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)

This review describes the ionic heterogeneity manifest in the pulmonary circulation, particularly as it pertains to hypoxic pulmonary vasoconstriction (HPV) and pulmonary arterial hypertension (PAH). Heterogeneity in potassium (K(+)) channels, key regulators of vascular tone, cell proliferation, and apoptosis rates, contribute to the diverse response of vascular segments to hypoxia and to the localization of pathological changes in PAH. Pulmonary artery (PA) and pulmonary vein (PV) smooth muscle cells (SMC) express several K(+) channel families, including calcium-sensitive (KCa), voltage-gated (K(v)), inward rectifier (Kir), and 2-pore channels. Diversity is created by heterogeneous occurrence of alternatively spliced, mRNA species, assembly of heterotetrameric channels from diverse alpha-subunits, and association of channels with regulatory beta-subunits. Local heterogeneity in transcription factor activity may underlie differences in channel expression. Enrichment of resistance PASMCs with O(2)-sensitive K(+) channels, such as K(v)1.5, partially explains the greater HPV in resistance versus conduit PAs. In addition, resistance PAs are unique in having mitochondria which dynamically alter production of reactive O(2) species (ROS) in proportion to PO(2), thereby regulating K(+) channel activity and controlling expression through transcription factors, such as HIF-1alpha. In intraparenchymal PVs, a coaxial layer of cardiomyocytes encompasses a media of typical vascular SMCs. PV cardiomyocytes have rhythmic contraction and their Kir-enriched channels may be relevant to genesis of atrial arrhythmias and pulmonary edema. K(v) channel expression is decreased in PAH, leading to elevations of cytosolic K(+) and Ca(2+) that impair apoptosis and increase proliferation. Understanding ionic diversity may allow development of therapies that locally increase K(+) channel current and expression to treat PHT.
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PMID:Potassium channel diversity in the pulmonary arteries and pulmonary veins: implications for regulation of the pulmonary vasculature in health and during pulmonary hypertension. 1758 56

A stay at high altitude exposes an individual to various environmental changes (cold, exercise, isolation) but the most stressful for the body is hypoxia. However, the cardiovascular system yields some efficient mechanisms of acclimatization to oxygen lack. Hypoxia activates the adrenergic system and induces a tachycardia that decreases during a prolonged stay at altitude. The desensitization of the adrenergic system leads to a decrease in maximal heart rate and a protection of the myocardium against an energy disequilibrium that could be potentially harmful for the heart. Hypoxia induces a peripheral vasodilation and a pulmonary vasoconstriction, leading to few changes in systemic blood pressure and an increase in pulmonary blood pressure (PHT) that can contribute to a high altitude pulmonary edema. Advice to a cardiac patient who plans to go to high altitude should take into account that all diseases aggravated by increased adrenergic activity or associated with a PHT or a hypoxemia (right-to-left shunt) will be aggravated at high altitude. As altitude increases, a patient with a coronary disease will present an ischemic threshold for a lower power output during an EKG exercise test. The only test allowing predicting the tolerance to high altitude is the hypoxia exercise test realized at 30% of maxVO(2)and at an equivalent altitude of 4,800m.
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PMID:[Altitude and the cardiovascular system]. 2242