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

This study was designed to determine whether indomethacin, a suggested treatment for adult respiratory distress syndrome (ARDS), would inhibit the efficacy of positive end-expiratory pressure (PEEP) in an animal model of ARDS. Functional residual capacity (FRC), alveolar-to-arterial oxygen difference (A-aPo2) and total lung water were measured in rabbits: 30 controls and 30 with oleic acid induced pulmonary oedema. Within each group, four treatments were administered: diluent (n = 12), PEEP (n = 6), indomethacin (n = 6), or PEEP + indomethacin (n = 6). Lung injury was induced at 30 mins and treatment commenced at 45 min. Oleic acid caused a significant increase at 3 h in % increase in A-aPo2 from baseline (105 +/- 12%) attenuated by PEEP (59 +/- 17%) and indomethacin (57 +/- 7%), with the combination of PEEP + indomethacin preventing a significant increase (26 +/- 9%). PEEP increase FRC in both saline and oleic acid animals; this was not reversed by indomethacin. Oleic acid caused an increase in total lung water (5.16 to 6.58 +/- 0.16 g), not influenced by any treatment. These findings suggest that indomethacin did not inhibit the efficacy of PEEP in this model of ARDS.
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PMID:Effects of indomethacin and PEEP on oleic acid induced pulmonary oedema in rabbits. 195 8

We have previously shown (Am. Rev. Respir. Dis. 136: 886-891, 1987) improved cardiac output in dogs with pulmonary edema ventilated with external continuous negative chest pressure ventilation (CNPV) using negative end-expiratory pressure (NEEP), compared with continuous positive-pressure ventilation (CPPV) using equivalent positive end-expiratory pressure (PEEP). The present study examined the effect on lung water of CNPV compared with CPPV to determine whether the increased venous return created by NEEP worsened pulmonary edema in dogs with acute lung injury. Oleic acid (0.06 ml/kg) was administered to 27 anesthetized dogs. Supine animals were then divided into three groups and ventilated for 6 h. The first group (n = 10) was treated with intermittent positive-pressure ventilation (IPPV) alone; the second (n = 9) received CNPV with 10 cmH2O NEEP; the third (n = 8) received CPPV with 10 cmH2O PEEP. CNPV and CPPV produced similar improvements in oxygenation over IPPV. However, cardiac output was significantly depressed by CPPV, but not by CNPV, when compared with IPPV. Although there were no differences in extravascular lung water (Qwl/dQl) between CNPV and CPPV, both significantly increased Qwl/dQl compared with IPPV (7.81 +/- 0.21 and 7.87 +/- 0.31 vs. 6.71 +/- 0.25, respectively, P less than 0.01 in both instances). CNPV and CPPV, but not IPPV, enhanced lung water accumulation in the perihilar areas where interstitial pressures may be most negative at higher lung volumes.
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PMID:Effect of negative-pressure ventilation on lung water in permeability pulmonary edema. 250 Dec 78

Hypoxic stimulation of the peripheral chemoreceptors has been reported to inhibit hypoxic pulmonary vasoconstriction. To evaluate the pathophysiological importance of this observation, we investigated the effects of surgical peripheral chemoreceptor denervation on pulmonary vascular tone and gas exchange in 17 pentobarbital-anesthetized dogs with oleic acid pulmonary edema. Pulmonary arterial pressure-cardiac index (Ppa/Q) plots, blood gases, and intrapulmonary shunt measured by the SF6 method were obtained at base line, after peripheral chemodenervation (n = 9) or after sham operation (n = 8), and again after 0.09 ml.kg-1 intravenous oleic acid. Over the range of Q studied (2-5 l.min-1.m-2), Ppa/Q plots were best fitted as first-order polynomials in most dogs in all experimental conditions. Chemoreceptor denervation increased Ppa at the lowest Q, while sham operation did not affect the Ppa/Q plots. Oleic acid increased Ppa over the entire range of Q and increased intrapulmonary shunt. This latter was measured at identical Q during the construction of the Ppa/Q plots. Chemoreceptor-denervated dogs, compared with sham-operated dogs, had the same pulmonary hypertension but lower intrapulmonary shunt (36 +/- 4 vs. 48 +/- 5%, means +/- SE, P less than 0.04) and venous admixture (43 +/- 4 vs. 54 +/- 3%, P less than 0.02). We conclude that in intact dogs chemoreceptor denervation attenuates the rise in intrapulmonary shunt after oleic acid lung injury. Whether this improvement in gas exchange is related to an enhanced hypoxic pulmonary vasoconstriction is uncertain.
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PMID:Sinoaortic deafferentation reduces intrapulmonary shunt in dogs with oleic acid lung injury. 279 84

