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)

All hypervolemia or any decrease in plasma oncotic pressure leads to deterioration in lesional pulmonary edema. The aim of albumin infusions is to restore the plasma oncotic pressure and to oppose the passage of water into the extravascular space. This therapy is however debatable owing to the abnormal increase in the permeability of the alveolo-capillary membrane to proteins. Diuretics enable one to lower the volemia and to maintain the pulmonary capillary pressure at its minimum level. However, strict hemodynamic supervision is absolutely necessary. Cortico-steroids have been recommended without serious physiopathological justification. However, they have a preventive action on interstitial edema in endotoxic shock.
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PMID:[Reduction and anti-inflammatory technics in non-hemodynamic pulmonary edemas]. 0 65

Patients with shock lung syndrome were identified as those who developed acute respiratory failure after a profound episode of hypotension secondary to hemorrhagic, gram-negative, or endotoxic shock. In this study, each of the 10 patients with shock lung syndrome received methylprednisolone sodium succinate, 30 mg. per kilogram, intravenously every 6 hours for 48 hours. In addition, all patients were supported with mechanical ventilation, with or without positive end-expiratory pressure (PEEP). Arterial oxygenation improved markedly, and pulmonary edema resolved in all patients. Nine were discharged from the hospital and one died subsequently of disseminated intravascular coagulation. This study demonstrated a significant improvement in mortality rate with repeated pharmacologic doses of methylprednisolone compared to previously reported mortality rates of 60 to 90 per cent in patients with shock lung syndrome treated without repeated pharmacologic doses of steroid therapy.
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PMID:Methylprednisolone. Pharmacologic doses in shock lung syndrome. 126 66

TNF is a major mediator in the pathogenesis of endotoxic shock, and its inhibition has a protective effect in various animal models of sepsis or endotoxin (lipopolysaccharide, LPS) toxicity. LPS treatment also induces an oxidative damage mediated by increased production of reactive oxygen intermediates. N-Acetylcysteine (NAC) is an antioxidant and a precursor of the synthesis of glutathione (GSH) and was reported to protect against LPS toxicity and LPS-induced pulmonary edema. In this study we investigated the effect of NAC on TNF production and LPS lethality in mice. The results indicated that oral administration of NAC protects against LPS toxicity and inhibits the increase in serum TNF levels in LPS-treated mice. The inhibition was not confined to the released form of TNF, since NAC also inhibited LPS-induced spleen-associated TNF. On the other hand, the inhibitor of GSH synthesis, DL-buthionine-(SR)-sulfoximine (BSO), had the opposite effect of potentiating LPS-induced TNF production, and this was associated with a decrease in liver GSH levels. Repletion of liver GSH with NAC reversed this effect. NAC was also active in inhibiting TNF production and hepatotoxicity in mice treated with LPS in association with a sensitizing dose of Actinomycin D. These data indicate that GSH can be an endogenous modulator of TNF production in vivo. On the other hand, NAC pretreatment did not inhibit other effects of LPS, particularly induction of serum IL-6, spleen IL-1 alpha, and corticosterone, in the same experimental model, suggesting that the observed effect could be specific for TNF.
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PMID:N-acetylcysteine and glutathione as inhibitors of tumor necrosis factor production. 154 68

We used a selective leukotriene (LT) D4/E4 receptor antagonist (LY 203647) to investigate the role of cysteinyl LTs as mediators of several important pathophysiological events in a porcine model of endotoxic shock. Pentobarbital-anesthetized pigs (11.8-17.5 kg) were mechanically ventilated with 100% O2. Pigs in groups I (n = 10), IIA (n = 10), and IIB (n = 5) were infused with Escherichia coli lipopolysaccharide (LPS; 250 micrograms/kg) from time (t) = 0-20 min. Pigs in group III (n = 3) were normal controls. All pigs were resuscitated from t = 0-240 min with Ringer lactate (0.8 ml.kg-1.min-1). Pigs in group I received no further treatment. At t = 30 min, groups IIA and IIB were injected with LY 203647 (30 mg/kg) and were started on an infusion of the compound at 10 (group IIA) or 30 mg.kg-1.h-1 (group IIB). Delayed treatment with LY 203647 significantly (P less than 0.05) and persistently ameliorated LPS-induced pulmonary hypertension. The compound also abrogated LPS-induced pulmonary edema, as assessed by gravimetrically determined lung extravascular wet-to-dry weight ratios. Despite its beneficial effect on pulmonary edema, delayed treatment with LY 203647 did not improve arterial oxygenation. Delayed treatment with LY 203647 transiently improved mesenteric perfusion. These data suggest that cysteinyl LTs are important mediators in porcine endotoxicosis.
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PMID:Delayed treatment with an LTD4/E4 antagonist limits pulmonary edema in endotoxic pigs. 185 25

