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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the mechanism of pulmonary edema after seawater drowning (PE-SWD), the indexes of blood-gas and acid-base in rabbits artery blood were measured by the blood-gas analyser. The activity of Na(+)-K(+)-ATPase, cytochrome oxidase(CYTO) and alkaline phospharase(ALP) in the lungs were measured and analysed by computer image system. C-fos mRNA and Fos protein in the lungs were respectively determined by situ hybrioization and immunohisto chemical techniques. The distribution of phospholipid and Ca2+ of rabbits lungs was quantitatively analysed by ultrastructural location method. The results showed that, five parameters of PaO2, oxygen saturation(SaO2), pH, actual bicarbonite(AB) and base excess(BE) and the activity of Na(+)-K(+)-ATPase and CYTO decreased remarkably in PE-SWD. Both c-fos mRNA and Fos protein expression in pulmonary epithelial cells in PE-SWD were significantly elevated compared with the normal controls(P < 0.01). The phospholipids products in the pulmonary alveolar type II epithelial cells were decreased, however, the Ca2+ precipitate pellets inside the lung capillary endothelial cells and the pulmonary alveolar type I and II epithelial cells increased obviously. The arthors suggest that the injuny action of the seawater, hypoxia and metabolic acidosis may be the mian three mechanisms of the pulmonary edema induced seawater drowning. The lowering activity of Na(+)-K(+)-ATPase and CYTO in the lungs and calcium overload in the cells are not only evil consequence resulted from above three factors, but also the importent causes leading to the worse of PE-SWD. The transmiting line of Ca(2+)-fos may be also a key link to bring about the worse of PE-SWD.
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PMID:[Study on the mechanism of pulmonary edema after seawater drowning in rabbit]. 1255 79

The standard treatment for acute heart failure (synonymous with pulmonary edema) is an upright posture, oxygen, morphine (often accompanied by an antiemetic), and intravenous diuretics. This treatment has remained unchanged for many years, and the precise mechanism by which each of these methods alleviates symptoms in patients is unclear. Nitrates, oral or intravenous, are also used with benefit, and have some hemodynamic advantages over intravenous diuretics. Recently, three new forms of treatment have been investigated. The use of milrinone, a phosphodiesterase inhibitor, for exacerbation of heart failure in patients with a background of chronic heart failure was not advantageous. The trials of levosimendan, a calcium sensitizer, in patients with pulmonary edema hinted at benefit. Nesiritide, a formulation of brain natriuretic peptide, does bring about hemodynamic improvement in acute heart failure, and is at least as effective as nitroglycerin, easier to prescribe, but prone to cause hypotension. These are small but important advances that increase our knowledge of the pathophysiology of acute heart failure, and also provide an indication of which drugs are preferable for the treatment of this distressing condition.
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PMID:New therapies for the management of acute heart failure. 1269 42

Conversion of atrial fibrillation and flutter to sinus rhythm results in a transient mechanical dysfunction of atrium and atrial appendage, termed atrial stunning. Atrial stunning has been reported with all modes of conversion of atrial fibrillation and flutter to sinus rhythm including both transthoracic and low energy internal electrical, pharmacological, and spontaneous cardioversion, and conversion by overdrive pacing and by radiofrequency ablation. Atrial stunning is a function of the underlying arrhythmia becoming apparent at the restoration of sinus rhythm, not the function of the mode of conversion, and does not develop after the unsuccessful attempts of cardioversion or the delivery of electric current to the heart during rhythms other than atrial fibrillation or flutter. Tachycardia-induced atrial cardiomyopathy, cytosolic calcium accumulation, and atrial hibernation are the suggested mechanisms of atrial stunning. Atrial stunning is at maximum immediately after cardioversion and improves progressively with a complete resolution within a few minutes to 4-6 weeks depending on the duration of the preceding atrial fibrillation, atrial size, and structural heart disease. Atrial stunning causes postcardioversion thromboembolism despite restoration of sinus rhythm. Duration of anticoagulation therapy after successful cardioversion should depend on the duration of atrial stunning. Lack of improvement in cardiac output and functional recovery of patients immediately after cardioversion is attributed to the atrial stunning. Verapamil, acetylstrophenathidine, isoproterenol, and dofetilide have been reported to protect from atrial stunning in animal and small human studies. Right atrium stunning is less marked and improves earlier than that of left atrium, resulting in a differential atrial stunning explaining the rare occurrence of pulmonary edema after cardioversion.
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PMID:Atrial stunning: basics and clinical considerations. 1465 42

