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

Pulmonary complications are a major cause of death in patients in various forms of shock. The exact causes of the pulmonary complications are unknown. This study evaluates the functional characteristics of intralobar pulmonary arteries (IPA) and veins (IPV) obtained from swine subjected to splanchnic arterial occlusion (SAO) shock ans subsequent cardiovascular collapse and sham-shocked swine subjected to surgery but no occlusion. The contractile response of pulmonary arteries to norepinephrine (NE) and serotonin (5-HT) were depressed when obtained from pigs subjected to SAO shock. The depression in the sensitivity to 5-HT and maximal tension development to 5-HT and NE was selective, since the responses to potassium ion were not depressed. IPA obtained from swine with SAO shock were more sensitive to the relaxant actions of arachidonic acid, a precursor for bisenoic prostaglandins, than were IPA from sham-shocked swine. This was not observed when prostaglandins were used as agonists. This suggests that synthesis of prostaglandin differs in the pulmonary vasculature of sham-shocked and SAO-shocked animals. IPV obtained from swine in SAO shock were less sensitive to 5-HT and NE but more sensitive to arachidonic acid and 9 alpha, 11 alpha-epoxymethano-PGH2, a thromboxane like compound. IPV obtained from swine in SAO shock converted more arachidonic acid into a substance with the chromatographic mobility of thromboxane B2. The data suggest that alterations in the prostaglandin system within the pulmonary artery and vein may contribute to the pulmonary complications of SAO shock. The alterations appear to include an enhanced synthesis of prostacyclin as well as thromboxane-like substance. Because the veins were more sensitive than the arteries to 9 alpha, 11 alpha-epoxymethano-PGH2, thromboxanes or endoperoxides may elevate venous tone and contribute to the pulmonary edema associated with shock states.
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PMID:Pulmonary vascular smooth muscle function in porcine splanchnic arterial occlusion shock. 724 87

The therapeutic efficacy of 100 mg spironolactone once daily in patients with congestive heart failure was evaluated in a multi-centre study in general practice. One hundred and fifteen patients were admitted to the study. Clinical and haemotological assessments were made at entry and at regular intervals throughout the 48-week study period. Body weight decreased and the incidence of both pitting and pulmonary oedema was reduced during spironolactone treatment. Plasma sodium level was consistently reduced and plasma potassium increased to accepted normal levels. Seventy-nine patients remained free of side-effects throughout the treatment period.
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PMID:Spironolactone in the long-term management of patients with congestive heart failure. 743 70

Effects of different perfusion conditions and storage of isolated dog lungs on the process of edema development were studied. Sixty-nine mongrel dogs were used in the study. In case of a 15 min perfusion via the pulmonary artery and 12 h storage lung condition depended mainly on the type of solution and addition of protective drugs to this solution. Euro-Collins and low-potassium electrolytic solution markedly increased capillary hydrostatic pressure and drastically reduced plasma colloid-osmotic pressure. As a result filtration coefficient increased and as soon as an hour after reperfusion onset a marked pulmonary edema developed. Use of LPD solution without drugs added for 2.5 h reperfusion was associated with a moderate increase of capillary hydrostatic pressure and negligible decrease of plasma colloid-osmotic pressure. If the reperfusion were longer plasma colloid-osmotic pressure reduced, this leading to development of moderate pulmonary edema. A 15 min lung perfusion via the pulmonary artery and 12 h storage at 1 degree C in LPD solution with membrane protectors and antioxidants was associated with virtually unchanged capillary hydrostatic pressure, plasma colloid-osmotic pressure, and filtration coefficient and, hence, no pulmonary edema.
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PMID:[The quality of the preservation of lungs using different solutions (an experimental study)]. 750 22

Scorpion envenoming results in a severe autonomic storm with a massive release of catecholamines, increased angiotensin II and inhibition of insulin secretion. These hormonal alterations could be responsible for the pathogenesis of a variety of clinical manifestations. Under these conditions, scorpion envenoming essentially results in a syndrome of fuel-energy deficits and an inability to utilize the existing metabolic substrates by vital organs causing multi-organ system failure and death. Based on our animal experiments in which insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming and treating the poisonous scorpion sting victims with insulin, we consider that insulin has a primary metabolic role in preventing and reversing the cardiovascular, haemodynamic, and neurological manifestations and pulmonary oedema induced by scorpion envenoming. The use of continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg/hr, with supplementation of potassium as needed and maintenance of fluid electrolytes and acid-based balance, has become a routine protocol in our setting for treating the victims of scorpion envenoming.
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PMID:Scorpion envenoming and the role of insulin. 780 39

