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

Fluid exchange disorders due to capillary lesions are numerous and their extent depends on the underlying disease as well as the capillary structure of the affected organ. The inflammatory cascade, triggered by sepsis or reperfusion injury, is mediated by several humoral mediators and activated blood cells. These include pro-inflammatory cytokines, arachidonic acid, proteases, oxygen free radicals, polymorphonuclears, procoagulant, complement and fibrinolytic system. The interaction between these mediators leads to a loss of endothelial integrity, a loss of basment membrane and a disruption of the interstitial matrix, with wasting of the endothelial cytoskeleton. The alteration in permeability induces transcapillary exudation of water and protein in the interstitial space, leading to organ dysfunction, mainly the lungs and splanchnic organs. Nitric oxyde, by modulating the response of the endothelium to the cellular interaction may protect against capillary injury. Capillary "stress lesions" following microvascular hypertension are the physiological basis of neurogenic or high altitude pulmonary oedema, and overinflation injury from mechanical ventilation. The anatomic specific features of the cerebral capillaries resulted in the well known concept of blood brain barrier with it's changeing morphology. Under the effect of humoral mediators and cellular interactions, the endothelial cells are able, via a calcium-mediated mechanism, to contract and to modify capillary permeability, leading to vasogenic oedema.
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PMID:[Transvascular fluid exchange disturbed by capillary injuries]. 888 82

Severe congestive heart failure and cardiogenic shock don't resemble a homogeneous clinical picture, but a syndrome that is based on very different etiologies. What all the etiologies have in common is the inadequate peripheral O2-supply to essential organs with or without signs of severe pulmonary congestion up to pulmonary edema. For prognosis and therapy is a fast diagnostical clarification of the causes crucial. The therapeutical procedure for the various etiologies may be diametrically opposed. For the therapy is it also dicisive to distinguish between acute myocardial failure, e.g. acute myocardial infarction, and the development of myocardial failure from a longer existing consistent congestive heart failure (cardiomyopathy). Whenever possible, next to symptomatically therapy of cardiogenic shock the basic conditions of the disease should be cured (e.g., PTCA, lysis with acute myocardial infarction, lysis in acute pulmonary embolism). In myogenic cardiogenic shock the use of positive-inotropic substances with and without simultaneous vasodilatory effects, if necessary in combination with other vasodilators, may be life-saving. Up until now there still doesn't exist an alternative to the catecholamines in the acute phase, initially they should be used as a first-line-therapy to stabilize the hemodynamics. The insertion of a Swan-Ganz-catheter for invasive therapy-monitoring, especially for the regulation of the therapy is a "condition sine qua non" for every patient with unstable hemodynamics. Because of the prompt beta-receptor-down-regulation during shock, caused by endogenous catecholamines, successful therapy with exogenous catecholamines is limited (adrenaline, dopamine, dobutamine), on account of the acceleration and intensification of the beta-receptor-down-regulation process. Possible beta-receptor independent alternatives are beta 2-agonists (dopexamine), PDE-III-inhibitors (amrinone, milrinone, enoximone) as well as H2-receptor agonists (impromidine, arpromidine) and finally the calcium-sensitisers (pimobendane). First results give rise to optimism to effectively reduce the mortality of congestive heart failure. The combination of these new pharmacological possibilities with interventional transcutaneous applicable assist-systems (aortic counterpulsationpump IABP, hemopump, transcutaneous heart-lung-machine) as well as the transitory application of an artificial heart (Novacor) can possibly increase the success of these therapeutic strategies. So far there are no convincing results shown in the world literature.
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PMID:[Pharmacotherapy of severe heart failure with inodilators--new approaches]. 902 10

A 34-year-old housewife with alcohol dependence vomited severely, lost consciousness, and died after she took more than 20 ml of 1% calcium cyanamide, and alcoholic beverage containing about 129 g of ethyl alcohol. An autopsy was performed around 16 h after death. The body weighed 55.5 kg, and moderate lung edema was found. Ethanol concentrations were 4.24 mg/g in the left heart blood, 4.39 mg/g in the right heart blood, and 21.55 mg/g in the stomach contents. Cyanamide concentrations were 0.63 microgram/g in the left heart blood, 0.20 microgram/g in the right heart blood, and 0.22 microgram/g in the stomach contents. The cause of death was determined to be acute ethanol intoxication with alcohol-cyanamide reaction.
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PMID:A fatal case of drinking and cyanamide intake. 918 22

