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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the truly elderly, a complex balance between compensatory processes and impaired organ function allows reasonably normal physical function. It is argued that beta blockade should have certain desirable qualities to minimize any impairment of organ function, thereby upsetting the quality of life. Thus a simple pharmacokinetic pattern without hepatic metabolism is less likely to cause unexpected variation in blood levels of the beta blocking agents and to have fewer risks of interactions with other drugs including nicotine. Renal-excreted beta blockers--such as atenolol, nadolol, and celiprolol--do, however, need downward dose adjustment when the glomerular filtration rates fall. The elderly are frequently categorized as having a low renin profile, which in the view of some workers may make a vasodilatory beta blocker more desirable. Hemodynamic advantages of such agents include the prime site of attack in hypertension on the increased peripheral vascular resistance, increasingly fundamental with a prolonged duration of hypertension and therefore with the aging process. Furthermore, a normal heart rate with a sustained cardiac output may avoid symptomatic bradycardia. In the elderly, respiratory function may be impaired so that loss of elastic recoil causes elderly emphysema. A highly cardioselective beta blocker should be an advantage. Finally, minimal interference with glucose and lipid metabolism should also be desirable goals.
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PMID:Required beta blocker profile in the elderly. 167 3

Bacterial infections is one of the most important complications in the patients with pulmonary tuberculosis. We reported the causative microorganisms in these cases with special reference to various clinical features and presented the recommended treatment and prophylaxis against respiratory bacterial infections in the patients with pulmonary tuberculosis sequelae. In 1988 and 1989, 63 patients with tuberculosis sequela were demonstrated to have been infected with respiratory pathogenic bacteria by the quantitative sputum culture method (greater than or equal to 10(7)/ml) in Tokyo National Chest Hospital. The male/female ratio of these patients was 3.5, and their average age was 62.5 years. Causative microorganisms of the secondary infections in the patients with tuberculosis sequela were essentially similar in those with other lower respiratory tract infections, i.e., chronic bronchitis, bronchiectasis, diffuse panbonchiolitis, chronic pulmonary emphysema, etc. Pseudomonas aeruginosa, other glucose-nonfermentative Gram-negative bacilli (GNF-GNB), and glucose-fermentative Gram-negative bacilli (GF-GNB) were the major pathogenic bacteria responsible for the chronic respiratory failure and/or fatal outcome in the post-tuberculous patients. Patients with complications, including aspergillosis, atypical mycobacteriosis, bronchial asthma, and so forth, showed no specific causative microorganism for the secondary infections except frequent isolation of Haemophilus influenzae. Our clinical observations clearly demonstrated that there were differences between the causative microorganisms in patients hospitalized during 1988 to 1989 and those in patients without admission. Gram-negative bacilli, including P. aeruginosa, GNF-GNB and GF-GNB, and Staphylococcus aureus were predominant in hospitalized patients. On the contrary, Streptococcus pneumoniae, H. influenzae, and Branhamella catarrhalis were major pathogenic bacteria in patients without hospitalization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tuberculosis sequelae: secondary bacterial infections]. 207 64

We instilled 2 mg of pancreatic elastase into the lungs, and insufflated a further 2 mg into the trachea of 6 male ferrets. Six control animals were given 0.9% NaCl (lungs) and glucose powder (trachea). This combined treatment was administered on days 1, 8 and 15. On these days, and again on days 29 and 39, we obtained chest x-rays. On the 39th day, we removed the lungs and measured the mean linear intercept. In tracheal sections, we measured goblet cell density, glandular structure and function by quantitative histology and autoradiography. Although, up to day 39, no emphysema developed, both structural and functional changes occurred in the glands: the volume density of the serous glands (S) decreased, that of the mucous glands (M) increased, the ratio S/M decreased from 2.0 to 1.5 (p = 0.05). The turnover of radioactive sulphur (indication of mucus synthesis) was significantly increased in animals treated with elastase (p = 0.001). Goblet cells increased from 0.9 +/- 0.4 to 3.4 +/- 1.8 cells per mm epithelium (p = 0.05). The results show that elastase induces structural and functional changes in submucosal glands and goblet cell hyperplasia, independently of emphysema.
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PMID:[Elastase-induced hyperfunction of submucous glands develops independent of elastase-induced emphysema]. 236 25

