Biomedical subjects
Publications and source records attributed to E Hoffer.
Aortobronchial fistula presenting as massive hemoptysis is a rapidly fatal process that is extremely difficult to manage. We report a case in which endovascular occlusion of a fistula between a thoracic aortic pseudoaneurysm and lung was successfully managed by placement of an aortic endovascular stent-graft. Stent-grafting is a promising technique in managing complications of thoracic aneurysms and grafts.
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We report the case of a 73-year-old woman who presents an acute mitral regurgitation secondary to fibro-elastic degenerescence. A mitral valvuloplasty is rapidly performed with complete disappearance of valvular insufficiency and the patient leaves the hospital ten days later. Degenerative mitral regurgitation is commonly seen in elderly patients. This constitutes an excellent indication for mitral valvuloplasty, rather than valve replacement. In our experience, mitral valvuloplasty leads to a complete correction of valvular regurgitation without neither stenosis, nor subvalvular obstruction. Left ventricular function is preserved, as subvalvular apparatus is conserved. This approach allows, in the absence of specific indication, anticoagulation withdrawn two to three months later.
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The present work is focused on the formation of the inflammatory mediator leukotriene B4 (LTB4) in the lungs of paraquat (PQ)-intoxicated rats. The levels of LTB4 and the number of neutrophils in lung lavages of PQ-intoxicated rats, measured 12 h after 30 mg/kg PQ, increased significantly compared with those of control animals; administration of 50 mg/kg IP N-acetylcysteine (NAC), 8 h after PQ, inhibited this effect. The release of LTB4 from alveolar macrophages (AM) or alveolar epithelial type II cells from healthy animals incubated with PQ and/or NAC did not offer' an explanation for the effect of these chemicals on LTB4 in the bronchoalveolar lavage fluid (BALF). The PQ-enhanced, NAC-inhibited release of arachidonic acid (AA) by alveolar epithelial type II cells did, however, explain our in vivo results, when one assumes that the AM synthesize their 5-lipoxygenase products from alveolar epithelial cell-derived AA, an hypothesis demonstrated already by other researchers.
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Identification of myocardial viability is of great clinical importance in patients with acute coronary events or chronic coronary artery disease. Stress echocardiography has emerged as a new accurate and cost-effective imaging modality to detect contractile reserve. Numerous studies have recently been published in this field. This article summarizes the main findings of these investigations and presents practical aspects of the method.
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The authors report a case of tricuspid blood culture-negative endocarditis where serologic investigations showed high titers of antibodies against. Chlamydia pneumoniae, thus suggesting its possible role as the causal agent. The treatment consisted of polymicrobial therapy using ciprofloxacine and doxycycline with favorable response thus avoiding surgical intervention. In all cases of culture-negative endocarditis not responding to classic empiric antibiotics, Chlamydia infection should be suspected. Although rare cases of endocarditis due to Chlamydia pneumoniae have been reported in the literature, to our knowledge, this is the first case of isolated tricuspid valve endocarditis due to this agent to be reported.
A protective effect of N-acetylcysteine in oxidative lung damage was reported by a number of workers; however, the mechanism underlying this effect was not thoroughly elucidated. The present research investigates the protection by N-acetylcysteine against paraquat-induced cytotoxicity to alveolar type II cells, which are known to be specific targets of paraquat toxicity in vivo. We found that addition of 1 mM N-acetylcysteine to alveolar type II cells incubated with 1 mM paraquat reduced the cytotoxic index from 17.4 +/- 1.3% to 9.3 +/- 1.5%. This effect could not be explained by the interference of N-acetylcysteine with the active uptake of paraquat by type II cells. Incubation of these cells with N-acetylcysteine enhances their glutathione content, thus reducing the paraquat- induced depletion of glutathione in these cells. These results suggest that N-acetylcysteine exerts its protective effect by acting as a precursor for glutathione in alveolar type II cells.
Total carbamazepine (CBZ) levels in serum of 61 epileptic children were compared with saliva levels. Both resting and stimulated saliva was analyzed. The salivary levels were 38.6% of serum CBZ levels. A highly significant correlation was noted (r = 0.89, p < 0.001). Stimulation had no effect on saliva CBZ levels (r = 0.97). Salivary and serum CBZ levels were not affected by storing the samples for 7 days at room temperature. The data indicate that salivary CBZ may provide a reliable alternative monitoring method to Tegretol therapy, especially in children, in whom blood sampling is difficult. Furthermore, the samples may be collected at home and delivered to the laboratory by mail.
Liposomes with various lipid composition and sizes, prepared by two different techniques were evaluated for their potential to deliver desferrioxamine to lungs as a treatment against oxidative lung damage. Multilamellar vesicles (MLV) and reverse evaporation vesicles were prepared out of a lipid mixture containing dipalmitoyl phosphatidylcholine, stearyl amine, cholesterol and vitamin E. The administration of desferrioxamine-encapsulated liposomes to rats by the intravenous route at a dose of 100 mg kg-1, significantly prolonged the presence of desferrioxamine in all the tested organs when compared with the administration of free desferrioxamine. The injection of reverse evaporation vesicles extruded through a 2 microns polycarbonate membrane exhibited a longer residence time of the desferrioxamine and of liposomal vitamin E in lungs compared with the other types of liposomes tested. The examination of liposome components in the bronchoalveolar lavage fluid (BALF) and the alveolar macrophages recovered from BALF revealed that about 7 x 10(-3)% of the administered desferrioxamine dose was recovered by this technique at 3 and 17 h after liposome administration. This high residual concentration in the alveolar space confirms the hypothesis that liposomes can be delivered to the lung tissue when encapsulated in alveolar macrophages.
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Hyperoxia has been used extensively as a model of acute lung injury. The drug pentoxifylline has been shown to have a protective effect in other models of lung injury. We sought to determine whether pentoxifylline protects against hyperoxic lung injury in rats by decreasing the accumulation of neutrophils within the lung. A total of 84 rats were studied. Twenty four rats were randomized into four groups. Two groups of rats were pretreated for 48 h with either pentoxifylline (20 mg.kg-1) or saline, and then exposed to > 95% O2 for 60 h while treatments continued. Two groups of control rats received the same treatment regimens as the O2-exposed animals, but breathed room air. Neutrophil accumulation in the lung was quantified both by histology and myeloperoxidase activity. Lung neutrophil accumulation increased in the oxygen-exposed group receiving pentoxifylline as compared to oxygen- or air-exposed rats receiving saline injections. Total glutathione was higher in lung homogenates from the hyperoxic, pentoxifylline-treated group than in homogenates from the other three groups. To study survival, 60 rats were exposed to > 95% O2 for 120 h, 30 rats were pretreated with pentoxifylline, and 30 received saline. Survival after 120 h of exposure to hyperoxia was not altered by pentoxifylline treatment (pentoxifylline treated: 6 out of 30 survived; saline treated: 2 out of 30 survived). We conclude that pentoxifylline does not reduce mortality or lung injury in rats exposed to hyperoxia and is associated with an increase in lung neutrophil accumulation.
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