A 10-year-old male cat was presented with sudden onset of respiratory difficulties. Clinical examination revealed an acute dyspnoea with cyanosis associated with a left systolic heart murmur. Standard thoracic radiographs excluded pulmonary oedema and showed very few pulmonary changes given the intensity of the respiratory compromise. Echocardiographic examination revealed hypertrophic cardiomyopathy and a thrombus in the right pulmonary artery. Pulmonary scintigraphy confirmed a pulmonary thromboembolism with hypovascularisation of the left cranial lobe and of the ventral segment of the right lobe. Conservative treatment was instituted using an antibiotic (doxycycline), anticoagulants (heparin, coumadine) and a calcium inhibitor (diltiazem). The cat was given absolute rest. The general condition of the animal improved.
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PMID:Diagnosis of pulmonary thromboembolism in a cat using echocardiography and pulmonary scintigraphy. 923 34

Pulmonary air embolism induces the generation of vasoactive and cytotoxic substances leading to lung injury. In the present study we investigated, in isolated and perfused rat lungs, the involvement of arachidonic acid metabolites in the alterations of vascular pressure, lung water content, and the filtration coefficient (Kf). We also tested the effects of a beta-agonist, a calcium channel blocker, and a cyclo-oxygenase inhibitor on the hemodynamic and the permeability changes following pulmonary air embolism. The artificially ventilated rat lungs were removed en bloc and suspended in a humidified chamber at 37 degrees C. The salt and buffered perfusate contained 4% Ficoll as albumin substitute for osmotic balance. We introduced air bubbles through the pulmonary artery. Air embolism increased pulmonary arterial resistance and caused pulmonary hypertension. Lungs receiving air infusion contained 88.6 +/- 0.6% water, which was significantly greater than the lung water content in the control groups (81.9 +/- 0.4%). Air embolism increased Kf by 145 +/- 19% from the baseline value. Pretreatment with indomethacin, isoproterenol, or nifedipine significantly reduced post-air-embolism lung water content to 85.8 +/- 0.5%, 84.1 +/- 0.4%, and 86.5 +/- 04%, respectively, and reduced the Kf increase to 17 +/- 8%, 1 +/- 9%, and 72 +/- 8%, respectively. These interventions did not alter the hemodynamic responses, except for the isoproterenol infusion, which shortened the half-time (T1/2) for pressure recovery after ending air infusion compared to the group with air embolism alone. Our results showed that indomethacin prevented vascular permeability increase and reduced pulmonary edema, suggesting that the cyclo-oxygenase products partially mediate the lung injury following air embolism. Furthermore, isoproterenol and nifedipine prevented or reduced the permeability increase, suggesting that alterations of the intracellular cAMP and cytosolic Ca2+ level play an important role in the pathophysiology of pulmonary air embolism.
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PMID:Pharmacologic modulation of pulmonary vascular permeability during air embolism. 944 63

Transfusion-related acute lung injury (TRALI) is a serious complication of hemotherapy. During blood storage, lipids are generated and released into the plasma. In this study, the role of these lipids in TRALI was investigated using an isolated, perfused rat lung model. Rats were pretreated with endotoxin (LPS) or saline in vivo and the lungs were isolated, ventilated, and perfused with saline, or (a) 5% (vol/ vol) fresh human plasma, (b) plasma from stored blood from the day of isolation (D.0) or from the day of outdate (D.42), (c) lipid extracts from D.42 plasma, or (d) purified lysophosphatidylcholines. Lungs from saline or LPS-pretreated rats perfused with fresh (D.0) plasma showed no pulmonary damage as compared with saline perfused controls. LPS pretreatment/D.42 plasma perfusion caused acute lung injury (ALI) manifested by dramatic changes in both pulmonary artery pressure and edema. Incubation of LPS pre-tx rats with mibefradil, a Ca2+ channel blocker, or WEB 2170, a platelet-activating factor (PAF) receptor antagonist, inhibited ALI caused by D.42 plasma. Lung histology showed neutrophil sequestration without ALI with LPS pretreatment/saline or D.0 plasma perfusion, but ALI with LPS pretreatment/D.42 plasma perfusion, and inhibition of D.42 plasma induced ALI with WEB 2170 or mibefradil. A significant increase in leukotriene E4 was present in LPS-pretreated/D.42 plasma-perfused lungs that was inhibited by WEB 2170. Lastly, significant pulmonary edema was produced when lipid extracts of D.42 plasma or lysophosphatidylcholines were perfused into LPS-pretreated lungs. Lipids caused ALI without vasoconstriction, except at the highest dose employed. In conclusion, both plasma and lipids from stored blood produced pulmonary damage in a model of acute lung injury. TRALI, like the adult respiratory distress syndrome, may be the result of two insults: one derived from stored blood and the other from the clinical condition of the patient.
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PMID:Plasma and lipids from stored packed red blood cells cause acute lung injury in an animal model. 952 89

