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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The respiratory pathophysiology of A2 influenza infection was studied in mice treated with small-particle aerosols (SPA) of rimantadine or ribavirin. Untreated infections in mice resulted in survival rates of 15% or less and were characterized by (i) severe hypoventilation (decreased P(O2) and increased P(CO2)), (ii) compensated respiratory acidosis (increased P(CO2) and HCO(3) (-), with normal pH), (iii) pneumonia with increased ratio of wet/dry lung weight, and (iv) hypothermia. Treatment with SPA of rimantadine (21 mg/kg per day for 4 days) beginning 72 h after virus challenge significantly improved survival rate (80%) but failed to alter lung pathology from that found in infected, untreated mice. Rimantadine treatment decreased somewhat the severity of hypoventilation, respiratory acidosis, lung wet weight, hypothermia, and lung virus titers from that observed in infected, untreated mice. SPA of ribavirin (26 mg/kg per day for 4 days) initiated 6 h after SPA exposure of mice to virus significantly improved survival rate (95%) and reduced lung virus titers and lung pathology. Gas exchange and pulmonary edema in ribavirin-treated, infected mice were significantly improved over those of infected, untreated controls. The mechanisms for increased survival rates induced by SPA of rimantadine remain uncertain, since increased survival rates could not be ascribed entirely to improvements in lung functions. In contrast, however, ribavirin treatment appeared to improve survival rates by reducing major lung pathology and pulmonary dysfunction. This was probably mediated through the antiviral effects of ribavirin.
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PMID:Effects of small-particle aerosols of rimantadine and ribavirin on arterial blood pH and gas tensions and lung water content of A2 influenza-infected mice. 1 87

There were two cases of fatal interstitial pneumonia secondary to bleomycin sulfate administration. Although bleomycin pulmonary toxicity is generally thought to be dose-related and occurs infrequently with a total cummulative dose less than 300 to 400 units, the two reactions reported here occurred with doses of 105 and 165 units. Fatal bleomycin-induced pneumonia has been previously reported at these low dosages, and physicians should be aware that this toxic reaction may occur as an idiosyncratic response. Previous thoracic irradiation may be a predisposing factor. Patients receiving bleomycin should be meticulously monitored by interrogation for cough, dyspnea, and chest pain; by auscultation for rales; by serial chest roentgenograms; and by determinations of vital capacity and single-breath carbon monoxide diffusing capacity.
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PMID:Fatal pulmonary reaction from low doses of bleomycin. An idiosyncratic tissue response. 5 5

Eikenella corrodens is a gram-negative rod that has been identified as a cause of endocarditis, osteomyelitis, pneumonia, cellulitis, and other infections. Because it is difficult to grow unless it is incubated in 10% carbon dioxide and because it may be overgrown by other organisms, it can be overlooked as a sinus pathogen. This is a report of the isolation of E corrodens from the sinuses of three patients with sinusitis. Three important features of infection with E corrodens, which are illustrated by these cases, are as follows: (1) the indolence of E corrodens infections; (2) the unusual susceptibility pattern of E corrodens; and (3) the fact that E corrodens is often isolated in mixed culture. The purulent contents of sinus cavities should be cultured in aerobic, anaerobic, and 10% carbon dioxide atmospheres.
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PMID:Sinus infection due to Eikenella corrodens. 35 19

Adult respiratory distress syndrome (ARDS) is a common medical emergency in respiratory care complicating a great variety of traumas and diseases. An animal model from Lewe miniature pigs has been developed to study the ARDS under standardized conditions; it is based on aspiration pneumonitis, a disorder often observed in ARDS, injuring the lung alveolar surfactant system. The experimental study was conducted under neuroleptanalgesia. ARDS was produced by intratracheal application of hydrochloric acid (0.2 mol/l) in an amount of 1.0 ml/kg body wt. The animals were ventilated automatically by a standardized ventilatory pattern in IPP mode. In all animals the time course of oxygenation ratio (Pa,O2/F1O2), arterial CO2 tension (Pa,CO2), ratio of alveolo--arterial oxygen tension difference to inspired oxygen fraction (Aa,DO2/F1O2), oxygen exchange ratio ((AaDO2/Pa,O2), lung compliance (CL), inspiratory airway resistance (RrsI), dead space ratio VD/VT), pulmonary artery pressure (PAP) and systemic blood pressure were studied. Changes in quasi-static volume--pressure curves, percentage change in lung water content and gross pathological finding were used to integrate the findings into a system of pathophysiological changes in ARDS. The animal group to which hydrochloric acid was administered shows severe pulmonary distress leading to death within 3.5--7.5 h. No significant changes in the measured parameters could be observed in the control group over a 14 h period. The results suggest that aspiration pneumonitis in Lewe miniature pigs is very suitable to investigate various problems in pathogenesis of ARDS. The model provides reproducible results which correlate very well with findings in different ARDS states. The models serves both to compare clinical states and to search for newer therapeutic manoeuvres.
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PMID:Gas exchange, pulmonary mechanics and haemodynamics in adult respiratory distress syndrome: experimental results in Lewe miniature pigs. 49 31

