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

Lipid mediators of inflammation cause pulmonary edema, yet it is unclear to what degree hemodynamic alterations or increased vascular permeability contribute to lung edema formation. The isolated rat lung preparation was used to examine the effect of leukotriene C4 (LTC4) and platelet-activating factor (PAF) on pulmonary arterial pressure (Ppa), lung microvascular pressure (Pmv), lung wet-to-dry weight ratio, and the 125I-albumin escape index. We first defined the response of the isolated rat lung perfused with protein-free salt solution to hydrodynamic stress by raising the lung outflow pressure. Sustained elevation of the lung outflow pressure less than 5.5 cmH2O (4.01 mmHg) caused a negligible increase in Ppa and wet-to-dry lung weight ratio. Elevation of outflow pressures greater than 7.5 cmH2O (5.4 mmHg) increased the vascular albumin escape index more than the lung wet-to-dry weight ratio. Dibutyryl adenosine 3',5'-cyclic monophosphate (db-cAMP) inhibited the increase in albumin escape index because of increased lung outflow pressure, suggesting perhaps a pressure-independent microvascular membrane effect of db-cAMP. Both LTC4 (2-micrograms bolus) and PAF (2-2,000 ng/ml perfusate) increased the albumin escape index in association with increases in Ppa and Pmv. Because the increased albumin escape index after LTC4 or PAF injection was largely accounted for by the increased vascular pressures and because db-cAMP and papaverine inhibited the rise in vascular pressures and in the albumin escape index, we conclude that vasoconstriction is an important contributor to LTC4- and PAF-induced edema formation in rat lungs.
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PMID:Importance of vasoconstriction in lipid mediator-induced pulmonary edema. 274 28

Repeated lung inflation with very high tidal volumes (VT) is associated with the production of permeability pulmonary edema in animal models using previously normal lungs. We studied the effect of mechanical ventilation, at VT values approaching those used clinically, on lung weight gain (lung water) in salt-perfused rabbit lungs diffusely injured by the administration of oleic acid. Lungs ventilated at a VT of 18 ml/kg gained significantly more weight at 30 through 90 min than did lungs ventilated at 6 ml/kg. These differences in weight gain were not associated with differences in the evolution of thromboxane B2 in the perfusate. The impact of VT on lung water and outcome in patients with lung injury deserves further study.
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PMID:High tidal volume ventilation produces increased lung water in oleic acid-injured rabbit lungs. 276 64

Patients with heart failure should stop smoking, maintain an optimal weight and limit their intake of salt. Alcohol abuse should be avoided. The detection and early treatment of hypertension appears to have had a major impact in preventing heart failure. Diuretics revolutionized the treatment of congestive heart failure and their proper and appropriate use can alleviate peripheral and pulmonary oedema. Diuretics should not be overused and care should be taken to avoid hypokalaemia. Controversy surrounds the use of digoxin in patients in sinus rhythm; the drug should be used in patients in atrial fibrillation. The use of an inotropic drug may be harmful in the presence of coronary artery disease. A reduction in the current use of digoxin might be of benefit to many patients with heart failure. When the drug is prescribed it should be used in a therapeutic and not homeopathic dose. Recent interest has been directed toward the use of vasodilators and the angiotensin-converting enzyme inhibitors in patients with heart failure. In my opinion, these drugs should be used after patients have been treated with thiazide and loop diuretics. Vasodilators are particularly beneficial in acute heart failure or in patients with chronic heart failure when the symptoms are related to fluid overload and volume expansion. The cause of symptoms in patients with chronic heart failure optimally treated with diuretics is controversial. Shortness of breath may not be simply related to the left atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing ideas in the treatment of heart failure--an overview. 330 Sep 78

During a 3-year period (1984 through 1987), 40 patients with smoke inhalation, cutaneous burns, or a combination of both injuries were studied. Injuries were assigned to the three categories on the basis of bronchoscopic findings and clinical history. Eleven patients had simultaneously sustained a common smoke-inhalation injury without burns while trapped in a burning ship; twelve patients had massive cutaneous burns over 50% of the total body surface area (TBSA); and seventeen patients had cutaneous burns over more than 30% of the TBSA and inhalation injury. Colloid oncotic pressure was maintained with salt-poor albumin infusion. Central venous pressure, arterial saturation, inspired oxygen, arterial pressure, and urine output were continuously monitored. Extravascular lung water (EVLW) and cardiac output were measured by the double indicator (thermal dye dilution) technique. EVLW remained normal throughout the study period in the group of patients with burns alone. In the first 24 hours after injury, EVLW increased in both groups with smoke injury and remained elevated for more than 48 hours after injury in patients with smoke injury only. The group with both smoke-inhalation and burn injuries showed an early increase in EVLW, which returned to normal by 28 hours after injury and which remained normal until 5 days after injury. The EVLW level then increased again until the end of the study period. In this study, lung edema formation is attributed to the toxic effect of smoke inhalation.
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PMID:Extravascular lung water changes following smoke inhalation and massive burn injury. 330

