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)

Beta-adrenergic receptors (betaAR) regulate active Na+ transport in the alveolar epithelium and accelerate clearance of excess airspace fluid. Accumulating data indicates that the cystic fibrosis transmembrane conductance regulator (CFTR) is important for upregulation of the active ion transport that is needed to maintain alveolar fluid homeostasis during pulmonary edema. We hypothesized that betaAR regulation of alveolar active transport may be mediated via a CFTR dependent pathway. To test this hypothesis we used a recombinant adenovirus that expresses a human CFTR cDNA (adCFTR) to increase CFTR function in the alveolar epithelium of normal rats and mice. Alveolar fluid clearance (AFC), an index of alveolar active Na+ transport, was 92% greater in CFTR overexpressing lungs than controls. Addition of the Cl- channel blockers NPPB, glibenclamide, or bumetanide and experiments using Cl- free alveolar instillate solutions indicate that the accelerated AFC in this model is due to increased Cl- channel function. Conversely, CFTR overexpression in mice with no beta1- or beta2-adrenergic receptors had no effect on AFC. Overexpression of a human beta2AR in the alveolar epithelium significantly increased AFC in normal mice but had no effect in mice with a non-functional human CFTR gene (Deltaphi508 mutation). These studies indicate that upregulation of alveolar CFTR function speeds clearance of excess fluid from the airspace and that CFTRs effect on active Na+ transport requires the betaAR. These studies reveal a previously undetected interdependency between CFTR and betaAR that is essential for upregulation of active Na+ transport and fluid clearance in the alveolus.
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PMID:Interdependency of beta-adrenergic receptors and CFTR in regulation of alveolar active Na+ transport. 1580 12

For expansion of the extravascular space, secretion of antidiuretic hormone and increment of vascular permeability, a large quantity of non-functional extracellular fluid is accumulated in an extravascular space from all over the operation. Extracellular fluid returns from an extravascular space to blood vessels in refilling stage, and decrement of a pulmonary vascular bed after pneumoresection make it easy to cause pulmonary edema and tachyarrhythmia. Therefore volume of postoperative infusion is apt to be limited after pneumoresection. However, the fluid management that extremely imbalanced in dry side increases the risk of arrhythmia, myocardial infarction and cerebral infarction. It is important to perform reasonable fluid therapy without excess and deficiency postoperatively while observing amount of urine, specific gravity of urine, heart rate, blood pressure, volume of chest drainage and central venous pressure. We have few opportunity to consider about nutritional management after pneumoresection so that ingestion is started for an early postoperative period. But, the grave case that ingestion cannot start for an early postoperative period should start total parenteral nutrition or enteral feeding. In that case, the enteral feeding which is more physiological than intravenous nutrition is recommended.
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PMID:[Fluid and nutritional management after pneumoresection]. 2071 9