To determine the prevalence of pulmonary dysfunction in lupus erythematosus, 24 patients with systemic lupus erythematosus (SLE) and 5 patients with discoid lupus erythematosus (DLE) were studied. Diffusing capacity for carbon monoxide was abnormal in 17 (71 percent) SLE patients. A restrictive ventilatory defect was present in 6 (25 percent) and arterial hypoxemia in 4 of 23 (17 percent). The mean ratio of forced expiratory volume in one second to forced vital capacity (FVC) was 83 percent. To test for the presence of small airways disease, maximum expiratory flow rate at 50 percent of FVC was measured on air and on an 80 percent helium-20 percent oxygen mixture. Ten patients (5 smokers and 5 nonsmokers) with SLE were nonresponders to helium suggesting small airways disease. Pulmonary dysfunction was present in 90 percent (9/10) of SLE patients with a previous history of pleuritis and/or pneumonitis, and in 71 percent (10/14) without respiratory symptoms or history of lung disease and with a normal chest radiograph. Pulmonary function tests were normal in DLE patients except for an abnormal response to helium and/or mild arterial hypoxemia in two patients, all of whom were smokers. These data indicate that there is a high prevalence of pulmonary function abnormalities in SLE including patients without clinically evident pleuropulmonary disease.
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PMID:Systemic and discoid lupus erythematosus: analysis of pulmonary function. 68 97

The indices of P a-A CO2, P A-a O2 and VD/VT were evaluated in a group of children treated with controlled ventilation (IPPV) for: pneumonia, congenital heart disease, respiratory distress syndrome or central nervous system diseases. The P A-a O2 index is regarded as the most useful one, since it enables the possibility to select a F IO2 value for obtaining an optimal P aO2. For calculation of VD/VT according to Bohr's formula during connection of the child to respirator P ECO2 was determined planimetrically from the capnographic curve. P a-A CO2 was recognized as a less useful index and difficult to interpret.
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PMID:Evaluation of P a-A CO2, P A-a O2 and VD/VT measurements during controlled respiration in children. Preliminary communication. 79 76

A marked increase in the carbon monoxide level in the blood sufficient to interfere with oxygen binding of hemoglobin was observed in a 43-year-old man during the course of extracorporeal membrane oxygenator support for acute respiratory failure from viral pneumonitis. The increased carbon monoxide level in this man was temporally related to the transfusion of large amounts of old bank blood. The etiology of an increased level of carbon monoxide in the blood during extracorporeal circulation is discussed and solutions to this problem are suggested.
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PMID:Carbon monoxide accumulation during extracoporeal membrane oxygenation for acute respiratory failure. 97 68

Patients with neurological disorders may have a reduced ventilatory response to a rising PaCO2. This is often unpredictable and may become apparent only when other complications, e.g. infections (pneumonia), occur or when the patient is subjected to general anaesthesia. This paper described a simple method suitable for screening patients who may have an impaired capacity of eliminating CO2 when stressed. Ventilatory changes were determined during the continuous recording of the CO2 concentration in end-tidal air in 20 healthy subjects, who were breathing first air and then gas mixtures containing 21% O2 and 2.5 or 5% CO2. A prediction interval with 90 and 95% probability limits was constructed for healthy individuals. The normally expected change in minute ventilation per m2 body surface area per change in PACO2 (delta versicle E/m2, l/min/delta PACO2, for this technique is also given.
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PMID:A simple technique for the determination of the ventilatory response to rising arterial CO2 tensions, suitable for patients with neurological disorders. 106 79

Progressive pulmonary insufficiency appears to be a universal response to the lung to a variety of injuries which damage the pulmonary-capillary emdothelium. Persistent hyperventilation, unresponsive to the administration of oxygen, is the earliest clinical sign of this complication of trauma and should prompt close monitoring of pulmonary function (measurement of arterial blood gas and pH levels, Vd/Vt A-aDo2, minute ventilation, vital capacity and inspiratory force) to assess the severity of the disease, the need for mechanical ventilatory support and the effectiveness of treatment. Other pulmonary complications of burn injury range from carbon monoxide poisoning and narcotics overdosage in the immediate postburn period through marked hyperventilation directly related to burn size occurring in the absence of significant parenchymal change to later occurring hematogenous and airborne pneumonia. Inhalation injury, a chemical tracheobronchitis which significantly increases the mortality of a given-sized burn, may be present immediately postburn but clinically inapparent for 48-72 hours. 133Xenon lung scans permit early diagnosis of this pulmonary injury and the timely institution of a graduated therapeutic response keyed to the severity of pulmonary disability. Knowledge of the pathogenesis of each of these complications is requisite for the physician caring for burn patients and permits the employment of rational preventive and therapeutic measures.
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PMID:Progressive pulmonary insufficiency and other pulmonary complications of thermal injury. 109 77

We have investigated the possibility that afferent vagal stimuli may be responsible for the excessive ventilatory drive during exercise characteristic of many diffuse pulmonary parenchymal diseases. Studies were performed on four conscious dogs with cervical vagal loops, in whom experimental pneumonitis was induced by the intravenous administration of complete Freund's adjuvant. Control measurements were made over a 3-mo interval prior to induction of disease which then ran a course of 6 wk. The disease was characterized histologically by a diffuse interstitial pneumonitis during the first week, and by a proliferative granulomatosis during the subsequent 4-5 wk. Physiologic disturbances at rest included decreased total lung and functional residual capacities; increased lung elastic recoil; and decreased carbon monoxide diffusing capacity. During mild-to-moderate steady-state exercise, the minute volume of ventilation (VE) and respiratory frequency (f) were increased significantly compared to control values; tidal volume (VT) was decreased significantly; and exercise tolerance (ET) was impaired. Complete cervical vagal blockade abolished the abnormally high VE, decreased f, and increased VT in all dogs, and improved ET in at least two dogs. The results indicate that afferent vagal stimuli were responsible for the excessive ventilation during exercise and contributed to the abnormal pattern of breathing.
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PMID:Role of vagal stimuli in exercise ventilation in dogs with experimental pneumonitis. 115 May 97


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