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)

Microaggregate filtration and separation of the cellular components of stored autologous blood have not changed the functional and morphological damage in primate lungs from stored-blood perfusion. Pharmacologic prevention of these "shock lung" changes was attempted with trasylol and with methylprednisolone pretreatment. In an in situ primate lung perfusion model, fresh and stored blood was perfused in untreated baboons and in groups of seven animals each pretreated with Trasylol or methylprednisolone. Pulmonary damage from stored-blood perfusion was evident by pulmonary edema, increase in pulmonary vascular resistance, decreases in effective compliance and arteriovenous pO2 gradient as well as by morphological criteria. Some protection was afforded by methylprednisolone and, to a lesser extent, trasylol pretreatment against this damage in primate lung form and function induced by stored-blood perfusion.
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PMID:Protection of primate lung from stored-blood perfusion by peptidase inhibition and target membrane stabilization. 9 51

Acute pulmonary edema, evidenced by increased lung/body weight ratios, was evoked in rats within 5 min following the intravenous injection of 16-40 mug/kg of adrenaline. This change was accompanied by a decrease of 40% of circulatory kininogen not due to generalized plasma protein loss. Rats treated 10-20 min prior to adrenaline with 10 mg/kg of acetylsalicylate (Aspirin), 1000 KIU/kg of Kunitz anti-protease (Trasylol), or 10 mg/kg of soybean trysin inhibitor (SBTI), failed to exhibit pulmonary edema or decreased plasma kininogen levels, but were as sensitive as untreated animals to the arterial hypertensive effect of adrenaline. 4.8 mug/kg of carbamylcholine administered together with 40 mug/kg of adrenaline, prevented pulmonary edema. Carbamylcholine did not reduce plasma kininogen consumption by adrenaline, but effectively decreased the raised systolic arterial blood pressure, the increased systolic-diastolic pressure interval as well as the reflex slowing of the heart presented by adrenaline-treated rats. It seems that in the adrenaline-treated rat, pulmonary edema results from the joined action of vasopressor effects leading to hydrostatically forced outflow of vascular fluid, and of kinin release leading to increased peripheral vascular permeability.
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PMID:Contribution of vasopressor and plasma kininogen changes towards acute adrenaline pulmonary edema in the rat. 108 87

In the present study the pathogenesis of the pulmonary damage following infusion of thrombin in combination with a fibrinolysis inhibitor, AMCA, in the dog was elucidated. An important mechanism in the development of the pulmonary damage following infusion of thrombin and AMCA seems to be an increased vascular permeability in the pulmonary microvasculature leading to pulmonary oedema. The question whether this pulmonary damage can be prevented by antihistamine (mepyramine maleate), antiserotonins (methysergide, reserpine) antiprostaglandins (acetylsalicylic acid, indomethacin, polyphloretin phosphate), 'anti-inflammatory agents' (methylprednisolone, calcium) or an anti-adrenergic agent (phenoxybenzamine) was investigated. None of these agents did prevent the lung damage following thrombin and AMCA. In order to study the possible role of bronchoconstriction, the complement system and the kinin system for this damage dogs were also artificially ventilated with an increased end-expiratory pressure, decomplemented with cobra venom factor or treated with Trasylol respectively. Neither were these treatments effective in preventing the pulmonary damage. The findings of the present study suggest that the permeability increasing substance involved in the pathogenesis of the pulmonary damage following thrombin and AMCA is not histamine, serotonin, prostaglandins or bradykinin. Therefore another, still unknown factor, may be of greater importance for this damage.
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PMID:Pulmonary damage following pulmonary microembolism in the dog. Effect of various types of treatment. 126 37

High doses (10-40 micrograms/Kg, i.v.), of epinephrine evoke conspicuous consumption of circulatory rat kininogen (Kg), an effect not observed in animals pre-treated with either soybean trypsin inhibitor (SBTI, 10 mg/Kg, i.v.), Trasylol (1000 KIU/Kg, i.v.) or Aspirin (10 mg/Kg). Kg consumption by epinephrine is accompanied by a raise in rat plasma TAME-esterase attributed to the activation of plasma kallikrein by pro-kininogenase generated in circulatory basophils or mast cells exposed to epinephrine. The severe pulmonary edema observed in rats given epinephrine, is very markedly reduced in animals pre-treated with either SBTI, Trasylol or Aspirin at doses which inhibit Kg consumption by the catecholamine. Indomethacin (1-10 mg/kg) did not reduce REPE nor inhibit Kg loss. These results indicate that while kinin released via the action of epinephrine-activated basophils and/or mast cells, could play a major role in REPE, the same cannot be suggested for prostaglandins, whose eventual formation in the epinephrine-treated lung, would be expected to be fully prevented by Indomethacin. Since Aspirin, known as a less effective inhibitor of PG formation than Indomethacin, was nevertheless a highly effective inhibitor of both REPE and Kg consumption, an explanation for the action of Aspirin not involving the lung PG system, is clearly called for.
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PMID:Role in kinin in rat epinephrine pulmonary edema (REPE). 243 18

The amiloride-sensitive epithelial Na(+) channel (ENaC) is essential for fluid clearance from the airways. An experimental animal model with a reduced expression of ENaC, the alpha-ENaC transgenic rescue mouse, is prone to develop edema under hypoxia exposure. This strongly suggests an involvement of ENaC in the pathogenesis of pulmonary edema. To investigate the pathogenesis of this type of edema, primary cultures of tracheal cells from these mice were studied in vitro. An ~60% reduction in baseline amiloride-sensitive Na(+) transport was observed, but the pharmacological characteristics and physiological regulation of the channel were similar to those observed in cells from wild-type mice. Aprotinin, an inhibitor of serine proteases, blocked 50-60% of the basal transepithelial current, hypoxia induced downregulation of Na(+) transport, and beta-adrenergic stimulation was effective to stimulate Na(+) transport after the hypoxia-induced decrease. When downregulation of ENaC activity (such as observed under hypoxia) is added to a low "constitutive" ENaC expression, the resulting reduced Na(+) transport rate may be insufficient for airway fluid clearance and favor pulmonary edema.
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PMID:Selected contribution: limiting Na(+) transport rate in airway epithelia from alpha-ENaC transgenic mice: a model for pulmonary edema. 1238 79