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

The use of vasodilators represents a new approach to the treatment of cardiac insufficiency, either chronic or acute. Their field of action is venous, arterial or mixed. Decreasing the pre-load, the "venous" vasodilators lighten the congestive symptoms of cardiac insufficiency. By decreasing the post-load, the "arterial" vasodilation increases the cardiac output. Some vasodilators, venously administered, imply a continuous hemodynamic checking (Sodium Nitroprussiate, Phentolamine, injectable Trinitrine). Others are active orally (Trinitrine, Isosorbide Dinitrate, Hydralazine, etc.). Vasodilating treatment is recommended for acute cardiac insufficiency, particularly during myocardium infarct and some acute valvular insufficiencies. It is also successfully used in acute lung edema. Finally it takes an increasing importance in the treatment of chronic cardiac insufficiency.
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PMID:[Vasodilators in the treatment of cardiac insufficiency (author's transl)]. 53 77

In experiments on 50 dogs with toxic acute edema of the lung, induced with intravenous injection of 0.1% silver nitrate, the authors have studied the efficacy of accessory artificial circulation and "conservative" therapy. During the perfusion a discharge of the right portions, adequate extracorporeal gas metabolism, normalization of blood gas and acid-base balance were noted; an intensity of pulmonary edema is descreased. An intensive therapy for pulmonary edema was found to be more effective in association of "conservative" treatment with venoarterial perfusion and blood oxygenation.
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PMID:[Accessory artificial circulation in complex treatment of experimental acute toxic pulmonary edema]. 96 Apr 88

Investigation of the parameters of toxicity of 8 zinc compounds revealed some differences in the degree of their risk for persons working with them. The following TSELs (tentative safe exposure levels of harmful substances) have been determined: 0.5 mg/m3 for zinc nitrate and hydrogen and dihydrogen zinc phosphates, 2 mg/m3 for zinc carbonate and zinc selenide, as well as MAC (maximum allowable concentration) for zinc sulphide equal to 5 mg/m3. No TSEL have been set for zinc caprylate and zinc stearate, but intratracheal administration of 50 mg caprylate caused 100%, of stearate 50% death of experimental animals due to pulmonary edema. Maximum tolerable doses were 10 and 1 mg, respectively. Zinc nitrate shows an expressed irritative effect on the skin and a highly expressed effect on the conjunctiva. Zinc phosphates, zinc caprylate and zinc stearate are resorbed by the skin. In all cases, working persons must be protected from the effect of the compounds under study because even though the toxicity of a compound may be rather low, highly noxious compounds may develop in the course of the technological process, e.g., in mechanical treatment of zinc selenide and zinc sulphide monocrystals, hydrogen selenide and hydrogen sulphide, respectively, can be isolated.
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PMID:Toxicity and character of the effect of some zinc compounds. 322 Oct 90

Long acting nitrate derivatives have varying hemodynamic effects of a piridoxilate-pentaerithrityle tetranitrate administration. The purpose of this study was to assess the hemodynamic effects of a piridoxilate-pentaerithrityle tetranitrate compound and measure their duration of action. The study was carried out in 11 patients with left ventricular incompetence. All other medications, except for anticoagulants, had been discontinued 5 days earlier and patients fasted during the investigations. Each patient was given the active product (100 mg pentaerithrityle tetranitrate) and the placebo orally, under double blind conditions. Pulmonary vascular pressure, peripheral arterial pressure, heart rate and cardiac output were measured over 8 hours for 2 consecutive days. The results show a decrease in the left ventricular preload from the 30th minute to the eighth hour, which is statistically significant from the first to the fourth hour. No changes were recorded in the postload or in any of the other parameters measured or derived. These findings suggest that the compound has an anti-anginal action by diminishing the pressure in the ventricular wall and reverses pulmonary edema in left ventricular failure. The long duration of action (at least 8 hours) allows prolonged dosage intervals.
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PMID:[Prolonged hemodynamic effects of pentaerythrityl tetranitrate combined with piridoxylate]. 630 89