The Dahl selected rat lines, one susceptible to salt-induced hypertension (DS) and the other resistant to salt-induced hypertension (DR), were subchronically exposed to filtered air, 0.4, 1.4, or 4.0 ppm acrolein. All of the DS rats exposed to 4.0 ppm acrolein died within the first 11 days, while 60% of the DR animals survived. Neither dose dependent blood pressure changes nor altered behavioral characteristics were evident following acrolein exposure. Exposure to 4.0 ppm acrolein increased the level of several serum enzymes. This concentration of acrolein also led to pulmonary edema and a significant increase in lung connective tissue. There was a marked difference in the pulmonary pathology observed in DS and DR rats exposed to 4.0 ppm acrolein. The lungs of the DS rats exhibited severe airway epithelial necrosis with edema and hemorrhage, while surviving DR rats primarily showed a proliferative change. Following exposure to 0.4 to 1.4 ppm acrolein, both rat lines displayed similar pathologic change. Epithelial hyperplasia and/or clusters of macrophages were usually found near terminal bronchiolar areas. These findings suggest that further investigation of the physiopathologic sensitivity of the DS rat line may elucidate a model for investigating the underlying characteristics of stress susceptible populations.
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PMID:The impact of inhaled acrolein on hypertension-sensitive and resistant rats. 378 45

Acute lung disease is commonly associated with interstitial pulmonary edema and a tendency towards partial or total alveolar collapse. To counteract this tendency mechanical ventilation is successfully used in most cases. Mechanical ventilation, however, leads to a harmful retention of water and salt, which may worsen interstitial pulmonary edema and further impair gas exchange. This problem seems to be less known. A survey of the effects of currently used modes of mechanical ventilation on excretory function and hemodynamics of the kidneys is given together with a short review of the possible afferent and efferent mechanisms which mediate the renal response to mechanical ventilation. Some clinical suggestions are made to break through the vicious cycle between mechanical ventilation and kidney function.
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PMID:[Artificial respiration and kidney function disorder--a vicious circle?]. 389 Jun 7

Platelet activating factor (PAF), a suspected mediator of acute lung injury, has been shown to potentiate contraction in isolated porcine carotid arteries. Such an action of PAF, if it occurred in the pulmonary circulation, could be of significance to the evolution of pulmonary hypertension in acute lung injury. Accordingly, we used isolated rat lungs perfused at a constant flow rate with physiologic salt solution to test the hypothesis that PAF-induced lung injury is associated with pulmonary vascular hyperresponsiveness to constrictor stimuli. PAF in concentrations of 0.1 to 10 ng/ml failed to influence pressor responses evoked by i.a. bolus injections of angiotensin II (Ang II) whereas 1 micrograms/ml of PAF significantly blunted Ang II-induced vasoconstriction. Similarly, 1 micrograms/ml, but not 0.1 ng/ml, of PAF attenuated constriction induced by ventilation with 3% O2. PAF at all concentrations tested failed to influence pressor responses evoked by i.a. bolus injections of KCI. Concentrations of PAF which blunted Ang II and hypoxic responses were associated with increased lung wet-to-dry weight ratios indicative of pulmonary edema. Another agent that provokes edema, cytochalasin B, also increased lung wet-to-dry weight ratios and blunted Ang II-, hypoxia-, and KCI-induced pressor responses. PAF delivered as i.a. bolus injections caused acute vasodilation in preparations preconstricted with Ang II but not in those preconstricted with KCI. Collectively, these observations demonstrate that PAF fails to augment and instead blunts pulmonary vascular responsiveness to pressor stimuli, possibly by mechanisms that relate to PAF-induced edema formation and/or vasodilation.
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PMID:Impact of platelet activating factor on vascular responsiveness in isolated rat lungs. 394 67

