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

Basic therapeutic methods based on early diagnosis of septic ARDS were described. Concerning early diagnosis exertional hypoxemia and increased broncho-vascular markings on chest X-ray were observed in the pre-ARDS stage of septic patients. These findings were also observed in the initial stage of endotoxin-induced pulmonary edema in rabbits and the basic mechanisms were thought to be as follows, based or our experimental studies. The former is related on impairment of alveolar diffusion and the latter reflect increased peri-vascular cuffing due to increase in pulmonary edema. The diffuse infiltrative shadows on the both back area in CT scanning was also a helpful sign indicating the early stage of pulmonary edema. This finding was seen at the stage at which the edematous shadow had not yet appeared on conventional chest X-ray. Increase in serum laminin and decrease in plasma fibronectin were also important biochemical findings predicting ARDS in gram negative sepsis. Using these findings, it is considered that early prediction of septic ARDS is possible. Concerning therapeutic methods based on early prediction, the usefulness of cortico-steroids and the protease inhibitor "Urinastatin" were observed in experimental in vitro and in vivo studies. Some findings induced by endotoxin administration in rats or rabbits, such as the increase in endotoxin in peripheral blood, the distraction of PMN-elastase, the increase in pulmonary lymph flow and mortality within 48 hours were significantly suppressed by simultaneous treatment by corticosteroid. In an in vitro study, PMN superoxide production and elastase release following incubation of endotoxin and PMNs were significantly inhibited by adding a concomitant level of corticosteroid and/or urinastatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sepsis and ARDS]. 203 89

Toxic oxygen metabolites (TOM) have been suggested to be mediators of permeability edema associated with the adult respiratory distress syndrome (ARDS). Because corticosteroids have possible beneficial effects in ARDS, we have examined the effect of methylprednisolone (MP) on TOM-induced lung edema in isolated, plasma-perfused rat lungs. TOM were generated by adding xanthine oxidase (XO) and hypoxanthine (HX) to the perfusate. Microvascular permeability was assessed by fluid filtration rate (FFR). FFR was determined before and 30 min after administration of XO and HX by measuring the weight increase of the lungs for the last 3 min during a standard 5 min elevation of the outlet pressure. MP was administered in two different ways: 1) Added to the perfusate 5 or 60 min before XO and HX (0.1 and 1 mg ml-1), and 2) given as pretreatment to the rats 12 and 2 hr before preparation of the lungs (40 mg kg -1). XO and HX significantly increased FFR compared to lungs perfused with untreated plasma. Pretreatment with MP significantly attenuated the increase in FFR caused by XO and HX. Addition of MP to the perfusate also inhibited the effect of TOM. This latter protection occurred irrespective of when MP was added before XO and HX. However, when the highest dose of MP was added 5 min before XO and HX, there was a loss of the protective effect. In summary, this study provides evidence that MP may directly prevent microvascular injury induced by TOM in isolated perfused rat lungs. The effect was dependent on the dose of MP applied, but not on when MP was administered prior to exposure to TOM.
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PMID:Toxic oxygen metabolites increase microvascular permeability in isolated perfused rat lungs: the effect of methylprednisolone. 206 43

The endothelial cells of pulmonary blood vessel play an significant role in lung vessel permeability, especially in acute lung damage and adult respiratory distress syndrome. In this study, bovine pulmonary endothelial cells were isolated, cultured and identified by means of reverse microscopic, scanning electromicroscopic, transmission electro- microscopic and immunofluorescence microscopic observation. Then they were labeled with 51Cr. Hydrogen peroxide (H2O2), H2O2 with catalase, xanthine oxidase (XO) with hypoxanthine (HX), human neutrophil elastase (HNE), cathepsin-G (C-G) and endotoxin (ET) were incubated with the labeled cells for half hour in various experimental groups respectively. The amount of 51Cr in the suspension released from the damaged cells was counted with r-radiometer. The results show that HNE, ET, H2O2 and superoxide anion (the latter is produced from the reaction between XO and HX) could at some degree damage the membrane of endothelial cells, and the inflammatory mediators of human neutrophils might play an important role in the development of pulmonary edema.
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PMID:[Effect of the products released from the activated human neutrophils and endotoxin on bovine pulmonary endothelial cells]. 208 56