Severe ethylene glycol toxicity can cause profound morbidity and is almost universally fatal if untreated. Central nervous system depression with intoxication, pulmonary edema, and acute oliguric renal failure with crystalluria are among the most commonly encountered complications of ingestion. The previously reported gastrointestinal side effects of ethylene glycol toxicity are mostly nonspecific, including nausea, abdominal pain, and cramping. In addition, hepatic damage due to calcium oxalate deposition has been reported. We describe a patient who developed acute colonic ischemia following ethylene glycol intoxication. Three months after the ingestion, the patient presented with severe abdominal pain secondary to a colonic stricture and perforation, necessitating emergent colectomy. Histology of the resected colon revealed polarizable polyhedral crystals suggestive of oxalate deposition. The pathophysiology underlying ethylene glycol intoxication, treatment strategies, and gastrointestinal toxicity are discussed.
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PMID:Ethylene glycol toxicity associated with ischemia, perforation, and colonic oxalate crystal deposition. 1510 May 24

Chronic hypoxia results in both structural changes in the pulmonary artery and a sustained increase in pulmonary vascular tone. This study investigated the effects of subacute moderate hypoxia on expression and function of potassium (K+) channels in rat pulmonary artery myocytes (PASMCs). The rats were kept at 0.67 atmospheres for 6, 12, or 24 h. We found that the expression of mRNA for voltage-activated K+ channels (Kv)1.2, Kv1.5, and Kv2.1 is reduced after less than 24 h of this moderate hypoxia. K+ current (Ik) is significantly inhibited in PASMCs from rats hypoxic for 24 h, resting membrane potential is depolarized and cytosolic [Ca2+] is increased in these cells. In addition, antibodies to Kv1.2, Kv1.5, and Kv2.1 inhibit Ik, cause membrane depolarization and attenuate both hypoxia- and 4-AP-induced elevation in [Ca2+]i in PASMCs from normoxic rats but not from 24 h hypoxic rats. Subacute hypoxia does not completely remove the mRNA for Kv1.2, Kv1.5, and Kv2.1, but antibodies against these channels no longer alter Ik or cytosolic calcium, suggesting that subacute hypoxia may inactivate the channels as well as reduce expression. As the expression of mRNA for Kv1.2, Kv1.5, and Kv2.1 is sensitive to subacute hypoxia and decreased expression/function of these channels has physiologic effects on membrane potential and cytosolic calcium, it seems likely that these Kv channels may also be involved in the mechanism of high-altitude pulmonary edema and possibly in the signaling of chronic hypoxic pulmonary hypertension.
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PMID:Subacute hypoxia decreases voltage-activated potassium channel expression and function in pulmonary artery myocytes. 1515 18

Humans encounter hypoxia throughout their lives. This occurs by destiny in utero, through disease, and by desire, in our quest for altitude. Hypoxic pulmonary vasoconstriction (HPV) is a widely conserved, homeostatic, vasomotor response of resistance pulmonary arteries to alveolar hypoxia. HPV mediates ventilation-perfusion matching and, by reducing shunt fraction, optimizes systemic Po(2). HPV is intrinsic to the lung, and, although modulated by the endothelium, the core mechanism is in the smooth muscle cell (SMC). The Redox Theory for the mechanism of HPV proposes the coordinated action of a redox sensor (the proximal mitochondrial electron transport chain) that generates a diffusible mediator [a reactive O(2) species (ROS)] that regulates an effector protein [voltage-gated potassium (K(v)) and calcium channels]. A similar mechanism for regulating O(2) uptake/distribution is partially recapitulated in simpler organisms and in the other specialized mammalian O(2)-sensitive tissues, including the carotid body and ductus arteriosus. Inhibition of O(2)-sensitive K(v) channels, particularly K(v)1.5 and K(v)2.1, depolarizes pulmonary artery SMCs, activating voltage-gated Ca(2+) channels and causing Ca(2+) influx and vasoconstriction. Downstream of this pathway, there is important regulation of the contractile apparatus' sensitivity to calcium by rho kinase. Controversy remains as to whether hypoxia decreases or increases ROS and which electron transport chain complex generates the ROS (I and/or III). Possible roles for cyclic adenosine diphosphate ribose and an unidentified endothelial constricting factor are also proposed by some groups. Modulation of HPV has therapeutic relevance to cor pulmonale, high-altitude pulmonary edema, and sleep apnea. HPV is clinically exploited in single-lung anesthesia, and its mechanisms intersect with those of pulmonary arterial hypertension.
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PMID:Hypoxic pulmonary vasoconstriction. 1559 9