Generalized circulatory changes, manifesting as pulmonary oedema, acute renal failure, liver damage and severe hypotension, are well recognized aspects of acute falciparum malaria. The organ pathology is thought to be associated with a restricted local blood flow. These aspects of falciparum malaria are strikingly analogous to the shock syndrome which follows trauma, the injection of indotoxin, or some bacterial infections. Two of the cyclooxygenase products of arachidonic acid, thromboxane A2 and prostacyclin, acting through their opposing effects on vasoactivity and platelet aggregation, are emerging as the major controlling influences of vascular homeostasis. The effects of thromboxane, which constricts blood vessels and aggregates platelets, appear to dominate during traumatic or endotoxic shock. Thus thromboxane is potentially one of the main mediators of endotoxicity, and as such, from our previously published model, is likely to be important in the pathogenesis of the circulatory disturbances seen in acute malaria. This suggestion is consistent with earlier evidence that the autonomic nerve supply and bradykinin may have an important role in the pathogenesis of the haemodynamic changes in this disease. It also implies that pharmacological antagonists of thromboxane may provide useful specific therapy for the main life-threatening aspects of acute falciparum malaria.
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PMID:Thromboxane may be important in the organ damage and hypotension of malaria. 727 28

The effect of TCV-309, a newly developed platelet activating factor (PAF) antagonist, on the wet/dry weight ratio of the lung (index of pulmonary edema) and the pulmonary surface activity (index of pulmonary compliance) was evaluated in comparison with that of CV-3988 (PAF-antagonist). Administration of TCV-309 (1 mg/kg) or CV-3988 (10 mg/kg) significantly reduced the wet/dry weight ratio which was increased by endotoxin administration (3 mg/kg). It also augmented the pulmonary surface activity. Administration of either TCV-309 or CV-3988 alleviated the histologic lesions caused by endotoxic shock. These results suggest that lung injury during endotoxic shock can be controlled by TCV-309 as by CV-3988.
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PMID:Effect of platelet activating factor antagonist (TCV-309) on lung injury in dogs with experimentally endotoxin-induced shock. 851 12

Sera obtained from a group of pigs (n = 5) fed a diet amended with fumonisin containing Fusarium moniliforme culture material was used to determine the levels of Tumor Necrosis Factor-Alpha (TNF) activity by a functional bioassay utilizing the TNF sensitive WEHI 140 mouse fibrosarcoma cell line. Two pigs developed signs consistent with pulmonary edema which was confirmed by pathologic examination in only one pig. Significant, time dependent increases in TNF-like activity were observed in all pigs during the five days of the trial. Another group of pigs (n = 5) was given a defined daily dose of the same culture material by gastric intubation. Two pigs developed fulminant pulmonary edema and sharp increases in TNF activity were observed during the 3 days of the trial in all pigs. In both cases the activity was not abrogated by addition of a neutralizing anti-human TNF monoclonal antibody suggesting that other factors may have been responsible for these effects, possibly the increased levels of sphingoid bases in the serum. Since the pig has become an important model in the study of TNF mediated endotoxic shock, these studies illustrate the relevance of certifying the absence of this important mycotoxin from corn based animal diets, specially if functional assays are used to monitor the activity of TNF in serum.
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PMID:Dietary Fusarium moniliforme culture material induces in vitro tumor necrosis factor-alpha like activity in the sera of swine. 913 10