Oxygen exposure for a sufficient duration at high partial pressure results in pulmonary edema in humans and animals. Although the specific mediators of oxygen toxicity are unknown, evidence suggests that oxygen-based radicals such as superoxide anion (O2.) are increased in the lungs in the presence of hyperoxia and contribute to this injury. A series of isomeric prostanoid compounds, the isoprostanes, are formed by the free radical-initiated lipid peroxidation of arachidonic acid (AA). One of these isomers, 8-iso-PGF2alpha, is elevated in the bronchial alveolar lavage fluid of rats exposed to 90% oxygen for 48 h and is associated with a significant increase in protein accumulation in the pulmonary extravascular space. Alveolar macrophages (AMs) are capable of producing large quantities of (O2.), suggesting a role in pulmonary oxygen toxicity. We hypothesized that isolated rat AMs exposed to hyperoxia generate increased amount of 8-iso-PGF2alpha. AMs were exposed to air or 90% oxygen for 6, 12, 24, 48, 72, 96, and 120 h in the absence and presence of AA and/or calcium ionophore (A23187) and 8-iso-PGF2alpha was measured in the culture media. Exposure of primary cultures of AMs to 90% oxygen resulted in a significant increase in 8-iso-PGF2alpha in the media (25 +/- 2 pg/mL) compared with air-exposed controls (14 +/- 1 pg/mL). The addition of 10 microM AA and 2 microM A23187 to the culture media resulted in a marked increase in 8-iso-PGF2alpha production by AMs exposed to air and 90% oxygen. However, treatment of AMs with the combination of AA and A23187, followed by exposure to 90% oxygen for 72 h, resulted in a 27-fold increase in 8-iso-PGF2alpha compared with media alone and 90% oxygen. AMs metabolized free and phospholipid-bound AA to 8-iso-PGF2alpha, an activity enhanced in the 90% oxygen environment. Finally, acetylsalicylic acid, a cyclooxygenase inhibitor and free radical scavenger, reduced but did not abolish production of 8-iso-PGF2alpha. This study provides evidence that AMs produce a free radical-mediated isomeric prostaglandin compound that may be involved in pulmonary oxygen toxicity.
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PMID:8-ISO-PGF2alpha production by alveolar macrophages exposed to hyperoxia. 956 55

A severely hypocalcaemic, hypomagnesaemic lactating bitch exhibited clinical signs of pulmonary oedema, paresis, dementia, gastrointestinal ileus and urinary bladder atony. The total calcium, ionised calcium and magnesium levels were extremely low. The clinical picture was very different from the one typically encountered in canine lactation tetany, and instead resembled bovine postparturient paresis. Muscle tremors, rigidity and seizures were not part of the acute clinical picture, but rather atony, weakness and paresis. General muscle dysfunction probably resulted from the extremely low ionised calcium levels in combination with very low levels of magnesium and possibly potassium. Heart failure and atony of the urinary bladder and intestines were probably a result of the severe hypocalcaemia. The alteration in calcium to magnesium ratio may have depressed neuromuscular transmission, leading to paresis and atony. The unusual electrocardiogram possibly also resulted from abnormal magnesium and calcium cation levels.
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PMID:Paresis and unusual electrocardiographic signs in a severely hypomagnesaemic, hypocalcaemic lactating bitch. 967 8