Nifedipine (Adalat) is marketed as an anti-hypertensive agent. Nifedipine inhibits voltage-dependent L-type calcium channels, which leads to vascular (and other) smooth muscle relaxation and negative inotropic and chronotropic effects on the heart. Vasodilation, followed by a baroreceptor-mediated increase in sympathetic tone then results in indirect cardiostimulation. Nifedipine was introduced as a tocolytic agent at a time when beta-agonists and magnesium sulphate dominated the arena for the prevention of preterm birth. The oral administration route, the availability of immediate and slow-release preparations, the low incidence of (mild) side effects, and its limited costs explain the attraction to this medication from the obstetric field and its rapid and widespread distribution. Currently, over 40 studies have been published on nifedipine's tocolytic effectiveness, including seven meta-analyses. The quality of the studies suffers particularly from performance bias because the majority of them failed to ensure adequate blinding to treatment both for providers and patients. Concerns about other methodological flaws include measurements, outcome assessment and attrition bias. In particular, the safety aspects of nifedipine for tocolysis have been under-assessed. Conclusions from the meta-analyses, favouring the use of nifedipine as a tocolytic agent, are not supported by close examination of the data. The tocolytic effectiveness and "safety" of nifedipine has been studied primarily in normal pregnancies. Based on its pharmacological properties, one should be cautious to administer nifedipine when the maternal cardiovascular condition is compromised, such as with intrauterine infection, twin pregnancy, maternal hypertension, cardiac disease, etc. Life-threatening pulmonary oedema and/or cardiac failure are definite risks and have been reported. Under such circumstances, the baroreceptor-mediated increase in sympathetic tone may not balance the cardiac-depressant activity of nifedipine.
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PMID:Nifedipine trials: effectiveness and safety aspects. 1571 1

Angiogenesis inhibitors, such as TNP-470 and the nontoxic HPMA copolymer-TNP-470 (caplostatin), are emerging as a class of anticancer drugs. We report that TNP-470 and caplostatin inhibit vascular hyperpermeability of tumor blood vessels as well as that induced in mouse skin by different mediators. Treatment with TNP-470 or angiostatin for 3 days was sufficient to reduce permeability of tumor blood vessels, delayed-type hypersensitivity, and pulmonary edema induced by IL-2. TNP-470 also inhibited VPF/VEGF-induced phosphorylation of VEGFR-2, calcium influx, and RhoA activation in endothelial cells. These results identify an activity of TNP-470, that of inhibiting vessel hyperpermeability. This activity likely contributes to TNP-470's antiangiogenic effect and suggests that caplostatin can be used in the treatment of cancer and inflammation.
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PMID:Inhibition of vessel permeability by TNP-470 and its polymer conjugate, caplostatin. 1576 63

Acetazolamide and other related carbonic anhydrase (CA) inhibitors have had a long history of effectiveness in prevention and treatment of acute mountain sickness (AMS) and remain the standard of care for this indication. Despite many decades of CA inhibitor use for AMS, the possibility has never been seriously entertained that these drugs might also afford protection against high altitude pulmonary edema (HAPE). In this paper, I will present our evidence and supporting data of others, that acetazolamide has inhibitory effects on the hypoxic response of the pulmonary circulation that may be useful in HAPE. Data from pulmonary artery smooth muscle cells, isolated perfused lungs, and live unanethetized animals all point to a potent reduction in hypoxic pulmonary vasoconstriction (HPV) by acetazolamide that may have clinical utility in HAPE and possibly other pulmonary hypertensive disorders. Astonishingly, the efficacy of acetazolamide as a HPV inhibitor does not appear to be related to carbonic anhydrase inhibition, since other potent CA inhibitors have no effect on HPV either in the conscious dog or on hypoxic calcium (Ca(2+)) signalling in rat pulmonary artery smooth muscle cells, despite enzyme presence in these cells. Although we have not yet determined the mechanism of action for acetazolamide in HPV, we have ruled out actions on membrane L-type Ca(2+) channels, normoxic and hypoxic membrane potential and rho-kinase activation. Based upon these negative findings in isolated pulmonary artery smooth muscle cells and preliminary data in Ca(2+) free media we propose that acetazolamide may act at the level of Ca(2+) release from the sarcoplasmic reticulum, a process which initiates and amplifies cell membrane Ca(2+) channel opening. In further work, we have developed and will use a methylated analog of acetazolamide to yield a molecule lacking CA inhibiting activity, but which in most other respects (size, pK(a), heterocyclic ring structure, electrostatic charge distribution) is equivalent to acetazolamide.
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PMID:Carbonic anhydrase inhibitors and hypoxic pulmonary vasoconstriction. 1637 58

Preterm labour and delivery remains a major cause of perinatal morbidity and mortality. Numerous drugs and interventions have been used to prevent and inhibit preterm labour but none have been found to be completely effective with the choice being further limited by troublesome side effects. This study compares in a prospective and randomised design the efficacy and safety of the calcium antagonist Nifedipine with the beta mimetic Isoxsuprine. 81.25% of patients receiving Nifedipine and 70% of those receiving Isoxsuprine achieved successful tocolysis. The mean prolongation of pregnancy with Nifedipine was 25+/-19.85 days and with Isoxsuprine it was 19.18+/-17.82 days. Maternal side effects were similar in both groups with hypotension and tachycardia being the commonest. Discontinuation rates were also similar with pulmonary oedema and severe hypotension being the reasons for foregoing tocolysis. It can be concluded that Nifedipine is a safe and effective alternative to Isoxsuprine for suppressing preterm labour.
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PMID:A comparative study between nifedipine and isoxsuprine in the suppression of preterm labour. 1638 3


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