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)

Isoproterenol inhalation increases the pulmonary edema induced in rats by phenylthiourea. Propranolol decreases this response while phenoxybenzamine has no effect upon it. It is proposed that the observed increase in toxicity is related to the beta-adrenergic effects of the isoproterenol and that the specific mechanism responsible might be an increase in pulmonary capillary hydrostatic pressure which is secondary to an increase in pulmonary blood flow.
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PMID:The action of isoproterenol on phenylthiourea induced pulmonary edema. 118 84

Intravenous Paf-acether (Paf, 15-80 micrograms kg-1) killed conscious Swiss mice in a dose-dependent manner, without causing platelet aggregation in the lung microvasculature, or pulmonary oedema. Propranolol (0.01-10 mg kg-1, i.p.) potentiated the effects of an LD20 of Paf dose-dependently, while the beta 1-adrenoceptor selective antagonist, metoprolol, was three orders of magnitude less potent in this respect. Salbutamol (1 mg kg-1, i.p.) provided complete protection against an LD80 of Paf. High doses of indomethacin, aspirin, benoxaprofen and FPL 55712 given i.p. failed to inhibit the effects of an LD80 of Paf, while BW 755C (50-100 mg kg-1) exerted a dose-dependent protection and benzydamine (50 mg kg-1) and nordihydroguaiaretic acid (200 mg kg-1) were partially active. Dexamethasone (1-5 mg kg-1, s.c.) exerted a dose-dependent protection, when administered at least 4 h before Paf. In mice anaesthetized with urethane, Paf (1-30 micrograms kg-1) produced hypotension which was not clearly dose-related. The effects of the highest dose were also tested on the resistance of the lungs to inflation and found to produce bronchoconstriction. It may be concluded that pharmacological manipulation of beta 2-adrenoceptors modulates Paf-induced death in mice, while arachidonate metabolites of the cyclo-oxygenase pathway and peptidoleukotrienes do not appear to be involved. However, lipoxygenase products, distinct from peptidoleukotrienes, may play a role in this phenomenon. It is suggested that bronchoconstriction, probably associated with cardiovascular effects, is a major determinant of the acute toxicity of Paf in mice.
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PMID:Paf-acether-induced death in mice: involvement of arachidonate metabolites and beta-adrenoceptors. 288 Jun 24

(+) Propranolol is considered to prevent adrenaline-induced pulmonary edema (A.P.E.) due to the beta-adrenoceptor blockade. However, local anaesthetics also are known to prevent pulmonary edema. To assess the role of beta-adrenergic blockade in A.P.E., the effect of a beta 1-blocker possessing local anaesthetic action (+/- Metaprolol) and a beta 1-blocker possessing no local anaesthetic action (+/- practolol) was studied along with propranolol derivatives. The study revealed that (+), (-), (+/-) propranolol and (+/-) metaprolol completely prevented A.P.E. whereas (+/-) practolol did not. This shows that local anaesthetic action but not the-beta adrenergic blockade may be responsible for prevention of A.P.E.
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PMID:Effect of some beta-adrenoceptor blockers and of (+) propranolol on adrenaline-induced pulmonary edema in mice. 613 33

Hemodynamic effects of combined nitroglycerin and propranolol administration were investigated in patients with acute myocardial infarction. After nitroglycerin infusion decreased the mean arterial pressure by 20 mm Hg for one hour, nitroglycerin was continued, and patients were given 0.033 mg/kg of propranolol every five minutes for a total dose of 0.1 mg/kg, or until there was a decrease in heart rate to less than 60 beats/min, an increase in left ventricular filling pressure (LVFP) to greater than 15 mm Hg, or a decrease in systolic arterial pressure to less than 85 mm Hg. Seven of eight patients with initial LVFP less than or equal to 15 mm Hg and three of seven with initial LVFP greater than 15 mm Hg received 0.1 mg/kg of propranolol. Propranolol significantly decreased heart rate. Although pressure time/minute decreased significantly, the magnitude of its decrease was small, suggesting only a minimal effect on myocardial oxygen demands. The LVFP increased after giving propranolol but remained less than the control value. Simultaneous administration of nitroglycerin likely prevented further increases, since LVFP increased after cessation of nitroglycerin infusion, and three patients subsequently had pulmonary edema. Propranolol administration resulted in a significant increase in peripheral vascular resistance and a decrease in cardiac output.
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PMID:Combined administration of nitroglycerin and propranolol to patients with acute myocardial infarction. 679 82

During hydrostatic pulmonary edema, active Na(+) transport and alveolar fluid reabsorption are decreased. Dopamine (DA) and isoproterenol (ISO) have been shown to increase active Na(+) transport in rat lungs by upregulating Na(+)-K(+)-ATPase in the alveolar epithelium. We studied the effects of DA and ISO in isolated rat lungs with increased left atrial pressure (Pla = 15 cmH(2)O) compared with control rats with normal Pla (Pla = 0). Alveolar fluid reabsorption decreased from control value of 0.51 +/- 0.02 to 0.27 +/- 0.02 ml/h when Pla was increased to 15 cmH(2)O (P < 0.001). DA and ISO increased the alveolar fluid reabsorption back to control levels. Treatment with the D(1) antagonist SCH-23390 inhibited the stimulatory effects of DA (0.30 +/- 0.02 ml/h), whereas fenoldopam, a specific D(1)-receptor agonist, increased alveolar fluid reabsorption in rats exposed to Pla of 15 cmH(2)O (0.47 +/- 0.04 ml/h). Propranolol, a beta-adrenergic-receptor antagonist, blocked the stimulatory effects of ISO; however, it did not affect alveolar fluid reabsorption in control or DA-treated rats. Amiloride (a Na(+) channel blocker) and ouabain (a Na(+)-K(+)-ATPase inhibitor), either alone or together, inhibited the stimulatory effects of DA. Colchicine, which disrupts the cellular microtubular transport of ion-transporting proteins to the plasma membrane, inhibited the stimulatory effects of DA, whereas the isomer beta-lumicolchicine did not block the stimulatory effects of DA. These data suggest that DA and ISO increase alveolar fluid reabsorption in a model of increased Pla by regulating active Na(+) transport in rat alveolar epithelium. The effects of DA and ISO are mediated by the activation of dopaminergic D(1) receptors and the beta-adrenergic receptors, respectively.
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PMID:Catecholamines increase lung edema clearance in rats with increased left atrial pressure. 1118 24