A 32 year old man was admitted for dyspnea, hemoptysis, macroscopic hematuria, hypertension (140/100), peripheral edema and hemodynamic decompensation. Lung Xrays revealed pulmonary edema and a cavity in the left apex. Laboratory determinations revealed an altered renal function with increased creatinine and urea levels and nephrotic syndrome. There was leucocyturia, hematuria and cylindruria. The sputum showed a large number of acid-fast bacilli. The patient began anti-tuberculosis treatment with three drugs (isoniacid, rifampicin, pirazinamide). On ultrasonography, both kidneys revealed ecogenic lesions with size, shape and cortico-medular relationship preserved. The patient persisted with altered renal function, steady levels of urea nitrogen, creatinine and potassium, preserved diuresis and hypertension. Bidimensional echocardiogram: LVDD 55 mm, hypoquinetic septum, pericardic effusion, thickened pericardium, pleural effusion, shortening fraction decreased. He received treatment for this congestive cardiac failure and hypertension with enalapril, nifedipine and fursemide. A percutaneous renal biopsy was performed with anatomopathologic diagnosis of diffuse encocapillar proliferative glomerulonephritis with crescents (15%) and total glomerular sclerosis (33%). Immunofluorescence: positive, immune-complexes with IgM and C3. The patient gradually recovered his normal renal function, improved his pleural effusions and normalized his cardiac function. He was discharged in good clinical condition on the 69th day of anti-tuberculosis treatment. An association between pulmonary tuberculosis and glomerulonephritis is discussed. It is proposed that renal lesions might be the consequence of the tuberculosis due to the sedimentation of circulating immune-complexes.
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PMID:[Immune complex glomerulonephritis associated with pulmonary tuberculosis]. 785 90

Previous studies have suggested that recovery from pulmonary edema may be dependent on active sodium ion transport. Most of the data supporting this concept came from work done in isolated type II cells, isolated lung preparations, or in models of alveolar flooding. There is a limited amount of information regarding the role of active sodium ion transport in vivo. Furthermore, most of this information was obtained in one model of pulmonary edema, the hyperoxic lung injury model. The purpose of these experiments was then to measure the activity of the sodium-potassium-adenosinetriphosphatase (Na(+)-K(+)-ATPase), the active component of the sodium transport process and an indirect marker of active sodium transport, during recovery from thiourea-induced pulmonary edema in rats. Na(+)-K(+)-ATPase activity was significantly increased during recovery from lung edema. This increase could not be accounted for by the Na(+)-K(+)-ATPase activity present in inflammatory cells recruited in the lung by the injury process or by a direct impact of thiourea on the enzyme. Alveolar flooding, induced by instillation of a protein-containing solution into the airways of ventilated rats also increased the activity of Na(+)-K(+)-ATPase, suggesting that activation of the enzyme is probably secondary to either the presence of edema or the physiological consequences associated with edema. The quantity of lung Na(+)-K(+)-ATPase protein was also elevated during edema resolution, indicating that augmented synthesis of this enzyme underlies the increased enzyme activity observed. The quantity of Na(+)-K(+)-ATPase protein in alveolar type II cells was also significantly enhanced during recovery from edema, suggesting that these cells contribute to active sodium transport in vivo. The results of this study suggest that active sodium transport could participate in the resolution of pulmonary edema.
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PMID:Increase of lung sodium-potassium-ATPase activity during recovery from high-permeability pulmonary edema. 899 59

Alveolar fluid is resorbed using active Na+ transport primarily through basolateral sodium-potassium-adenosinetriphosphatase (Na-K-ATPase) and apical Na+ channels that are particularly dense on the alveolar type II (ATII) epithelial cells. During lung injury with pulmonary edema, continued or accelerated Na+ and fluid resorption is critical for a favorable outcome. However, little is known of how ATII cell Na+ transport is affected during injury. These experiments examined the effects of acute lung injury on ATII cell Na-K-ATPase activity and expression using an established model of rats exposed to 100% O(2) for 60 h. Na-K-ATPase activity of ATII cells isolated immediately after exposure was assessed by ouabain-sensitive (86)Rb+ uptake in intact cells and by ouabain-sensitive P(i) production by cell membranes. In the presence of 1 mM ouabain, ouabain-sensitive Rb+ uptake was not different between normoxic and hyperoxic cells, but the apparent Na-K-ATPase maximal velocity (Vmax) of hyperoxic cell membranes was 75 +/- 8% of normoxic membranes (P < 0.05). On Western blots of ATII cell membranes, alpha1-subunit protein significantly decreased with hyperoxia (35 +/- 9% of normoxia; P < 0.05), whereas the amounts of the beta-subunit were unchanged (P > 0.05). On Northern blots of ATII cell total RNA, steady-state levels of both the alpha1- and beta1-subunit mRNA increased after hyperoxia (alpha1 = 2.5 +/- 1.3-fold; beta1 = 4.6 +/- 2.5-fold). Thus despite hyperoxic decreases in Na-K-ATPase Vmax and the amount of alpha1-protein, Rb+ uptake by Na-K-ATPase in intact cells was unchanged. The mRNA levels, protein amounts, and enzyme activity did not respond in parallel to hyperoxic injury, and the activity in intact cells correlated best with the amounts of the beta-subunit, the limiting component in de novo pump assembly in many tissues.
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PMID:Effects of hyperoxia on type II cell Na-K-ATPase function and expression. 912 12