The objective of this study was to elucidate the features of experimentally induced pulmonary edema at the lobular level, using high-resolution CT (HRCT) with pathological correlation. We selected the pig as the experimental animal because the pig has well-defined pulmonary lobules. Twelve Yorkshire pigs were included in this study. Five animals were used for studying normal anatomy of the pig lung. Pulmonary edema was induced by oleic acid infusion in 7 pigs. All computed tomographic (CT) scans were performed on a GE 9800 scanner, using 1.5 mm slice-thickness, 16 cm field of view with 512 X 512 matrix and bone reconstruction algorithm. The animals were killed after CT scans and the lungs were removed, inflated, fixed and dried, and subsequently sliced in sections which corresponded to the CT sections. Using CT images, specimen radiography, and histology, we studied the intralobular distribution of pulmonary edema in selected lobules of each animal. Oleic acid infusion caused multifocal hemorrhagic pulmonary edema within the pulmonary lobule. The distribution was uneven and areas surrounding the lobular bronchi were less involved. HRCT permits evaluation of morphological changes of oleic acid-induced pulmonary edema at the lobular level. The intralobular distribution of the lesions may provide additional information about the mechanism of permeability pulmonary edema.
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PMID:Intralobular distribution of oleic acid-induced pulmonary edema in the pig. Evaluation by high-resolution CT. 280 17

Lung injury following intravenous oleic acid is characterized by pulmonary edema, leukopenia and hypoxemia. Because leukotrienes can increase permeability and cause leukocyte adherence, we evaluated their potential role in oleic acid-induced lung injury in the anesthetized rat using a selective LTD4/E4 antagonist, LY171883. 99mTc-albumin and 99mTc-red blood cells (99mTc-RBC) were used to measure changes in the pulmonary permeability index and intravascular space by non-invasive scintigraphy. Intravenous oleic acid (0.06 ml/kg) increased the pulmonary permeability index 11 (P less than 0.01) and 5.8 fold (P less than 0.01) at 5 and 50 min after its injection compared to baseline, but had no effect on mean pulmonary arterial pressure or pulmonary distribution of 99mTc-RBC. Oleic acid also induced arterial hypoxemia, and increased bronchoalveolar lavage-fluid levels of immunoreactive (i) leukotriene LTC4 from 0.40 +/- 0.14 ng/ml to 2.27 +/- 0.55 ng/ml (mean +/- S.E.M., n = 4, P less than 0.05) and iLTB4 (from 0.42 +/- 0.05 ng/ml to 1.91 +/- 0.63 ng/ml, n = 5-7, P less than 0.01). LY171883 attenuated the elevated permeability by 24% and 68% at 5 (P less than 0.05) and 50 min (P less than 0.01), but did not alter the hypoxemia. These results support the hypothesis that oleic acid elevates leukotriene levels which may increase pulmonary vascular permeability. Furthermore, they suggest that the prevention of elevated pulmonary vascular permeability and edema may be necessary, but are clearly not sufficient to prevent arterial hypoxemia following oleic acid injury in the rat.
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PMID:Oleic acid-induced pulmonary injury in rats: potential role of sulfidopeptide leukotrienes. 284 82

We investigated the effects of varying inspired oxygen concentrations on the resolution of oleic acid-induced lung injury in rabbits. Rabbits were injected intravenously with oleic acid and maintained in room air, or exposed to 60, 70, or 80% oxygen for periods of 7 or 10 days. Oleic acid caused hemorrhagic pulmonary edema with hypoxemia. Hypoxemia was more profound in the oxygen-treated animals, a difference that was significant after 7 days' exposure to 60 and 70% oxygen, and after 4 days to 80% oxygen. Mortality was increased in the animals maintained in 80% oxygen. The data suggest that environmental oxygen concentrations greater than 60% interfere with the return to normal lung function following oleic acid injury in rabbits. The hypoxemia may be due to either mismatching of ventilation and perfusion or to a diffusion block resulting from the increased septal width. There was no evidence of massive pulmonary edema as a cause of the hypoxemia. It was not possible to distinguish between injury primarily caused by oxygen and its interference with the healing process.
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PMID:Oxygen and resolution of lung injury. 308 25

We investigated the effects of prostaglandin E1 (PGE1) and of sodium nitroprusside (NP) on multipoint pulmonary arterial pressure (PAP)/cardiac index (Q) plots in 24 pentobarbital-anesthetized and ventilated dogs with pulmonary hypertension secondary to oleic acid lung injury. The PAP/Q plots were rectilinear in all experimental conditions. In control dogs (n = 8), PAP was increased over the entire range of Q studied, from 1 to 4 L/min.m2, 90 min after oleic acid 0.09 ml/kg, and remained so during 2 consecutive 5-point PAP/Q plots, each of them being constructed in about 30 min. Oleic acid increased the extrapolated pressure intercept (p less than 0.001) but not the slope of the PAP/Q plots. Infusion of PGE1 0.4 micrograms/kg.min intravenously (n = 8) reduced PAP at each level of Q, with a reduction of the extrapolated pressure intercept (p less than 0.01) and no change in slope of the PAP/Q plots. In contrast, NP 5 micrograms/kg.min intravenously (n = 8) slightly reduced PAP only at the highest Q studied, without any significant change in extrapolated pressure intercept or slope of PAP/Q plots. Systemic blood pressure was decreased by 21% after PGE1 and by 24% after NP. Neither drug affected Q nor blood gases after oleic acid. The results suggest that pulmonary hypertension secondary to oleic acid pulmonary edema may be due more to an increase in effective outflow pressure of the pulmonary circulation than to an increase in incremental vascular resistance, and that active vasoconstriction contributes to this type of pulmonary hypertension.
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PMID:Pulmonary vascular pressure-flow plots in canine oleic acid pulmonary edema. Effects of prostaglandin E1 and nitroprusside. 314 86

