Peripheral chemoreceptor activity on exercise-induced hyperpnea in human.
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Biomedical subjects
Publications and source records attributed to Shinobu Osanai.
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To determine if doxapram stimulates the carotid body through the same mechanism as hypoxia, we compared the effects of doxapram and hypoxia on isolated-perfused carotid bodies in rabbits. Doxapram stimulated the carotid body in a dose-dependent manner. In Ca(2+)-free solution, neither doxapram nor hypoxia stimulated the carotid body. Although, doxapram had an additive effect on the carotid body chemosensory response to hypercapnia, a synergistic effect was not observed. Also, we investigated the various K(+) channel activators on the response to doxapram and hypoxia: pinacidil and levcromakalim as ATP-sensitive K(+) channel activators; NS-1619 as a Ca(2+)-sensitive K(+) channel activator; and halothane as a TASK-like background K(+) channel activator. The hypoxic response was partially reduced by halothane only, while pinacidil, levcromakalim and NS-1619 had no effect. Interestingly, the effect of doxapram was partially inhibited by NS-1619. Neither pinacidil nor levcromakalim affected the stimulatory effect of doxapram. We conclude that doxapram stimulates the carotid body via a different mechanism than hypoxic chemotransduction.
Exposure to cold is known as a potential exacerbating factor in asthmatics. However, few studies have investigated severity of symptoms during daily life in winter for asthmatics living in northern Hokkaido, the coldest region in Japan. We sent questionnaires to 126 asthmatics living in northern Hokkaido, and obtained answers from 116 patients (52 males, 64 females). Breathing difficulties during cold-air exposure were reported by 62.1% of patients. Furthermore, 19.6% of patients had experienced the need for bronchodilators following cold-air-induced attacks. Limitations to daily life in winter caused by exacerbated asthmatic symptoms were recognized by 48.3% of patients. Asthmatic exacerbation was experienced by 30% of patients in summer (May to August), compared to >35% in winter (September to April). No significant differences in results were noted between atopic and non-atopic patients. Improvements in respiratory symptoms during winter are thus necessary for better quality of life in asthmatics living in cold districts.
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Penicillin binding protein (pbp) gene alterations of 328 clinical isolates of Streptococcus pneumoniae were examined for a correlation with their antibiotic-resistance. The frequency of penicillin G (PEN-G) resistance was determined to clarify susceptibility to several antibiotics, namely PEN-G, ampicillin, sulbactam/ampicillin, cefozopram, panipenem (PAPM), clarithromycin (CLR), azithromycin (AZM) and levofloxacin (LVX). Oligonucleotide primers for three pbp genes (pbp1a, pbp2x and pbp2b) were used to detect mutations in pbp. Of the strains, 25.9% were classified as Pen-Gs, 68.0% as Pen-Gir and 6.1% as Pen-Gr. The polymerase chain reaction product for wild-type pbp1a was found in 185 isolates, that for wild-type pbp2x was found in 66 isolates and that for wild-type pbp2b was found in 213 isolates. None of these three genes was detectable in 100 isolates while all of them were detected in 64 isolates (1aw/2xw/2bw). Of those 64 isolates with 1aw/2xw/2bw, the minimum inhibitory concentration (MIC) of PEN-G was < or =0.06 mg/l for 54 isolates and 0.12 mg/l for 10 isolates. Of the 272 strains for which the MIC of PAPM was < or =0.03 mg/l, there were 85 Pen-Gs, 184 Pen-Gir and three Pen-Gr isolates. Three strains for which the MIC of LVX was > or =4.0 mg/l included one Pen-Gs and two Pen-Gir isolates. The MICs of CLR correlated significantly with those of AZM. The MIC of CLR was > or =1 mg/l for 216 isolates, and the MIC of AZM was > or =1 mg/l for 244 of them. These data suggested that PAPM may be effective against S. pneumoniae infection, although acquisition of resistance should be considered. LVX also seemed to be effective against S. pneumoniae.
Severe pulmonary hypertension is one of the fetal complications in various connective tissue diseases. We report a case of severe pulmonary hypertension associated with primary Sjögren's syndrome. In a lung biopsy specimen, there were findings of intimal and medial hypertrophy with narrowing vessel lumina and plexiform lesions. Moreover, deposits of immunoglobulin M, immunoglobulin A and complement protein C1q were found in the pulmonary arterial walls. Although pulmonary hypertension was refractory to oral prostacyclin, steroid therapy improved the clinical and hemodynamic conditions. In the present case, the immunological etiology may be related to the mechanisms of pulmonary hypertension associated with Sjögren's syndrome.
