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)

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

In order to assess the role of the kallikreinkinin (k-k) system in the pathogenesis of pulmonary oedema, we studied the contact phase factors of blood coagulation, as well as the haemodynamics and blood gas changes in 34 patients with pulmonary oedema, 23 of them with Adult Respiratory Distress Syndrome (ARDS) and 11 with cardiogenic pulmonary oedema (CPO). We have verified significant differences in the haemodynamic pattern and blood gases between the two groups of patients, which corroborate the previously established differences between both types of pulmonary oedema. Our results reveal k-k system activation in ARDS patients, with a significant fall in factor XII (p less than 0.05), prekallikrein (p less than 0.01), alpha-2-macroglobulin (p less than 0.01) and high molecular - weight kininogens (p less than 0.005), with a rise in C1-esterase inhibitor (p less than 0.001) in comparison with patients with CPO. All of the CPO patients had normal prekallikrein levels, whereas 15 out 23 ARDS cases (65%) had decreased prekallikrein values. Our results suggest that the k-k system activation could play a role in the pathogenesis of ARDS. Estimation of prekallikrein levels may be helpful in the differential diagnosis of ARDS.
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PMID:Contact phase of blood coagulation in cardiogenic pulmonary oedema (CPO) and adult respiratory distress syndrome (ARDS). 271 14

Adoptive immunotherapy, the administration of interleukin-2 (IL-2) and interleukin-2 activated cells, leads to tumor regression in some patients with advanced cancer. Although this new therapeutic modality offers hope for the future, at present, a multitude of toxicities limit the total dose and duration of therapy. Among the toxic side effects a purported third space or vascular leak syndrome is the most serious. In this review, we detail the evidence for a third space syndrome (peripheral edema, ascites, oliguria, elevated serum creatinine levels) and cardiopulmonary dysfunction (hypotension, respiratory distress, pulmonary edema, hypoxemia) with adoptive immunotherapy in human and animal studies. We conclude that IL-2 administration is associated with increased pulmonary microvascular permeability, infiltration of the lung parenchyma with large esterase negative lymphoid cells, hypoxemia, systemic hypotension, positive fluid balance and, in animals, transient pulmonary hypertension. These abnormalities do not seem to be caused by IL-2 directly; the causes may be mediated by IL-2 activated lymphocytes or other IL-2 activated cellular mediators.
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PMID:Cardiopulmonary toxicity of adoptive immunotherapy. 306 15

Organophosphorus chemical warfare agents (nerve agents) are to be feared in military operations as well as in terrorist attacks. Among them, VX (O-ethyl-S-[2-(diisopropylamino)ethyl] methylphosphonothioate) is a low volatility liquid that represents a percutaneous as well as an inhalation hazard if aerosolized. It is a potent irreversible cholinesterase (ChE) inhibitor that causes severe signs and symptoms, including respiratory dysfunction that stems from different mechanisms. VX-induced pulmonary oedema was previously reported in dogs but mechanisms involved are not well understood, and its clinical significance remains to be assessed. An experimental model was thus developed to study VX-induced cardiovascular changes and pulmonary oedema in isoflurane-anaesthetized swine. In the course of this study, we observed a fast and unexpected rebound of plasma ChE activity following inhibition provoked by the intravenous injection of 6 and 12 microg kg(-1) of VX. In whole blood ChE activity, the rebound could stay unnoticed. Further investigations showed that the rebound of plasma esterase activity was neither related to spontaneous reactivation of ChE nor to VX-induced increase in paraoxonase/carboxylesterase activities. A bias in Ellman assay, haemoconcentration or severe liver cytolysis were also ruled out. All in all, these results suggest that the rebound was likely due to the release of butyrylcholinesterase into the blood stream from ChE producing organs. Nature of the organ(s) and mechanisms involved in enzyme release will need further investigations as it may represent a mechanism of defence, i.e. VX scavenging, that could advantageously be exploited.
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PMID:An unexpected plasma cholinesterase activity rebound after challenge with a high dose of the nerve agent VX. 1845 Mar 56