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)

We earlier showed that the ionotropic glutamate receptor agonist N-methyl D-aspartate (NMDA) induces excitotoxic pulmonary edema, and that endogenous activation of NMDA receptors (NMDAR) could mediate lung injury caused by oxidative stress. In this study, we searched for evidence of NMDAR expression in the rat lung and in the alveolar macrophage (AM) cell line NR8383, and for possible regulation of receptor expression by NMDA. The presence of mRNA for NMDAR 1 and the four known NMDAR 2 subtypes (A, B, C, and D) was examined by reverse transcriptase-polymerase chain reaction using isoform-specific primers. NMDAR 1 was expressed in all lung regions examined (peripheral, midlung, and mainstem), as well as in trachea and the AMs. Expression of NMDAR 2A and 2B subtypes was not detected, whereas NMDAR 2C was present only in peripheral and mid-lung samples. NMDAR 2D was the dominant subtype expressed in the peripheral, gas-exchange zone of lung and in alveolar macrophages, and this expression was upregulated in lungs treated with NMDA. Western blot confirmed the presence of NMDAR 1 protein in all lung regions and in AMs. These findings provide a molecular-biological basis for the excitotoxic actions of glutamate in rat lungs and airways, and raise the question of a possible physiologic role for NMDAR in lung and airway function.
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PMID:Ionotropic glutamate receptors in lungs and airways: molecular basis for glutamate toxicity. 1285 8

The present study was undertaken to evaluate possible roles of L-glutamate ionotropic receptors in neurogenic pulmonary edema. Perfusion of L-glutamate into the fourth ventricles of rats increased nitric oxide (NO) signals in the efflux solution concentration-dependently, significantly reducing both the occurrence and severity of neurogenic pulmonary edema. This effect was completely reversed by prior intracisternal injection of an NO synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), or an N-methyl-D-aspartate (NMDA) receptor antagonist, dizocilpine maleate (MK-801), and partially by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a 2-amino-3-hydroxy-5-methyl-4-isoxazol propionic acid (AMPA)/kainic acid receptor antagonist. Administration of MK-801 or CNQX alone, without L-glutamate, almost completely prevented neurogenic pulmonary edema development. These results suggest that endogenous L-glutamate may facilitate underlining disease process, whereas L-glutamate exogenously applied into the fourth ventricle may have an inhibitory action via release of NO, through ionotropic receptors.
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PMID:A role for L-glutamate ionotropic receptors in the development of rat neurogenic pulmonary edema. 1538 Oct 47

A two-day-old, full-term male infant was admitted to the neonatal intensive care unit with heart failure. He was found to be non-dysmorphic, with no clinical evidence of sepsis. Physical examination was significant for hepatomegaly, active precordium, pansystolic murmur and hypotension requiring ionotropic support. A cranial bruit was detected on auscultation. Chest radiography revealed cardiomegaly and pulmonary oedema due to heart failure. Electrocardiogram and two-dimensional echocardiography were normal. Magnetic resonance imaging of the brain showed a large vein of Galen malformation, extensive cerebral ischaemia and multiple cerebral infarcts. This case illustrates the importance of auscultation of the cranium to rule out vein of Galen malformation, a potential cause of high-output cardiac failure in neonates in the absence of other common causes of heart failure.
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PMID:Clinics in diagnostic imaging (132). Vein of Galen malformation. 2114 Jan 18