Ruminal bacteria can perform biochemical transformations on plant constituents that may affect the health of ruminant animals. Reactions carried out by ruminal bacteria on oxalates and some pyrrolizidine alkaloids include decarboxylation, hydrolysis and reduction steps. Prior exposure of ruminal bacteria to these substances increases the rate of detoxification, indicating an adaptive response by the bacteria to these substrates. The formation of toxic substances by ruminal bacteria also occurs and may involve similar reactions. Hydrolysis of cyanogenic glycosides and miserotoxins , reduction of nitrate and S-methylcysteine sulfoxide to nitrite and dimethyl disulfide can result in toxicity in ruminants. Similarly, the deamination and decarboxylation reactions associated with the degradation of tryptophan and tryosine result in the formation of 3-methylindole and p-cresol, which are toxic. Formation of 3-methylindole results from fermentation of tryptophan to indoleacetic acid, with subsequent decarboxylation of indoleacetic acid to 3-methylindole by a Lactobacillus sp. The 3-methylindole causes acute pulmonary edema and emphysema in ruminants as a result of mixed function oxidase metabolism in tissues. The 3-methylindole is also the cause of naturally-occurring acute bovine pulmonary edema and emphysema after abrupt pasture change. Inhibition of ruminal 3-methylindole formation by monensin and other antibiotics lowers ruminal 3-methylindole concentrations and prevents acute lung injury in experimental animals.
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PMID:Ruminal metabolism of plant toxins with emphasis on indolic compounds. 637 6

We tested whether NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, can prevent interleukin 2 (IL-2)-induced capillary leakage in tumour-bearing mice without compromising the therapeutic benefits of IL-2. C3H/HeJ female mice transplanted s.c. with 2.5 x 10(5) C3-L5 mammary carcinoma cells were treated with: nothing, IL-2 (ten injections of 15,000 Cetus units i.p. every 8 h), L-NAME (0.1, 0.5, or 1 mg ml-1 drinking water), IL-2 + L-NAME (0.1 or 0.5 or 1 mg ml-1 drinking water). Therapies were given in one round (IL-2, days 10-13; L-NAME, days 9-13) or in two rounds (IL-2, days 10-13 and 20-23; L-NAME, days 9-13 and days 19-23) after tumour transplantation. Capillary leakage was measured from the water contents of the pleural cavities, lungs, spleen and kidneys. Effects of the therapies on the primary tumour size and the number of spontaneous lung metastases were also recorded. NO production was measured as the nitrite + nitrate levels in the serum and in the pleural effusion. After the first round of therapies, addition of L-NAME significantly reduced IL-2-induced pulmonary oedema and water retention in the spleen in a dose-dependent manner. It also significantly reduced the IL-2-induced rise in NO levels in the serum and pleural fluid, but did not affect IL-2-induced pleural effusion or water retention in the kidney. At later stages of tumour growth (day 23), tumours themselves induced significant fluid retention in the lungs and the kidney, which was not aggravated further with the second round of IL-2 therapy. At this time, L-NAME therapy alone ameliorated tumour-induced pulmonary oedema. During both rounds of therapy different doses of L-NAME alone caused a reduction of primary tumour growth as well as spontaneous lung metastases, which improved further with the addition of IL-2. The combination therapy was at least as effective as IL-2 therapy. In summary, L-NAME had anti-tumour effects in vivo, reduced the severity of IL-2-induced capillary leakage in some organs and did not compromise anti-tumour efficacy of IL-2 therapy. Thus, L-NAME could be a valuable adjunct to IL-2-based cancer therapy.
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PMID:NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, ameliorates interleukin 2-induced capillary leakage and reduces tumour growth in adenocarcinoma-bearing mice. 854 5

We tested whether treatment with an inhibitor of nitric oxide synthesis (Ng-methyl-L-arginine, MeArg) can ameliorate interleukin-2(IL-2)-therapy-induced capillary leak syndrome in healthy or tumor-bearing mice without compromising the antitumor effects of IL-2 therapy. Healthy or C3-L5-mammary-adenocarcinoma-bearing C3H/HeJ mice were treated with one or two rounds of various doses of IL-2 (ten injections, i. p., every 8 h) or MeArg (ten injections s. c., every 8 h) or their combination. In an additional experiment, MeArg was given chronically in the drinking water, rather than s. c. to healthy mice subjected to one round of therapy as above. Mice were killed 1 h after their last IL-2 injection to measure the water content of the lungs and pleural cavities (markers of capillary leakage), NO production (given by NO2- and NO3- levels in the serum and pleural effusion), as well as the effect of therapies on the primary tumor size and number of spontaneous lung metastatic nodules. Results revealed that all doses of IL-2 (7500-35000 Cetus U/injection), as well as both rounds of IL-2 therapy, caused capillary leakage. However, no pleural effusion was seen after the second round in any of the IL-2-treated groups. MeArg therapy, given subcutaneously (5-20 mgkg(-1) injection(-1) in healthy and 20 mgkg(-1) injection(-1) in tumor-bearing mice), did not ameliorate IL-2-induced capillary leakage in either group of mice, and did not compromise antitumor effects of IL-2. However, subcutaneous MeArg therapy alone reduced the growth of the primary tumors, the occurrence of lung metastases and the amount of tumor-induced pulmonary edema. When MeArg therapy was given orally (1 mg/ml drinking water), a substantial drop in NO production, as well as reduction in capillary leakage was noted in IL-2-treated healthy mice. These findings suggest that NO inhibitors could be a valuable adjunct to IL-2 therapy of cancer and infectious diseases.
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PMID:Effects of N(g)-methyl-L-arginine, an inhibitor of nitric oxide synthesis, on interleukin-2-induced capillary leakage and antitumor responses in healthy and tumor-bearing mice. 862 65

