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)

Following onset of acute cardiogenic pulmonary edema in 21 patients, increases in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with decreases in plasma volume. Accordingly, there was a loss of hypo-oncotic fluid into the extravascular spaces. Following treatment with oxygen, furosemide, and morphine sulfate and reversal of clinical and radiographic signs of pulmonary edema, declines in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with increases in plasma volume. Hypo-oncotic edema fluid was therefore reabsorbed into the vascular compartment. The concept that acute heeart failure with pulmonary edema is associated with an increase in intravascular volume is therefore not supported. To the contrary, there is a reduction of blood volume during acute pulmonary edema. During reversal of acute pulmonary edema with diuresis, there was re-expansion rather than contraction of blood volume.
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PMID:Blood volume prior to and following treatment of acute cardiogenic pulmonary edema. 61 25

In order to compare the venodilation effect of morphine in normal individuals (22) with that in patients (13) with heart failure morphine sulfate (0.1 mg/kg) was administered to 13 patients with mild pulmonary edema. After morphine congestive symptoms improved and venodilation was induced as determined by two independent techniques: venous pressure fell 10.2 mm Hg by the isolated hand technique and the venous volume of the forearm increased by 0.48 cc/100 ml, measured by equilibration technique. Neither finding differed from those in normal individuals. Reflex venoconstriction noted on the taking of a single deep breath was unaffected by morphine administration and was similar to that observed in normal subjects. Since the drug morphine sulfate does not cause a major pooling of blood in the limbs, the favorable effect of narcotics in patients with pulmonary edema must be caused by other mechanisms such as splanchnic pooling, afterload reduction or reduced breathing effort.
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PMID:The effects of morphine on venous tone in patients with acute pulmonary edema. 93 31

We tested the hypothesis that dextran sulfate and heparin sulfate inhibit platelet-activating factor- (PAF) induced pulmonary edema in the isolated perfused guinea pig lung via a charge-dependent mechanism. Dextran sulfate prevented the changes in pulmonary capillary pressure (Ppc, 7.8 +/- 0.9 vs. 14.0 +/- 0.7 cmH2O), lung weight gain (dW, +0.48 +/- 0.29 vs. +8.41 +/- 2.07 g), and pulmonary edema formation or wet-to-dry weight ratio [(W-D)/D, 6.5 +/- 0.3 vs. 13.2 +/- 2.6] occurring 60 min after PAF infusion (10(-11) M) into an isolated lung. The unsulfated form of dextran had no protective effect [Ppc, dW, and (W-D)/D, 11.9 +/- 1.4 cmH2O, +5.33 +/- 2.18 g, and 11.2 +/- 3.2, respectively]. The unrelated anionic compound, heparin sulfate, also inhibited the PAF response [Ppc, dW, and (W-D)/D, 7.0 +/- 0.5 cmH2O, +0.61 +/- 0.32 g, and 6.1 +/- 0.2, respectively], whereas the partially desulfated form of heparin was not effective in inhibiting PAF-induced edema [Ppc, dW, and (W-D)/D, 15.1 +/- 0.7 cmH2O, +6.07 +/- 1.58 g, and 10.0 +/- 1.2, respectively]. When the metachromatic dye crystal violet was used as an indicator of charge interactions, the sulfated compounds interacted with PAF in vitro. The data indicate that PAF-induced pulmonary edema is inhibited by sulfated polysaccharides, possibly via a charge interaction between negatively charged compounds and PAF.
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PMID:Dextran sulfate and heparin sulfate inhibit platelet-activating factor-induced pulmonary edema. 153 12

We report the case of a 24-year-old white female in need of tocolysis during the 25th week of pregnancy with i.v. hexoprenaline, while suffering from a discrete influenza-like syndrome with nasal discharge and sinusitis. A few hours later fulminant acute adult respiratory distress syndrome (ARDS) developed. ARDS is a rare (0.5-5%) but feared complication of tocolysis with beta-2 mimetic agents and magnesium sulfate. Its physiopathology is obscure, but iatrogenic hyperhydration and lesions of the alveolar-capillary membrane are suspected. In this case both factors were involved, but lesions of the alveolar-capillary membrane were predominant. A direct toxic effect of beta-2 mimetic agents on the alveolar-capillary membrane has not been demonstrated and other factors favoring pulmonary edema during tocolysis with beta-2 mimetic agents, especially infections, are discussed.
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PMID:[Lesional pulmonary edema associated with tocolysis by hexoprenaline sulfate]. 153 26