Hypertensive crisis is defined as a severe elevation in BP and is classified as either urgency or emergency. In hypertensive urgency there is no end-organ injury and no evidence that acute BP lowering is beneficial. Indeed, rapid uncontrolled pressure reduction may be harmful. Therefore, in hypertensive urgencies BP should be lowered gradually over 24 to 48 hours using oral antihypertensives. When the cause of transient BP elevations is easily identified, appropriate treatment should be given. When the cause is unknown, an oral antihypertensive should be given. The efficacy of available treatments appear similar; however, the underlying pathophysiological and clinical findings, mechanism of action and potential for adverse effects should guide choice. Captopril should be avoided in patients with bilateral renal artery stenosis or unilateral renal artery stenosis in patients with a solitary kidney. Nifedipine and other dihydropyridines increase heart rate whereas clonidine, beta-blockers and labetalol tend to decrease it. This is particularly important in patients with ischaemic heart disease. Labetalol and beta-blockers are contraindicated in patients with bronchospasm and bradycardia or heart blocks. Clonidine should be avoided if mental acuity is desired. In hypertensive emergency there is an immediate threat to the integrity of the cardiovascular system. BP should be immediately reduced to avoid further end organ damage. Sodium nitroprusside is the most popular agent. Nitroglycerin (glyceryl trinitrate) is preferred when there is acute coronary insufficiency. A beta-blocker may be added in some patients. Loop diuretics, nitroglycerin and sodium nitroprusside are effective in patients with concomitant pulmonary oedema. Enalaprilat is also theoretically helpful, especially when the renin system might be activated. Initial treatment of aortic dissection involves rapid, controlled titration of arterial pressure to normal levels using intravenous sodium nitroprusside and a beta-blocker. If beta-blockers are contraindicated, urapidil or trimetaphan camsilate are alternatives. Hydralazine is the drug of choice for patients with eclampsia. Labetalol, urapidil or calcium antagonists are possible alternatives if hydralazine fails or is contraindicated. For patients with catecholamine-induced crises, an alpha-blocker such as phentolamine should be given; labetalol or sodium nitroprusside with beta-blockers are alternatives. There are few, if any, comparative or randomised trials providing definitive conclusions about the efficacy and safety of comparative agents. Some investigators recommend decreasing the diastolic BP to no less than 100 to 110 mm Hg. A reasonable approach for most patients with hypertensive emergencies is to lower the mean arterial pressure by 25% over the initial 2 to 4 hours with the most specific antihypertensive regimen.
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PMID:Comparative tolerability profile of hypertensive crisis treatments. 970 48

It is well known that scorpion venom induces lung lesions and respiratory distress which are usually classified as pulmonary oedema (PO). Tityus discrepans is a scorpion that lives in the north-central area of Venezuela, is the most common source of human envenomation here and produces PO. We studied the action of the venom of Tityus discrepans on whole rabbits and on their isolated lungs perfused with Krebs saline with 1 g/l of bovine serum albumin (Krebs-BSA saline). Two milligram of venom were diluted in 250 ml of solution (approximately the rabbit's total blood volume) and used to perfuse isolated lungs. Lung oedema occurred in rabbits which received 1 mg/kg of scorpion venom i.p., heparin prevented the production of this lung oedema. T. discrepans venom produced PO, in rabbits pretreated with 15 mg/kg of ajoene. Yet, Tityus venom had no effects on isolated lungs perfused with citrated or heparinized blood, and in lungs perfused with Krebs-BSA with normal Ca2+. These result show that Tityus venom does not act directly on lungs. Otherwise, we have observed that abundant microthrombi occurred in all rabbit lungs exposed to venom in vivo, suggesting that these clotting alterations are fundamental to produce PO. The presence of intravascular microthrombi is not characteristic of the usual PO hinting that scorpion venom induced pulmonary alterations are a different clinical entity. We thus propose that the use of the term pulmonary oedema in scorpionism should abandoned in favor of scorpion venom respiratory distress syndrome.
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PMID:Tityus discrepans venom produces a respiratory distress syndrome in rabbits through an indirect mechanism. 992 Apr 89


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