A good model of adult respiratory distress syndrome is lung injury induced by phorbol myristate acetate (PMA). In the present study we examined the effect of mepacrine, an inhibitor of phospholipase A2, on lung injury induced by PMA in isolated blood-perfused rat lungs. In the isolated lung, saline (1 ml) or mepacrine (75 microM) alone in the perfusion system did not discernibly change the pulmonary arterial pressure (PAP) and lung weight (LW). After administration of PMA (0.16 micrograms/ml), severe hypertension and lung edema developed (delta PAP = 40.1 +/- 6.0 mmHg, p less than 0.001; delta LW = 5.5 +/- 0.7 g, p less than 0.001). Whereas, the addition of mepacrine (75 microM) prevented PMA-induced lung edema and pulmonary hypertension (delta PAP = 4.7 +/- 2.2 mmHg, delta LW = 0.2 +/- 0.2 g). To further elucidate the protective mechanism of mepacrine on lung injury, a vasodilator (nitroprusside) was given to decrease PAP levels to +6 mmHg from baseline values in the PMA group, as well as in the mepacrine-pretreated PMA (MPMA) group. During a subsequent venous pressure challenge, severe lung injury developed in the PMA group (delta LW = 9.5 +/- 2.1 g, p less than 0.001). However, with the same venous pressure challenge in the MPMA the lung weight was markedly less than that of the PMA group (delta LW = 1.0 +/- 0.2 g). Histologic findings examined by light microscopy presented intraalveolar hemorrhage and fluid accumulation, disruption of vascular basements and alveolar septa, and aggregation of inflammatory cells within the parenchyma in the lungs of the PMA group. In the MPMA group there was no evidence of intraalveolar hemorrhage and alveolar fluid accumulation, however, the occasional presence of granulocytes in the parenchyma and slight interstitial edema were still observed. In addition, depressed the chemiluminescence release from PMA activated granulocytes which were in a dose-dependent manner in vitro. These observations suggest that mepacrine inhibits PMA-induced lung injury chiefly by protection of vascular permeability. The mechanism of the protection may be due to the inhibition of oxygen radicals released from activated neutrophils and the reduction of neutrophil chemotaxis.
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PMID:The protective effect of mepacrine on acute lung edema induced by phorbol myristate acetate in rats. 209

The survival and ICU length of stay of 40 ARDS patients admitted to the ICU were analyzed to determine if a management strategy of lowering the pulmonary capillary wedge pressure (Ppw) was associated with an increased survival or a decreased ICU length of stay. ARDS was defined as three or four quadrant alveolar filling roentgenographically, a PaO2 less than 80 mm Hg with an FIO2 greater than .5 and a Ppw less than 18 mm Hg. Patients were divided into two groups: group 1 included all patients in whom there was a reduction of Ppw by at least 25 percent, and group 2 included patients in whom there was no, or less than a 25 percent reduction in Ppw. Survival was statistically different between the groups with 12 of 16 group 1 patients and seven of 24 group 2 patients surviving to hospital discharge. This difference remained statistically significant after stratifying patients by age and the APACHE II severity of illness index. We conclude that this retrospective analysis supports the notion that treatment of low pressure pulmonary edema with reduction of Ppw is associated with an increased survival.
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PMID:Improved survival in ARDS patients associated with a reduction in pulmonary capillary wedge pressure. 233 93

In an attempt to determine the physiologic parameters that best correlate with severity of lung edema (wet/dry [W/D] weight), we serially monitored multiple cardiopulmonary hemodynamics, airway pressure, and blood gases on both 100% oxygen and room air after graded infusions of oleic acid (OA) in dogs. We found significant increases in the intrapulmonary shunt fraction (Qsp/Qt), mean pulmonary arterial pressure (MPAP), pulmonary (PVR) and systemic vascular resistance (SVR), alveolar-arterial PO2 difference (P[A-a] O2), and peak airway pressure (Paw), but decreases in PaO2 and pH. These cardiopulmonary hemodynamic changes were similar to those found in adult respiratory distress syndrome (ARDS). This study showed that Qsp/Qt (r = .72, p less than .001), PaO2 (r = -.60, p less than .01), P(A-a)O2 (r = .55, p less than .01), pH (r = -.55, p less than .01), MPAP (r = .50, p less than .05) and Paw (r = .49, p less than .05) significantly correlated linearly with W/D. The significant correlation is not high enough clinically to predict the severity of acute permeability pulmonary edema considering only one parameter of cardiopulmonary hemodynamic change. Therefore, we propose the possible prediction of the severity of ARDS by considering all of the above hemodynamic changes together with Paw or dynamic compliance.
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PMID:Correlation between cardiopulmonary changes and severity of acute lung injury in dogs. 210 3

