UMLS:C0034063 - FACTA Search

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

We observed that the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L- phenylalanine (FMLP) induced pulmonary edema when polymorphonuclear leukocytes (PMNs) were added to isolated constant-flow buffer-perfused rabbit lungs. This study was designed to test the hypothesis that PMNs activated by FMLP induced lung injury by the modulation of reactive oxygen species (ROS), cyclooxygenase products, or cysteinyl leukotrienes (LTs). Addition of FMLP alone did not increase microvascular permeability (Kf). When PMNs were added to the isolated lung, FMLP caused an 80% increase in Kf. Wet-to-dry weight ratio was also significantly increased with PMNs + FMLP compared with FMLP only. There was a significant positive correlation between total myeloperoxidase activity in lung tissue and Kf values after FMLP (30 min). Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate or ibuprofen, had no effect on the PMN + FMLP-induced increase in Kf. However, the ROS inhibitor catalase and the nonantioxidant LT synthesis blocker MK 886 inhibited the PMN + FMLP increase in Kf. Perfusate levels of LTs (LTC4, -D4, and -E4) were significantly increased from baseline values 30 min after FMLP. Both MK 886 and catalase suppressed the elevation of LTs after PMN + FMLP. These results indicate that FMLP increased a pulmonary microvascular permeability in isolated buffer-perfused rabbit lungs that is PMN dependent and mediated by LT produced possibly by a result of ROS production.
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PMID:Mechanisms of increased pulmonary microvascular permeability induced by FMLP in isolated rabbit lungs. 133 54

We tested the hypothesis that tumor necrosis factor-alpha (TNF-alpha) primes the hemodynamic response to the neutrophil agonist N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) in lungs isolated from guinea pigs. Lungs were isolated from animals 18 h after injection of TNF-alpha (3.20 x 10(5) U/kg ip). The infusion of FMLP (300 nM) into lungs isolated after the intraperitoneal administration of TNF-alpha resulted in increases in lung weight, lung (wet-dry)-to-dry weight ratio [(wet-dry)/dry wt], pulmonary capillary pressure, lung myeloperoxidase activity and perfusate thromboxane (Tx)B2 levels. Animals pretreated with the maximal possible amount of endotoxin in the TNF-alpha (1.7 pg endotoxin) did not respond to FMLP. WEB-2086 (37 microM), a platelet-activating factor (PAF) receptor antagonist, added to the perfusate attenuated the hemodynamic and TxA2 response to FMLP. Dazoxiben (0.5 mM), a TxA2 synthetase inhibitor, prevented the FMLP effect. Polyethylene glycol (PEG)-catalase (500 U/ml) added to the perfusate did not affect the FMLP response; however, PEG-catalase (10(5) U/kg) given intraperitoneally with the TNF-alpha decreased the synergism induced by TNF-alpha with FMLP. The data suggest that TNF-alpha primes the lung to the effects of FMLP by increasing the population of resident neutrophils in the lung and/or by in vivo oxidant generation. The pulmonary hemodynamic response and lung edema induced by FMLP are mediated by PAF and TxA2.
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PMID:Tumor necrosis factor-alpha primes pulmonary hemodynamic response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine. 165 89

Adult respiratory distress syndrome (ARDS) is a non-cardiogenic pulmonary edema of various etiologies. Here we report the first application of proton nuclear magnetic resonance (NMR) for the detection of abnormal metabolites in plasma from patients with ARDS. By comparing plasma obtained from the systemic artery with that obtained from the pulmonary artery, we could study the metabolic status of the lung in patients with ARDS. Although their concentrations may vary, the peaks for acetate, acetoacetate, beta-hydroxybutyrate, phenylalanine, and other unidentified compounds in water-suppressed NMR of these patients' plasma were higher than in the normal controls. The proton NMR resonance at a chemical shift of about 7.4 ppm (relative to sodium tetradeutero-3-trimethyl-silylpropionate), presumably caused by phenylalanine and its related metabolites produced by a disordered amino acid metabolism, is detected in greater than 65% of the samples from ARDS patients. We discuss the detection of abnormal metabolites in terms of possible deranged metabolism of carbohydrates, lipids, or amino acids in this syndrome.
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PMID:Proton nuclear magnetic resonance studies of plasma to determine metabolic status of patients with adult respiratory distress syndrome. 270 52