While numerous studies have demonstrated that the myeloperoxidase system found in neutrophils can oxidize and functionally inactivate alpha 1-proteinase inhibitor in vitro, there is little direct evidence that this phenomenon is relevant in vivo. Using incubation with tritiated porcine pancreatic elastase followed by column chromatography to quantitate binding, we demonstrated recovery of microgram amounts of functional alpha 1-protease inhibitor from bronchoalveolar lavage of hamster lungs. When exposed to the myeloperoxidase system in vitro, hamster alpha 1-protease inhibitor was 97% inactivated. Functional alpha 1-protease inhibitor recovered by bronchoalveolar lavage 20 minutes after hamsters were given intratracheal injections with myeloperoxidase and either hydrogen peroxide or glucose plus glucose oxidase was only half that recovered from control animals. These studies suggest that the myeloperoxidase system is effective in oxidizing alpha 1-protease inhibitor in vivo. They support the concept that oxidation of alpha 1-protease inhibitor by myeloperoxidase from neutrophil granules in the presence of H2O2 and halide may produce elastase-antielastase imbalance in vivo and contribute to the development of acute lung injury and emphysema in humans.
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PMID:Myeloperoxidase-induced inactivation of alpha 1-antiprotease in hamsters. 298 79

The oxidative inactivation of alpha 1-proteinase (alpha 1AP) inhibitor is a one of mechanisms that may lead to the pulmonary emphysema. This process is caused by oxidants derived from atmosphere and released from lung phagocytes. These cells produce various oxidants hydrogen peroxide (H2O2), hypochlorous acid (HClO), hydroxyl (OH.) and superoxide (O2-) radicals after inflammatory stimulation. In this study I have investigated the effects of H2O2 (1.5 x 10(-5) to 1.5 x 10(-2) M) alone or with addition of FeCl2 (50 microM) in order to generate OH., chloramine-T (1.5 x 10(-5) to 1.5 x 10(-3) M) which generates HClO, glucose 10 mg/ml-glucose oxidase (12.5 to 80 mU/ml)-H2O2 generating system, xanthine 0.2 mM-xanthine oxidase (12.5 to 80 mU/ml)-O2-2 generating system on the elastase inhibitory activity of alpha 1AP in vitro. H2O2 was weak in alpha 1AP inactivation--only concentration of H2O2 1.5 x 10(-2) caused severe loss of its activity to 23 +/- 8% inhibition of elastase. Addition of FeCl2 to H2O2 and following OH. generation did not enhance its alpha 1AP inactivation. O2-2 generating system inhibited moderately alpha 1AP. The % inhibition of elastase at concentration of xanthine oxidase 80 mU/ml was 65 +/- 7. HClO was most effective as an alpha 1AP inactivator. All used chloramine-T concentrations completely suppressed alpha 1AP activity. The obtained results and in vivo consumption of H2O2 by polymorphonuclear leukocyte myeloperoxidase for HClO production suggest that scavenging of these reactive oxygen species may be useful in prevention of emphysema.
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PMID:The comparative study of reactive oxygen species generated by polymorphonuclear leukocytes as alpha 1-proteinase inhibitor inactivators-possible application for antioxidant prevention of emphysema. 307 84

A knowledge of the relationship between nutrition and the respiratory system applied in chronic airflow obstruction (BCO) enables a better understanding of the increased frequency (30 to 50%) of protein-energy malnutrition (MEP) in this population. The physiology of the wasting in chronic airflow obstruction seems to relate to hypermetabolism (HMB) which is not compensated by an increased alimentary intake. The HMB is linked to a rise in the work of the respiratory muscles whose efficiency is altered by intrathoracic hyperinfiltration and also the consequences of MEP on the mass and function of the respiratory muscles. In the animal MEP induced by alimentary restrictions leads to a model of pulmonary emphysema and to the diminution of the synthesis of surfactant. This emphysema seems to be principally due to an alteration of the process of protein synthesis and to a diminution of lysyl-oxydase activity. The nutrients (utilised notably by the venous route) have their own pharmacological role, and in addition they have an effect on the natural equilibrium of the energy and nitrogen balance. Lipids (rich in polyunsaturated fatty acids) intervene in the synthesis of prostaglandins, and exercise some effects on the inflammatory process and the activity in the bronchial and vascular smooth muscles. Based on this fact they have been used for their anti-inflammatory role at the pulmonary level in the treatment of mucoviscidosis. The administration of amino acids changes ventilation by acting on the central neuro-muscular command mechanism (VT/TI). The perfusion of amino acids enables a restoration of the chemo-sensitivity to oxygen and to CO2 abolished by the prolonged restricted diet. Finally the partial pressure of oxygen ought to be interpreted with respect to meal times because an oral dose of glucose can provoke an increase in the PaO2 of around 10 mmHg for healthy subjects and those with BCO. A preventive and therapeutic attitude vis a vis BCO should take account of the relationship between nutrition and the respiratory system in parallel with a correction of hypoxaemia in order to avoid the development of wasting.
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PMID:[Malnutrition and chronic obstructive bronchopathies]. 314 Mar 15