The safety of prehospital pharmacologic therapy has not been well studied. The authors evaluated field use of morphine sulfate (MS) in San Francisco County over a 6-month period. Paramedics assessed patients for ischemic chest pain (ICP) and/or pulmonary edema (PE), made base hospital contact, and administered 2- to 4-mg doses of intravenous morphine according to treatment protocols. Clinical assessments and patient responses to therapy were recorded by both field paramedics and emergency department (ED) physicians. Safety was evaluated by determining the (1) accuracy of paramedic field assessment, (2) appropriateness of field administration of MS, and (3) therapeutic complications. During the study period, paramedics administered MS to 84 patients. In 69 cases paramedic assessment of either ICP and/or PE corresponded to ED physician diagnosis. In five cases paramedics correctly recognized ICP but missed physical findings of PE. In this group the paramedics' assessment was considered inaccurate but the judgement to give MS was considered appropriate. In the remaining 10 cases paramedics identified ICP or PE but the ED physician diagnosed a different condition. These assessments were considered inaccurate and the management inappropriate. Therefore, overall paramedic accuracy was 77% (true rate 73% to 82%, 95% confidence interval); appropriateness of therapy was 88% (true rate 85% to 92%, 95% confidence interval); and the overall complication rate was 6% (true rate 2% to 12%, 95% confidence interval). Complications of respiratory depression or hypotension occurred in only one of the cases in which MS was inappropriately administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of pre-hospital therapy with morphine sulfate. 173 17

We tested the hypothesis that neutrophil sequestration is required for the development of tumor necrosis factor- (TNF) induced neutrophil- (PMN) dependent pulmonary edema. TNF (3.2 X 10(5) U/kg ip) was injected into guinea pigs 18 h before lung isolation. After isolation, the lung was perfused with a phosphate-buffered Ringer solution. Dextran sulfate (mol wt 500,000) prevented the changes in pulmonary capillary pressure (Ppc; 8.5 +/- 0.8 vs. 12.8 +/- 0.8 cmH2O), lung weight gain (dW; +0.240 +/- 0.135 vs. +1.951 +/- 0.311 g), and pulmonary edema formation or wet-to-dry wt ratio [(W - D)/D; 6.6 +/- 0.2 vs. 8.3 +/- 0.5] at 60 min induced by PMN infusion into a TNF-pretreated lung. The unsulfated form of dextran had no protective effect [Ppc, dW, and (W - D)/D at 60 min: 11.9 +/- 0.9 cmH2O, +1.650 +/- 0.255 g, and 7.3 +/- 0.2, respectively], whereas the use of another anionic compound, heparin, inhibited the TNF + PMN response [Ppc, dW, and (W - D)/D at 60 min: 5.6 +/- 0.4 cmH2O, +0.168 +/- 0.0.052 g, and 6.4 +/- 0.2, respectively]. Isolated lungs showed increased PMN myeloperoxidase (MPO) activity compared with control in TNF-treated lungs at baseline and 60 min after PMN infusion. Dextran sulfate, dextran, and heparin inhibited the increase in MPO activity. The data indicate that inhibition of PMN sequestration alone is not sufficient for the inhibition of PMN-mediated TNF-induced hydrostatic pulmonary edema and that a charge-dependent mechanism mediates the protective effect of dextran sulfate.
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PMID:Dextran sulfate inhibits PMN-dependent hydrostatic pulmonary edema induced by tumor necrosis factor. 185 40

The Fischer rat is known for its susceptibility to develop liver necrosis when challenged with paraquat (Smith et al., J. Pharmacol. Exp. Ther. 235: 172-177, 1985). We postulated that other organs, specifically the lung, may also be more susceptible to injury and examined whether lungs from Fischer (F) rats were injured more easily when challenged with active oxygen species than Sprague-Dawley (SD) rat lungs. We aimed to investigate whether increased susceptibility to oxidant injury was related to differences in lung antioxidant defenses. Perfused lungs from both rat strains were challenged by addition of H2O2 to the perfusate or by short-term hyperoxic ventilation. To assess nonoxidant modes of lung injury, we examined lung responses after exposure to protamine sulfate or neutrophil elastase. Intravascular H2O2 or 3 h in vitro hyperoxia caused lung edema in F but not SD rats, and elastase injured F rat lungs more than the lungs from SD rats. Protamine, however, injured the lungs from both strains to a similar degree. Catalase, but not superoxide dismutase or allopurinol, protected F rat lungs against edema, resulting from 3 h in vitro hyperoxia. The lung homogenate levels for reduced glutathione or conjugated dienes and the activities of lung tissue catalase, glutathione peroxidase, and cytochrome P-450 were not different between the two strains. Lung tissue ATP levels, however, were lower in F than in SD rats. Although the F rat strain appears to have an altered oxidant-antioxidant defense balance, the exact cause of the greater susceptibility to oxidant stress of the F rat strain remains elusive.
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PMID:Lung injury in Fischer but not Sprague-Dawley rats after short-term hyperoxia. 226 Jun 76