Mechanically ventilated, nonsurgical, critically ill patients represent a group not rigorously studied by energy expenditure measurements for formulating nutritional support guidelines. Most strategies for predicting caloric requirements in this group are based on studies of spontaneously breathing surgical patients. It is unclear whether "severity of disease" or "stress" factors employed in this group are justifiable in medical patients with compromised pulmonary function, who may be particularly prone to the complications of overfeeding. We therefore measured the energy expenditures of 73 consecutive ventilator-supported patients with various primary diagnoses in a medical ICU. These results are compared to estimates of caloric requirements based on the Harris-Benedict equations, without modification for severity of disease or other factors. These comparisons are (kcal/day +/- SE, measured vs predicted): sepsis, 1,982 +/- 97 vs 1,534 +/- 56 (p less than 0.0001); cardiogenic shock, 1,452 +/- 119 vs 1,339 +/- 62; cardiogenic pulmonary edema, 1,427 +/- 87 vs 1,338 +/- 93; ARDS, 1,732 +/- 203 vs 1,550 +/- 125; pneumonia, 1,508 +/- 148 vs 1,259 +/- 55; and "other" 1,585 +/- 104 vs 1,419 +/- 55. These data reveal that in mechanically ventilated nonsurgical patients without sepsis, no modifications of the Harris-Benedict equations are necessary; in those with sepsis an increase of approximately 20 percent over these predictions is appropriate.
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PMID:Energy expenditures of mechanically ventilated nonsurgical patients. 211 45

The effect of pulmonary injury induced by aspiration of HCl on plasma atrial natriuretic polypeptide (ANP) level was examined in rats given a constant infusion of water and electrolytes. In addition, using specific antiserum against ANP, we investigated the physiological role of ANP in rats after HCl aspiration. Rats were housed individually in metabolic cages and were given a constant infusion of sodium solution via catheters chronically inserted into the jugular vein. Plasma ANP levels were elevated at 3 and 24 h after tracheal injection of 0.2 ml of 0.1 N HCl via the cricothyroid membrane. Urine volume and urinary sodium excretion increased during the first 24 h after acid aspiration. However, this increase was reduced by the injection of anti-ANP serum. Furthermore, the injection of anti-ANP serum resulted in a significant (P less than 0.05) increase in wet lung weight from a value of 0.74 +/- 0.06 (HCl aspiration with normal rabbit serum injection) to 0.83 +/- 0.07% of body weight. These results indicate that ANP plays a physiological role in the regulation of urinary water and sodium excretion after pulmonary acid injury and suggest that ANP elevated in plasma after pulmonary injury may prevent pulmonary edema with its diuretic action and/or some direct action on water movement in the lung.
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PMID:Release of ANP and its physiological role in pulmonary injury due to HCl. 213 26

Parvovirus infection was confirmed by fluorescent antibody staining or viral culturing in 137 (22%) of 615 necropsy accessions from dogs at the Missouri Veterinary Medical Diagnostic Laboratory from Jan 1, 1987 through Sept 30, 1988. Septicemic colibacillosis was diagnosed in 88 (90%) of the 98 canine parvovirus-positive accessions in which liver or lung was cultured bacteriologically. Pulmonary edema or alveolitis similar to that seen in the human adult respiratory distress syndrome was observed in 63 (69%) of the 91 canine parvovirus-positive accessions in which the lungs were examined histologically.
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PMID:Coliform septicemia and pulmonary disease associated with canine parvoviral enteritis: 88 cases (1987-1988). 215 91

A 4 hr intravenous infusion of Escherichia coli endotoxin in a total dose of 100 mg/kg produced significant morphological and functional pulmonary alterations in pentobarbitone anesthetized rats. Lung vascular permeability index was increased from 2.11 +/- 0.34 in normal rats to 4.82 +/- 0.65 in untreated endotoxemic rats. Treatment of endotoxemic rats with recombinant human superoxide dismutase (r-HSOD) in doses of 0.1, 0.215, and 0.464 mg/kg.min i.v., infused concomitantly with endotoxin, dose-dependently reduced the permeability index to 3.28 +/- 0.96, 2.83 +/- 0.55 (P less than 0.05), and 2.16 +/- 0.65 (P less than 0.05). The wet lung weight was 523 +/- 15 and 664 +/- 46 mg/100 g bwt in normal and in untreated endotoxemic rats, respectively. r-HSOD dose-dependently inhibited the endotoxin-induced increase in wet lung weight to 617 +/- 40, 577 +/- 31, and 559 +/- 39 (P less than 0.05) mg/100 g bwt. r-HSOD (0.464 mg/kg.min) did not affect permeability index and wet lung weight in normal, nonintoxicated rats. Endotoxin infusion produced a significant increase in respiratory rate (max. +69%) and blood gas alterations, indicating a hyperventilatory hypocapnia in endotoxemic control rats. Infusion of r-HSOD (0.464 mg/kg.min) significantly inhibited the endotoxin-induced tachypnoe (max. +13%) and blunted the alterations in arterial hydrogen carbonate content and carbon dioxide tension. In conclusion, infusion of r-HSOD dose-dependently and significantly inhibited pulmonary edema formation and hyperventilatory dyspnoe in endotoxemic rats.
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PMID:Effects of recombinant human superoxide dismutase on increased lung vascular permeability and respiratory disorder in endotoxemic rats. 217 95


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