The effect of smoke inhalation on bradykinin metabolism was studied in the rat lung perfused with Ringer's bicarbonate solution. After smoke (from cotton, polyester, or seat cushion material) inhalation, tritium-labeled bradykinin was added to the Ringer's bicarbonate solution, and then the lung perfusion effluent aliquots containing bradykinin and its metabolic fragments were collected after a single transpulmonary passage. For the 20 control rats without smoke inhalation, 91% of the bradykinin dose was metabolized, with Pro-Pro (I), 49%, and Arg-Pro-Pro-Gly-Phe (II), 32%, being the predominant bradykinin cleavage fragments. For 12 rats with smoke inhalation, 89% of the bradykinin dose was metabolized, with I (28%) and II (36%) being the major bradykinin cleavage fragments. The type of smoke did not significantly alter the capacity of the rat lung to metabolize bradykinin. Exposure to smoke from seat cushion material for more than 3 minutes caused pulmonary edema and thickening, and smoke exposure for more than 5 minutes caused loss of integrity at the lung alveolar-capillary interface. In contrast, exposure to cotton or polyester smoke did not cause any observable gross changes of the lung. Electron microscopic examination of lung exposed to seat cushion material smoke revealed considerable damage, with the type I epithelium existing as patches on the alveolar surface and capillary endothelium separated from the basement lamina. Thus in our model acute, short-term inhalation of smoke did not significantly alter the amount of bradykinin metabolized by the pulmonary endothelium so long as the integrity of the lung alveolar-capillary interface was maintained, although there seemed to be a moderate shift in the amount of major cleavage fragments from I to II.
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PMID:The effect of smoke inhalation on bradykinin metabolism by the perfused and ventilated rat lung. 853 19

This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 microg/kg of AT I was found to be an adequate dose for inducing pulmonary edema. To elucidate the mechanism of AT I pulmonary edema and protective measures against it, we observed the effects of captopril (CAP, 5 and 10 mg/kg), an angiotensin converting enzyme inhibitor; losartan (LOS, 10 mg/kg), an angiotensin II (AT II)-receptor antagonist; and phentolamine (PHE, 10 mg/kg), an alpha-adrenergic receptor blocker, on AT I-induced pulmonary edema in rats. Similarly, we also observed the effects of CAP (10 and 20 mg/kg) on pulmonary edema induced by 25 microg/kg of adrenaline (ADR) in rats. The development of AT I-induced pulmonary edema was significantly suppressed by CAP and LOS, but was unaffected by PHE. In contrast, the development of ADR-induced pulmonary edema was not suppressed by CAP. These results suggest that AT I-induced pulmonary edema is developed via the AT II and a specific AT II-receptor, without the indirect action of adrenaline.
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PMID:Pulmonary edema induced by angiotensin I in rats. 951 4