Heart and lung transplantation has only provided long-term survival for patients with end-stage cardiopulmonary disease. Many more patients of potential recipients cannot receive the transplantation because of a pause of satisfactory donors. One of its reason is difficulty in prolonged heart-lung preservation and this has imposed a significant barrier to donor procurement. Using Autoperfusion of heart and lung, six hours preservation was successfully achieved in six mongrel dogs and an adequate condition for preservation was evaluated. 1. Glucose metabolism, 2. Electrolytes, 3. Acid-base balance, 4. Pulmonary blood flow, 5. Temperature, 6. Ventilation were considered important factors for long hours preservation. Heart and lung preserved for six hours were transplanted in thirteen dogs in heterotopic and orthotopic models and their functions were evaluated two hours after transplantation. The cardiac function was well preserved and pathological changes in cardiac muscle were minimum. But lung preservation was not so stable. Levels of PaO2 were variable and pathological changes of the donor lungs such as pulmonary edema, emphysema, etc were observed. Further studies were needed for lung preservation.
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PMID:[An experimental study on the heart and lung preservation and transplantation. Autoperfusion method and cardiac and pulmonary functions after transplantation]. 314 58

Positron emission tomography is a major technological advance in the characterisation of structure-function relationships within and between regions in normal and abnormal lungs (Hughes et al. 1985). The measurements are noninvasive and relatively exact since the geometric conditions are precisely defined. Regional expansion, flow (ventilation, perfusion), oxygen concentration (from VA/Q) and glucose metabolism can be measured in absolute terms per cubic centimetre of thorax or per gram of extravascular lung. Examples of structure-function relationships in normal subjects, emphysema, bronchitis and sarcoidosis are briefly presented.
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PMID:Contribution of the positron camera to studies of regional lung structure and function. 349 36

Findings from natural cases and experiments with cattle emphasise that flowering plants are the most important form of Bryophyllum (Kalanchoe) spp in poisonings in Australia. The main life-threatening lesion is myocardial. The effects on the alimentary tract are less important than was believed previously. B. tubiflorum, B. daigremontianum x B. tubiflorum, B. pinnatum and B. proliferum caused 41 recorded poisoning incidents affecting 379 cattle in Queensland between 1960 and 1984. Poisoning occurred between May and October--the flowering season of these plants. Experimental B. tubiflorum poisoning and natural poisonings produced anorexia, depression, ruminal atony, diarrhoea, heart rate and rhythm abnormalities, dyspnoea and death. Increased plasma concentrations of urea, creatinine and glucose and decreased chloride were measured experimentally. Both natural and experimental cases had myocardial degeneration and necrosis with haemorrhages of the heart and alimentary tract. Cattle with severe dyspnoea had atelectasis and emphysema of the lungs. Some cattle had mild nephrosis. The median lethal doses of B. tubiflorum flowers, roots and leaf plus stem were 0.7, 2.3 and 5.0 g dry matter/kg liveweight respectively (7, 7 and 40 g wet weight/kg). Bufadienolides have been isolated recently from B. tubiflorum flowers and the syndrome is consistent with cardiac glycoside poisoning.
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PMID:Hearts and flowers: Bryophyllum poisoning of cattle. 377 71

Intraruminal doses of L-tryptophan cause acute pulmonary edema and emphysema in cattle. The D and L isomers of tryptophan and 22 related indolic compounds were incubated with ruminal microorganisms in vitro. Incubation of L-[U-benzene ring-(14)C]tryptophan with ruminal microorganisms for 24 h resulted in 39% of the added radioactivity being incorporated into skatole, 7% into indole, and 4% into indoleacetate (IAA). D-Tryptophan was not degraded to any of these metabolites. The major pathway of skatole formation from L-tryptophan appeared to be by the decarboxylation of IAA. Incubation of [2-(14)C]IAA with ruminal microorganisms for 24 h resulted in 38% incorporation into skatole. L-[5-Hydroxy]tryptophan was degraded to 5-hydroxyskatole and 5-hydroxyindole, whereas 5-hydroxyindoleacetate was degraded to only 5-hydroxyskatole. Incubation of indolepyruvate, indolelactate, and indolealdehyde with ruminal microorganisms resulted in the formation of both skatole and indole. Under similar conditions, indoleacetaldehyde was converted to IAA and tryptophol. The addition of increasing concentrations of glucose (0 to 110 mM) reduced the formation of both skatole and indole from L-tryptophan and resulted in the accumulation of IAA. Antibiotics reduced the degradation of L-tryptophan to skatole and indole, with kanamycin and neomycin particularly effective in reducing the decarboxylation of IAA to skatole.
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PMID:Dissimilation of tryptophan and related indolic compounds by ruminal microorganisms in vitro. 454 42


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