With 2 groups of 10 patients the influence of an additional therapy with 1 g magnesium sulfate/h during i.v. tocolysis with the betamimetic fenoterol (2 micrograms/min) upon parameters of water and electrolyte balance has been investigated. The whole of the magnesium administered during the 24 hours investigational period has been eliminated via the kidneys. Most probably due to a competition within the distal tubulus hypermagnesemia was associated with hypocalcemia and hypercalciuria, followed by a rise in parathyroid hormone. As PTH is able to compensate hypocalcemia not only by means of bone mobilisation but also by an increase in enteral Ca absorption, estimated losses of calcium are minimal. These may be neglected, as additional therapy with magnesium sulfate--besides the advantages yet known (cardioprotection, saving of betamimetic dosage, reduction of drug tolerance development)--reduces betamimetic induced water retention, thus significantly diminishing lung edema hazard during tocolytic therapy.
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PMID:[Effect of co-medication with magnesium sulfate in beta-mimetic tocolysis on parameters of water-electrolyte balance]. 231 70

We studied the synergistic interaction between platelet-activating factor (PAF) and protamine sulfate, a cationic protein that causes pulmonary endothelial injury, in isolated rat lungs perfused with a physiological salt solution. A low dose of protamine (50 micrograms/ml) increased pulmonary artery perfusion pressure (Ppa) but did not increase wet lung-to-body weight ratio after 20 min. Pretreatment of the lungs with a noninjurious dose of PAF (1.6 nM) 10 min before protamine markedly potentiated protamine-induced pulmonary vasoconstriction and resulted in severe lung edema and increased lung tissue content of 6-keto-prostaglandin F1 alpha, thromboxane B2, and leukotriene C4. Pulmonary microvascular pressure (Pmv), measured by double occlusion, was markedly increased in lungs given PAF and protamine. These potentiating effects of PAF were blocked by WEB 2086 (10(-5) M), a specific PAF receptor antagonist. Pretreatment of the lungs with a high dose of histamine (10(-4) M) failed to enhance the effect of protamine on Ppa, Pmv, or wet lung-to-body weight ratio. Furthermore, PAF pretreatment enhanced elastase-, but not H2O2-, induced lung edema. To assess the role of hydrostatic pressure in edema formation, we compared lung permeability-surface area products (PS) in papaverine-treated lungs given either protamine alone or PAF + protamine and tested the effect of mechanical elevation of Pmv on protamine-induced lung edema. In the absence of vasoconstriction, PAF did not potentiate protamine-induced increase in lung PS. On the other hand, mechanically raising Pmv in protamine-treated lungs to a level similar to that measured in lungs given PAF + protamine did not result in a comparable degree of lung edema. We conclude that PAF potentiates protamine-induced lung edema predominantly by enhanced pulmonary venoconstriction. However, a pressure-independent effect of PAF on lung vasculature cannot be entirely excluded.
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PMID:PAF potentiates protamine-induced lung edema: role of pulmonary venoconstriction. 234 34

During a 12-year period, 254 cases of eclampsia were managed at this center. Eighty patients (32%) did not have edema, 58 (23%) had "relative hypertension," and 49 (19%) did not have proteinuria at the time of convulsions. Eclampsia developed at less than or equal to 20 weeks in 6 patients and beyond 48 hours post partum in 40 (16%). Convulsions developed in 33 while they were receiving standard doses of magnesium sulfate for preeclampsia during or after birth, and subsequent seizures developed in 36 (14%) after magnesium sulfate therapy was started. There was one maternal death (0.4%) and morbidity was frequent (acute renal failure, 4.7%; pulmonary edema, 4.3%; cardiorespiratory arrest, 3.1%; and aspiration, 2%. The use of multiple drug therapy was associated with significant maternal and neonatal complications. The total perinatal mortality was 11.8%, with the majority of them related to either abruptio placentae or extreme prematurity. These findings emphasize the need for intensive monitoring of women with preeclampsia throughout hospitalization and underscore the importance of maternal stabilization before and during transfer.
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PMID:Eclampsia. VI. Maternal-perinatal outcome in 254 consecutive cases. 240 30


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