Alkaptonuria is a rare disease of phenylalanine, aromatic amino acids, and tyrosine metabolism. Because of a genetic deficiency of the enzyme homogentisic acid oxidase, an accumulation of homogentisic acid causes ochronotic pigment deposition. The most common clinical manifestations are arthropathy, urinary calculi and discoloration, cutaneous and cartilaginous pigmentation, and cardiac valvular disease. Arthropathy and aortic stenosis are the most debilitating manifestations of the disease. A case of alkaptonuric aortic stenosis is described. A 75-year-old woman with a history of alkaptonuria presented in the emergency department with complaints of progressive dyspnea. Upon examination, the patient was hypertensive, tachypneic, and tachycardic with premature ventricular contractions. She had pitting edema of the lower extremities and complaints of generalized weakness. Chest x-rays revealed congestive heart failure and pulmonary edema. Diuretics were administered, and a continuous nitroglycerin infusion was initiated in the emergency department. The patient was admitted for further evaluation. The patient's respiratory status continued to decline. She was intubated endotracheally 1 day after admission. Subsequent cardiac evaluation revealed an ejection fraction of 35%, severe aortic stenosis, mild coronary artery disease, ischemic cardiomyopathy, and anteroapical akinesis. A dobutamine infusion was instituted for persistent hypotension, and renal dose dopamine was initiated for oliguric renal failure. The patient underwent an emergency operation for an aortic valve replacement with a Dacron patch 10 days after admission. Cardiopulmonary bypass and mild hypothermia were used during the procedure. The patient's hemodynamic status remained tenuous throughout the procedure. Although the first attempt to wean off cardiopulmonary bypass failed, the second attempt was successful with the aid of an intra-aortic balloon pump, inotropic support, and atrioventricular pacing. These measures were maintained during transport to the surgical intensive care unit. In the intensive care unit, the patient did not have an audible blood pressure or a palpable pulse without the support of the intra-aortic balloon pump and atrioventricular pacing. Coarse atrial fibrillation was the underlying electrocardiogram rhythm in the absence of atrioventricular pacing. Sodium bicarbonate was given without improvement. After discussion with the family, all life support measures were discontinued. The patient died 10 minutes after her arrival in the intensive care unit. Alkaptonuria's pathogenesis is manifested as both local and systemic in nature. Collagen vascular diseases share a similar pattern of multisystem involvement. Despite the negative outcome for the patient described, valuable insight can be obtained by studying this case and noting the anesthetic considerations specific to collagen vascular diseases in general.
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PMID:Alkaptonuric aortic stenosis: a case report. 1048 88

Previously we reported that alcohol abuse increases the incidence of the acute respiratory distress syndrome (ARDS) in septic patients, and that chronic ethanol ingestion in rats depletes alveolar epithelial glutathione and increases endotoxin-mediated lung edema. In this study we examined a potential mechanism by which ethanol-induced glutathione depletion could predispose to acute lung injury. We hypothesized that glutathione depletion activates matrix metalloproteinases (MMPs), thereby increasing degradation of the alveolar extracellular matrix (ECM) during sepsis. Ethanol-fed rats (20% vol/vol in water for 6 wk) were given endotoxin (2 mg/kg, intraperitoneally) followed 2 h later by lung isolation and ex vivo perfusion with n-formyl-methionyl-leucyl-phenylalanine (fMLP) (10(-)(7) M). Ethanol ingestion increased (p < 0.05) MMP-9 and MMP-2 activity, as determined by zymography, in the lung tissue and lavage fluid compared with control-fed rats, and increased (p < 0.05) levels of the 7S fragment of type IV collagen in the lung lavage fluid. Ethanol ingestion increased activation, but not production, of the MMP-9 and MMP-2 zymogens. Finally, although concomitant ingestion of N-acetylcysteine had no effect (p > 0.05) on MMP production, it increased (p > 0.05) lung glutathione levels, blocked (p < 0.05) MMP-9 and MMP-2 activation, and decreased (p < 0.05) levels of the 7S fragment of type IV collagen. We conclude that chronic ethanol ingestion, via glutathione depletion, activates MMPs during sepsis, thereby increasing degradation of the alveolar epithelial ECM. Lois M, Brown LAS, Moss IM, Roman J, Guidot DM. Ethanol ingestion increases activation of matrix metalloproteinases in rat lungs during acute endotoxemia.
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PMID:Ethanol ingestion increases activation of matrix metalloproteinases in rat lungs during acute endotoxemia. 1050 28