We tested whether NG-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of NO synthesis, can prevent interleukin-2 (IL-2)-induced capillary leakage. Healthy C3H/HeJ female mice were treated with: nothing; IL-2 (10 injections; 35,000, 15,000, or 7,500 Cetus U i.p. every 8 h); IL-2 + L-NAME (0.01, 0.1, 0.5, and 1 mg/ml of drinking water starting 1 day before IL-2 therapy and ending with IL-2 therapy); or L-NAME alone. In the first series of experiments, mice were killed 1 h after last IL-2 injection to measure pleural effusion, and water content of the lungs, spleen, and kidney (markers of capillary leakage), as well as NO2- + NO3- levels in the serum and pleural effusion. In the two additional series, the survival of treated mice was followed. All doses of IL-2-induced capillary leak syndrome as indicated by pleural effusion, pulmonary edema, and fluid retention in the spleen and kidney. NO production was positively correlated with manifestation and severity of this syndrome. NO2- + NO3- levels in the pleural effusion were directly related to IL-2 dose, and L-NAME treatment reduced both the NO production and severity of capillary leakage, excepting fluid retention in the kidney. However, L-NAME therapy prevented IL-2-induced mortality only when combined with a middle range IL-2 dose (15,000 U/injection). In summary, oral L-NAME therapy effectively prevented IL-2-induced capillary leakage in healthy mice, suggesting its potential value as a supplement in IL-2-based immunotherapy of cancer and infectious diseases.
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PMID:NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, ameliorates interleukin-2-induced capillary leak syndrome in healthy mice. 868 Jun 49

Levels of nitrite (NO2-) and nitrate (NO3-) were measured in pulmonary edema fluid and plasma from 34 patients with early acute lung injury (ALI) and 20 patients with hydrostatic pulmonary edema. Pulmonary edema fluid from patients with ALI had significantly higher levels of NO2- + NO3- compared with pulmonary edema fluid from patients with hydrostatic pulmonary edema (108 +/- 13 microM versus 66 +/- 9 microM; means +/- SEM; p < 0.05). In addition, patients with shock had higher plasma NO2- + NO3- levels than those without shock (79 +/- 11 microM versus 53 +/- 12 microM, p < 0.05). Acidemia and increased anion gap, markers of systemic hypoperfusion, were also associated with twofold higher plasma NO2- + NO3- levels (p < 0.01). Increased levels of NO2- + NO3- in edema fluid samples were associated with slower rates of alveolar fluid clearance. Nitrated pulmonary surfactant protein A (SP-A) was also detected in the edema fluid of patients with ALI after immunoprecipitation with a specific antibody against this protein. Previously, we have shown that nitration of SP-A impairs its host- defense properties. In aggregate, the results of this study indicate that reactive oxygen-nitrogen species may play a role in the pathogenesis of human ALI.
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PMID:Increased levels of nitrate and surfactant protein a nitration in the pulmonary edema fluid of patients with acute lung injury. 1120 43

In this retrospective cohort study, 172 patients presenting to two accident and emergency departments in the UK, with acute, cardiogenic pulmonary oedema were identified. The median age of the patients was 77 years and there was an equal sex distribution. The commonest therapy given in the acute treatment of this condition was frusemide, and less than 70% of the cohort received nitrates. Only 73.8% survived to hospital discharge, and only 50.6% were alive one year later. Using logistic regression analysis, the use of nitrate medication in the emergency department was associated with improved survival to hospital discharge (odds ratio 3.04; 95% confidence interval 1.15-8.01). It is recommended that nitrates are given to all patients presenting to emergency departments with acute cardiogenic pulmonary oedema whose blood pressure will allow the use of such therapy.
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PMID:Epidemiology, treatment and outcome of acidotic, acute, cardiogenic pulmonary oedema presenting to an emergency department. 1250 Oct 30


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