We examined the hypothesis that arachidonic acid can lead to pulmonary edema, increased pulmonary vascular permeability, and increased pulmonary vascular resistance (PVR) in an isolated dog lung. The lung was perfused with a dextran-salt solution to remove blood elements. Compared to controls, 20 mg/min sodium arachidonate into the pulmonary circulation led to edema and to an increase in a permeability and surface area index (PSI%), PVR, and cyclooxygenase (i.e. prostaglandin) production as measured by 6-keto-PGF1 alpha, TXB2 and PGF2 alpha. With 20 mg/min arachidonate, indomethacin inhibited the increase in cyclooxygenase production, reduced the increase in PVR and increased the edema and PSI%. Indomethacin, alone, did not produce edema or an increase in PSI% or PVR. Lower doses of arachidonate (0.1 to 5 mg/min) led to increasing cyclooxygenase production without obvious edema or an increase in PSI% or PVR. We conclude: 1) arachidonate can lead to pulmonary edema and an increase in PVR, and may lead to an increase in pulmonary vascular permeability; these effects of arachidonate do not require normal numbers of circulating blood elements; 2) arachidonate appears to contribute to pulmonary edema and increased PSI% by a noncyclooxygenase effect since inhibition of cyclooxygenase production did not prevent, and lower doses of cyclooxygenase production did not produce edema or an increase in PSI%; 3) the increase in PVR appeared to have a cyclooxygenase component since inhibition of cyclooxygenase production reduced the increase, and 4) indomethacin can increase the magnitude of edema and PSI% from arachidonate by an undefined mechanism.
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PMID:Inhibition of cyclooxygenase production does not prevent arachidonate from increasing extravascular lung water and albumin in an isolated dog lung. 643 62

The Dahl selected rat lines, one susceptible to salt-induced hypertension (DS) and the other resistant to salt-induced hypertension (DR), were exposed to filtered air, 0.4, 1.4, or 4.0 ppm acrolein for 6 h/day, 5 days/week for 62 days. All of the DS rats exposed to 4.0 ppm acrolein died within the first 11 days, while 60% of the DR animals survived the duration of the study. Neither dose dependent blood pressure changes nor altered behavioral characteristics were evident in either rat strain following acrolein exposure. Exposure to 4.0 ppm acrolein increased the level of several serum enzymes in the DR rats which survived. This concentration of acrolein also led to pulmonary edema and a significant increase in lung connective tissue in these animals. There was a marked difference in the pulmonary pathology observed in DS and DR rats exposed to 4.0 ppm acrolein. The lungs of moribund DS rats exhibited severe airway epithelial necrosis with edema and hemorrhage, while surviving DR rats primarily showed a proliferative change. Following exposure to 0.4 and 1.4 ppm acrolein, both rat lines displayed similar pathologic changes. Epithelial hyperplasia and/or clusters of macrophages were usually found near terminal bronchiolar areas. These findings suggest that further investigation of the physiopathologic sensitivity of the DS rat line may elucidate a model for investigating the underlying characteristics of stress susceptible populations.
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PMID:Selected responses of hypertension-sensitive and resistant rats to inhaled acrolein. 672 36

Pilocarpine, a parasympathomimetic drug used in the treatment of glaucoma, produces a variety of ocular and systemic adverse reactions. Ocular side effects include miosis, accommodative spasm, frontal headaches, twitching lids, conjunctival injection, cataractous changes, allergic reactions, iris cysts, retinal detachment, increased permeability of the blood-aqueous barrier, anterior chamber narrowing, and the potential for inducing an acute angle-closure attack. Systemic side effects include nausea, vomiting, tenesmus, abdominal spasm, salivation, lacrimation, sweating, pulmonary edema, and bronchial spasm. The systemic side effects can best be minimized initially through proper use of the medication and nasolacrimal occlusion. The Ocusert, a long-acting pilocarpine-incorporated ocular insert, is a recent advance in delivery technique that offers an adequate hypotensive action with fewer side effects. Pilopex is a promising new experimental pilocarpine polymer salt presently being studied in Israel. Photomydriasis, a process involving the use of a laser to enlarge miotic pupils also offers help for these patients. N-demethylated carbachol is a new parasympathomimetic drug currently under study for glaucoma therapy. Initial results show that it may have considerable ocular hypotensive action with fewer adverse effects.
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PMID:Miotics: side effects and ways to avoid them. 707 Jul 79


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