Although it has been suggested that some biological activities of platelet-activating factor (PAF) are mediated by, at least in part, reactive oxygen intermediates (ROI), the precise mechanisms underlying the interaction between the two remains to be elucidated. Antioxidants, such as alpha-tocopherol acid succinate, N-acetyl-L-Cysteine, pyrrolidinedithiocarbamate failed to inhibit PAF-induced immediate systemic reactions such as lethality, symptoms of disseminated intravascular coagulation, and histological changes such as pulmonary edema and hemorrhage in renal medullae 10 min following PAF injection. In contrast. antioxidants significantly inhibited both the in vivo and in vitro PAF-induced NF-kappaB activation and NF-kappaB-dependent TNF-alpha expression. The effects of the antioxidants were due to their inhibition of PAF-induced degradation of IkappaBalpha, a protein responsible for keeping NF-kappaB in an inactive form. A protein tyrosine kinase and N-tosyl-L-phenylalanine chloromethyl ketone sensitive serine protease were involved in both PAF- and H2O2-induced NF-kappaB activation. Collectively, these data indicate that the PAF-induced NF-kappaB activation is selectively mediated through the generation of ROI.
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PMID:Selective involvement of reactive oxygen intermediates in platelet-activating factor-mediated activation of NF-kappaB. 1092 4

Clusterin (CLU) is a multifunctional 75- to 80-kDa glycoprotein that is upregulated during cellular stress and might represent a defense mechanism during local cellular damage. Mechanisms discussed are antiapoptotic, antioxidative, and anticomplement properties as well as chaperone-like features protecting stressed proteins. The aim of this study was to investigate potential protective effects of CLU on pulmonary vasculature after in situ PMN activation in isolated rabbit lungs. The experiments were performed on 24 isolated and ventilated rabbit lungs that were perfused with 200 mL of Krebs-Henseleit-10% blood buffer with a constant flow of 150 mL/min in a recirculating system. It was tested whether pretreatment with CLU (2.5 microg/ml; n = 8) or catalase (CAT, 5000 U/ml; n = 8) before N-formyl-Met-Leu-Phe (fMLP; 10(-8) M) injection influenced pulmonary artery pressure (PAP) peak airway pressures (PAW) and edema formation as compared with controls (n = 8). Baseline values of PAP were 9-11 mmHg and PAW 11-13 cm H2O. Application of fMLP resulted in an acute significant (P < 0.01) increase of PAP (48 +/- 29 mmHg) within 2 min in the control group and PAW increased to 35 +/- 7 cm H2O within 30 min. Pretreatment with CLU completely suppressed the PAP and PAW response as a result of the fMLP challenge (P < 0.001), whereas a transient PAW increase up to 27 +/- 15 mmHg was observed after CAT. Complement factor C3a release was suppressed by CAT, whereas CLU blocked the complement cascade at the level of C5b-9 formation. Moreover, generation of thromboxane A(2) was reduced after CLU and CAT. Lung edema occurred in the fMLP group but was absent (P < 0.001) after CLU and CAT treatment. Both CLU and CAT prevented fMLP-induced lung injury. Stabilizing effects of CLU, point towards complement regulating features at the level of the terminal complement sequence. Elevated levels of CLU during inflammation could reflect a compensatory organ protective mechanism. Further studies are required to elucidate the clinical impact of the observed organ-protective properties of CLU.
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PMID:Clusterin protects the lung from leukocyte-induced injury. 1286 62

There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S(cv)O(2)), cerebro-vascular carbon dioxide reactivity (DeltaS(cv)O(2)), and brain structural damage (beta-amyloid precursor protein [betaAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 +/- 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better S(cv)O(2) (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO(2) evoked a 16 +/- 4% increase in S(cv)O(2), indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in betaAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO(2) reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
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PMID:Cerebral perfusion pressure directed therapy following traumatic brain injury and hypotension in swine. 1457 61

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