. A reliable discrimination between subjects susceptible to high altitude pulmonary oedema and acute mountain sickness with a low ventilatory response to hypoxia is not possible by Doppler echocardiographic estimations of hypoxic pulmonary vascular response.
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PMID:Ventilatory and pulmonary vascular response to hypoxia and susceptibility to high altitude pulmonary oedema. 862 Sep 46

Surfactant protein-A (SP-A) leaks into the circulation of patients with acute respiratory distress syndrome (ARDS) or acute cardiogenic pulmonary edema (APE) in a manner inversely related to lung function. Since surfactant protein-B (SP-B) is synthesized as a precursor considerably smaller than alveolar SP-A, we investigated whether it enters the circulation more readily. Reactivities consistent with SP-B proprotein (approximately 42 to approximately 45 kD) and the approximately 25 kD processing intermediate were detected in plasma. Plasma immunoreactive SP-B levels were significantly higher in ARDS (8,007+/-1,654 ng/ml [mean+/-SEM], n = 22) and APE (3,646+/-635 ng/ml, n = 10) patients compared with normal subjects (1,685+/-58 ng/ml, n = 33) and ventilated patients with no cardiorespiratory disease (1,829+/-184 ng/ml, n = 7). All groups had plasma SP-B/SP-A ratios approximately 6- to approximately 8-fold higher than in normal lavage or ARDS tracheal aspirate fluid, consistent with protein sieving. During admission, both plasma SP-B and the SP-B/SP-A ratio were inversely related to blood oxygenation (PaO2/FIO2) (p < 0.0001 and p < 0.025, n = 260 from 39 patients; Spearman) and static respiratory system compliance (deltaV/deltaP) (p < 0.0001 and p < 0.01, n = 168 from 25 patients). We describe in detail three patients and conclude that immunoreactive SP-B enters more readily than SP-A, is cleared acutely, and provides a better indicator of lung trauma.
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PMID:Surfactant proteins-A and -B are elevated in plasma of patients with acute respiratory failure. 935 25


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