Oleic acid (OA) injection into the lungs of dogs produces pulmonary edema and decreased cardiac output, and the result is combined hypoxic and stagnant hypoxia. Prostacyclin (PGI2) has some effects that may be beneficial in the alleviation of hypoxia. We studied 18 anesthetized dogs that were divided into three groups: (1) Six dogs acted as controls and did not receive OA or PGI2, (2) six dogs received OA but no PGI2, and (3) six dogs were first given OA and 1 hour later an infusion of PGI2 (100 ng/kg/min) was started and continued for 4 hours. All dogs were killed at the end of the study and their lungs were removed for weighing and preparation for microscopic examination. Compared with controls, OA caused a low cardiac output, high systemic and pulmonary vascular resistance, and increased right-to-left intrapulmonary shunt. The group that received OA and PGI2 demonstrated a well-maintained cardiac output and a low systemic vascular resistance. Right-to-left intrapulmonary shunt, however, increased in these dogs compared with the dogs not given PGI2. All animals given OA had similar wet/dry lung weights and histologic appearances. Our results suggest that the only beneficial effect of PGI2 in OA-induced lung injury is to improve the stagnant hypoxia, but this is associated with an aggravation of the hypoxic hypoxia. The result of these competing effects appears to be a mild overall improvement in oxygen delivery as suggested by the slightly higher mixed venous PO2 in the group that received PGI2.
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PMID:Hemodynamic and pathologic effects of prostacyclin on oleic acid-induced pulmonary injury. 327 13

To study the influence of Ethanolamine-Oleate (EO) used for endoscopic injection sclerotherapy for esophageal varices on the pulmonary hemodynamics, extra vascular lung water (EVLW), and pulmonary and systemic pressures measurements, and blood gas analysis were performed after injection of EO directly into the right atrium in 18 mongrel dogs. Studies were made in three groups, group A (6 dogs) in which the bolus of 1 ml/kg of EO was injected with 1 second; group B (6 dogs) in which 0.25 ml/kg of EO was injected for four times successively within a minute; and controls (6 dogs) the bolus of 1 ml/kg of saline was injected within 1 second. EVLW was measured by thermal-green dye double indicator dilution method. Pulmonary pressures were measured using Swan-Ganz catheter. Results were as follows. In group A, 4 of the 6 dogs died with a symptom of pulmonary edema within several minutes. In the other two, systemic and pulmonary artery pressure did not change, but EVLW and pulmonary artery resistance significantly increased compared to the controls. Intrapulmonary shunt ratio and PO2 were reduced significantly compared to the controls. In group B no systemic hemodynamic changes were observed. But again EVLW significantly increased. These results suggest that the injection sclerotherapy using EO affects pulmonary hemodynamics. And this effect of EO doesn't depend on the total amount of injected EO, but on the concentration of EO reaching the lung. Careful respiratory monitoring seems necessary in patients undergoing injection sclerotherapy.
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PMID:[Experimental studies on respiratory insufficiency after endoscopic injection sclerotherapy using ethanolamine-oleate]. 371 71

We compared the acute effects of bilateral arteriovenous may be related to levels of PvO2. The hydralazine-associated (p less than .05) decrease in resistance. Mixed venous oxygen fistulas to those of hydralazine infusion on hemodynamics and pulmonary gas exchange in dogs with pulmonary edema induced by administration of oleic acid. Oleic acid significantly (p less than .01) increased intrapulmonary shunt (Qsp/Qt) and pulmonary and systemic vascular resistance, and reduced cardiac output. Once the lesion stabilized, both opening the fistula and infusing hydralazine produced a similar and significant (p less than .01) increase in cardiac output, and a significant (p less than .05) decrease in resistance. Mixed venous oxygen tension (PvO2) closely followed the changes in cardiac output; however, PaO2 did not change. Qsp/Qt significantly (p less than .01) increased with the fistulas open and with hydralazine infusion. Closure of the fistulas or bleeding the animal at the end of the experiment reversed the changes in cardiac output and Qsp/Qt. The comparable increases in cardiac output and Qsp/Qt produced by opening the fistulas or infusing hydralazine may be related to levels of PvO2. The hydralazine-associated PvO2 increase indicates that this drug increased oxygen transport to the tissues even as Qsp/Qt became larger.
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PMID:Effect of hydralazine on intrapulmonary shunt. 372 Mar 26


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