A 49-year-old woman was referred to our hospital because abnormal masses had been found in the left lung on chest radiography. This examination and CT scanning on admission both revealed a 12 x 8 mm mass in the left S5 and a 31 x 25 mm mass in the left S8. Calcification was not found in the tumors. Bronchoscopy showed narrowing of the left B5 and B8 bronchi by irregularity of the mucous membrane. No malignant cells were found in the cytological specimens, which were obtained by brushing and washing of the bronchi. Although the radiological findings suggested benign tumors, surgical resection was performed to confirm the diagnosis. The tumor in the left S5 was diagnosed as a hamartoma because it contained cartilage, lipoid tissue and lymphatic follicles. The tumor in the left S8 was diagnosed as a sclerosing hemangioma because vasculo-capillary formation by the cells with epithelial origin was seen. The pathological diagnosis of the two tumors differed, but a similar mechanism of tumorigenesis was suggested.
The effects of ambient O(2) tension on epithelial metabolism and nitric oxide (NO) production (VNO) in the nasal airway were examined in nine healthy volunteers. Nasal VNO, O(2) consumption (VO(2)), and CO(2) production (VCO(2)) were measured during normoxia followed by gradual hypoxia from 21 to 0% O(2) concentration. Nasal VO(2), VCO(2), and respiratory quotient during normoxia were determined to be 1.19 +/- 0.04 ml/min, 1.60 +/- 0.04 ml/min, and 1.35 +/- 0.04, respectively. Hypoxia exposure to the nasal cavity significantly decreased both VCO(2) and VNO [VCO(2): 1.60 +/- 0.04 to 0.96 +/- 0.03 ml/min (P < 0.01), VNO: 530 +/- 15 to 336 +/- 9 nl/min (P < 0.01)]. VNO was reduced commensurately with gradual decline in O(2) tension, and the apparent K(m) value for O(2) was determined to be 23.0 microM. These results indicate that the nasal epithelial cells exchange O(2) and CO(2) with ambient air in the course of their metabolism and that nasal epithelial cells can synthesize NO by using ambient O(2) as a substrate. We conclude that air-borne O(2) diffuses into the epithelium where it may be utilized for either cell metabolism or NO synthesis.
Pulmonary sarcoidosis in association with dermatomyositis has rarely been reported. A 52-year-old woman was admitted for evaluation of a previously unrecognized bilateral hilar lymphadenopathy on a chest radiogram in August 1995. She had been receiving oral corticosteroids for dermatomyositis, which was confirmed by the typical skin rash and the myogenic changes on an electromyogram in 1977. She had no respiratory symptoms at the time of admission. Chest computed tomography showed hilar and mediastinal lymphadenopathy with reticular shadows in the peripheral lung parenchyma. A 67gallium-citrate scintigram apparently revealed accumulation in bilateral hilums. The tuberculin skin reaction was negative. Flowcytometry of bronchoalveolar lavage fluid indicated a CD4/CD8 ratio of 5.37. Thoracoscopic biopsy specimens sampled from the mediastinal lymph nodes and the lung demonstrated non-caseating granulomas. A definitive diagnosis of pulmonary sarcoidosis was made from these findings. The chest radiographic findings were spontaneously resolved after three years with no increase in the dosage of oral corticosteroids. It is well known that an abnormal immune response playa an important role in development of dermatomyositis and sarcoidosis. This case suggested close associations in both diseases.
A 58-year-old man, a dairy farmer, was admitted to Engaru Kosei Hospital because of cough, fever and dyspnea following repeated exposure to moldy silage in a silo. Chest radiography showed ground-glass opacity and tiny nodules in both lung fields. Arterial blood gas analysis showed severe hypoxia (PaO2, 30.8 torr). The patient was referred to Asahikawa Medical College Hospital for a diagnostic evaluation. At the time of admission, his symptoms were slightly resolved and the lung density on the chest radiograph was decreased. Pulmonary function tests revealed restrictive ventilatory impairment with a reduction in diffusing capacity. Bronchoscopic examination revealed mild lymphocytosis in the bronchoalveolar lavage fluid (BALF). Neither bacteria nor fungi were cultured from the BALF. Transbronchial lung biopsy specimens showed alveolitis with lymphocyte infiltration. The symptoms and signs disappeared spontaneously without any specific treatment, such as corticosteroids or antibiotics. A provocation test consisting of silage handling elicited recurrence of his symptoms, a decrease in diffusing capacity, and hypoxia. A definitive diagnosis of hypersensitivity pneumonitis (HP) was made from these findings. Samplings from the silage revealed a gross growth of the yeast Saccharomyces cerevisiae. A serum-precipitating antibody gave a positive reaction for an extract of S. cerevisiae. These results suggested that repetitive exposure to S. cerevisiae had led to sensitization through the patient's occupational environment, resulting in the development of HP.