Acute respiratory distress syndrome (ARDS) is the result of severe injuries of different etiologies of the capillary system in patients with previously healthy lungs, resulting in noncardiogenic pulmonary edema. The authors studied 42 infants in whom the histopathologic aspects were suggestive for ARDS. The etiologic factors of this syndrome were: severe gastroenteritis with hypovolemic or endotoxic shock (13 cases), sepsis (9 cases), fulminans purpura (2 cases), severe neurological disorders (13 cases), pulmonary infections (5 cases). In such conditions, if the infant presents hyperpnea followed by generalised cyanosis, refractory to oxygen therapy, and if there are clinical and radiologic signs of acute pulmonary edema, the diagnosis of ARDS must be considered and a complete intensive care therapy is compulsory in order to alleviate the severe prognosis of this syndrome.
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PMID:Etiological, clinical and pathomorphological aspects of acute respiratory distress syndrome in children. 1075 53

We evaluated the role of endothelin-1 (ET-1) and the involvement of nitric oxide in cardiovascular and respiratory dysfunction, during endotoxic shock, in 18 anaesthetised, mechanically ventilated pigs, divided into three groups. Group 1 was i.v. infused with LPS (20 microg/Kg/h for 240 min). Group 2 was pre-treated with bosentan, a dual inhibitor of ET-1 receptors, and at 180 min of endotoxic shock, L-NAME (N(G)-nitro-L-arginine methyl ester, 10 mg/Kg), a non-selective inhibitor of NO synthases, was i.v. administered. Group 3 was infused with LPS and L-NAME was administered similarly to group 2. Results show that LPS caused systemic hypotension, pulmonary biphasic hypertension, decrease in compliance (C(rs)) and increase in resistance (R(max,rs)) of respiratory system. Bosentan completely abolished the pulmonary hypertension and the changes in C(rs)and R(max,rs). L-NAME does not affect the LPS-dependent changes in respiratory mechanics, but it worsens the cardiovascular effects, causing death of pigs. Pre-treatment with bosentan prevents this deleterious effect. Our study demonstrates that the LPS-dependent respiratory effects are mediated by ET-1, which, probably causing pulmonary oedema, is responsible for the decrease in C(rs)and the increase of R(max,rs).
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PMID:Improvement of respiratory function by bosentan during endotoxic shock in the pig. 1154 27

Most recently we have shown that 4-aminotetrahydrobiopterin (4-ABH4), an analogue of tetrahydrobiopterin (cofactor of NO synthase), even administered 2 h after endotoxin challenge, improves survival rate in rats. The following experiment was performed to examine the effects of 4-ABH4 with respect to endotoxin-induced hemodynamic alterations and organ failure. At 2 h after endotoxic challenge (10 mg kg(-1) body weight) animals received 4-ABH4 at a dose of 1, 10, or 100 mg kg(-1) body weight. The controls were treated similarly but received saline at the same volume. Eight hours after endotoxin challenge cardiac index and stroke volume were significantly increased in animals treated with 10 mg 4-ABH4 compared to controls (0.23 +/- 0.06 vs. 0.16 +/- 0.04 mL min(-1) kg(-1) and 0.29 +/- 0.05 vs. 0.22 +/- 0.03 mL beat(-1)) while mean arterial pressure and peripheral vascular resistance index did not significantly differ among the groups. Plasma alanine aminotransferase (ALT) and creatinine levels were significantly increased in endotoxin controls compared with laboratory controls (ALT: 1643 +/- 1436 vs. 74 +/- 17 U L(-1); Creatinine: 91 +/- 29 vs. 42 +/- 3 micromol L(-1)) which was attenuated in animals treated with 10 mg kg(-1) 4-ABH4 (ALT: 417 +/- 318 U L(-1); Creatinine: 78 +/- 26 micromol L(-1)). Moreover, endotoxin-induced lung edema and intestinal necrosis were significantly reduced by 4-ABH4. Our study provides information that tetrahydrobiopterin analogue, 4-ABH4, improves LPS induced hemodynamic conditions and organ injury. This may, at least in part, account for the previously observed protection of rats by 4-ABH4 against endotoxin-induced mortality in the same endotoxic shock model.
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PMID:A 4-amino analogue of tetrahydrobiopterin attenuates endotoxin-induced hemodynamic alterations and organ injury in rats. 1216 80


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