Recently much interests have focused on the imbalance between the release of thromboxane A2 (TXA2) and prostaglandin I2 (PGI2), which may contribute to the development of pulmonary vascular injury. TXB2 has potents of platelet aggregation and vasoconstriction, while PGI2 has against in its activities. We investigated the effect of new PGI2 analogue (ONO-1301), which is a novel prostacyclin mimetic with inhibitory activity against thromboxane synthetase, on the early graft function in canine left single lung allotransplantation model. 19 donor dogs were divided into three groups. Seven dogs were comprised control group and received heparin administration (400 Unit/kg) before pulmonary arterial flushing with 50 ml/kg of 4 degrees C low potassium dextran glucose (LPDG) solution. Each six dogs were comprised I2-10 and I2-50 groups respectively, with receiving a 10-minute infusion of ONO-1301 (10 micrograms/kg/min) before flushing. The pulmonary cold preservation was performed with LPDG solution at 4 degrees C for 18 hours. After left single lung transplantation, in control group, saline solution was administered to the recipient for 10 minutes encompassing the reperfusion process (starting from 5 minutes prior to reperfusion). In I2-10 group, the ONO-1301 (10 micrograms/kg/min) was administered in the same manner. In I2-50 group, the ONO-1301 was administered from the same timing as I2-10 group, but for 50 minutes. The recipient dogs were observed for 6 hours after ligation of the right pulmonary artery and bronchus. We measured the transplanted lung function, including arterial blood gas and pulmonary hemodynamics, and plasma 6-keto-PGF1 alpha, TXB2 and lipid peroxide levels of left atrial blood. Pulmonary histological investigation was performed after preservation and sacrifice the recipient dog. All recipient dogs were survived for observation period. I2 groups provided significantly better gas exchange and pulmonary hemodynamics than control group. The 6-keto-PGF alpha levels in control group peaked after an early rise in TXB2 levels, and reached maximum at one hour after contra-lateral ligations. These prostanoid release levels rose again at 6 hours. While in I2 groups, the levels of them were significantly lower compared with control group. Histological examination of the transplanted lung after assessment, revealed disruption of alveoli forced by pulmonary edema in control group. In contrast, there was minimal fluid extravasation without alveolar disruption in both I2-10 and I2-50 groups. There were no significant differences between I2-10 and I2-50 groups. Although it dose not protect the implanted lung completely from developing edema, the ONO-1301 administration (10 micrograms/kg/min) to the donor and the recipient resulted in prevention of TXA2 and PGI2 release and improvement of the respiratory function and pulmonary hemodynamics after reperfusion. We conclude that it seems beneficial to administer the ONO-1301 to the donor and the recipient in order to regulate the prostanoid release and maintain the early graft function.
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PMID:[Beneficial effect of a stable PGI2 analogue (ONO-1301) on prostanoid release after reperfusion in canine left single lung allotransplantation model]. 945 4

The efficacy and safety of the angiotensin converting enzyme inhibitor enalapril in dogs with naturally acquired class III or class IV heart failure was evaluated in this study. Eighteen small-breed dogs with insufficiency of their mitral valves, but without other diseases were included in this study over a period of six months. When necessary due to massive pulmonary edema or high serum potassium concentrations, furosemide was added to the therapy with enalapril. No other drugs, including digitalis, were used in this study. The treatment was followed by anamnesis, clinical examinations, electrocardiography, radiography, echocardiography and laboratory diagnosis. Examinations were performed before treatment and after one week, after six weeks and after six months of treatment. 72% of the dogs improved in NYHA classification until the end of the study (p < 0.05). The incidence of seizures due to syncopes or severe respiratory distress decreased during this study (p < 0.01). For 28% of the dogs this treatment was not successful. In the electrocardiographic, radiographic and laboratory examinations statistically significant changes could not be recorded. The decrease in heart rate did not reach statistical significance. The echocardiographic investigation evaluated a significant decrease in fractional shortening and in the diastolic diameter of the left ventricular wall (p < 0.05 respectively p < 0.01), but no significant change in the diastolic or systolic diameter of the interventricular septum. The average oral dose of enalapril was 0.38 mg/kg body weight b.i.d., the average dose of furosemide was 0.37 mg/kg body weight b.i.d. in the first week of the study and was raised to 0.74 mg/kg body weight b.i.d. until the end of the study. Side effects like diarrhea, vomiting or reduced appetite did not increase during the course of the study. However one dog was excluded from the study because of repeated vomiting after six weeks of treatment. This study shows the beneficial clinical and hemodynamic effects and the security of the therapy with enalapril for dogs with heart failure due to mitral insufficiency.
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PMID:[Treatment of mitral valve insufficiency in dogs with the ACE inhibitor enalapril. A clinical progress study]. 953 70

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


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