[Sulpyrine inhalation challenge test monitored continuously by respiratory impedance and 81mKr ventilation image].

Continuous changes of respiratory impedance by the oscillation method using Asthograph and 81mKr ventilation image during saline and sulpyrine solution (100 mg/ml, 250 mg/ml) provocation were simultaneously measured in 15 adult asthmatics and 7 normal individuals. Estimation of airway obstruction by respiratory impedance using Asthograph was difficult during sulpyrine inhalation, since respiratory impedance increased gradually. In addition to the measurement of respiratory impedance, images of 81mKr ventilation were also obtained to estimate the regional ventilatory distribution. Estimation of the airway obstruction was easily obtained. Another advantage of 81mKr ventilation image is that it can estimate the regional ventilatory distribution. The site of airway obstruction provoked by sulpyrine was observed predominantly in the lower lung field. The results of our present study were as follows. 1) In 3 patient, increase of respiratory impedance and defect of 81mKr ventilation image were observed. Two cases in this group were clinically diagnosed as having aspirin-induced asthma. 2) In 7 patients, a defect of 81mKr ventilation image was observed, but no increase of respiratory impedance was observed. Five cases in this group could not be clinically diagnosed as having aspirin-induced asthma. 3) In 5 patients, neither defect of 81mKr ventilation image nor increase of respiratory impedance could be detected. These results suggest that 81mKr ventilation image on sulpyrine inhalation challenge test is a useful method for evaluating regional ventilatory distribution, but should be further investigated for application to aspirin-induced asthma.

[A case of alveolar hydatid disease of the lung in the Kansai district of Japan].

A 78-year-old man was admitted to hospital because of episodes of high grade fever and multiple nodular shadows on chest roentgenogram. He had a past history of percutaneous drainage and partial resection of the left lobe of the liver for liver abscess of unknown origin in 1987. The high grade fever was secondary to sepsis due to Citrobacter freundii. The sepsis improved with antibiotic therapy, but the abnormal shadows on chest roentgenogram did not improved. Immunoserological tests indicated a probable diagnosis of alveolar hydatid disease of the lung, which is very rare in the Kansai district of Japan. Open lung biopsy was performed and the diagnosis of alveolar hydatid disease of the lung was confirmed.

Decreased sodium dependent D-glucose transport across renal brush-border membranes in cis-diamminedichloride platinum induced acute renal failure.

Na-coupled D-glucose transport in rabbits with cis-diamminedichloride platinum (CDDP; cisplatin) induced acute renal failure (ARF) has been studied. ARF occurred at 3 days after injection of CDDP (3 mg/kg i.v.). Na-coupled D-glucose transport into brush-border membrane vesicles (BBMV) from both outer cortex (OC) and outer medulla (OM) of ARF rabbits under zero-trans condition was decreased. Increased Km (i.e., decreased affinity of transport carrier for D-glucose) in OC and decreased Vmax (i.e., decreased number of glucose carrier) in OM were observed in CDDP-induced ARF rabbits. Decrease glucose transport was also observed under equilibrium exchange condition. Intravesicular volume of BBMV from OC and OM of ARF rabbits was decreased. In homogenate and BBMV from OC and OM of ARF rabbits, activities of gamma-glutamyl transpeptidase and alkaline phosphatase (marker enzymes of brush-border membrane) were decreased. Activities of succinate dehydrogenase, glucose-6-phosphatase, and Na-K ATPase (marker enzymes of mitochondria, endoplasmic reticulum, and basal lateral membrane, respectively) were not affected by CDDP administration. These results suggested that one of the main target sites of CDDP in kidney is brush-border membrane (BBM) along the proximal tubule, that is, not only Na-coupled D-glucose transport carrier protein but also other proteins in BBM.

[Content and localization of leukotriene C4 in lung tissue during biphasic allergic bronchoconstriction in the guinea pig].

Leukotriene C4 (LTC4) is a very potent bronchoconstrictor, and is believed to be an important mediator during immediate (IAR) and late asthmatic response (LAR). No direct measurement of LTC4 in lung tissue during IAR and LAR has been reported, however, and its localized site in the lung remains unclear. In an effort to clarify these issues, the content of LTC4 in lung tissue was evaluated at the onset of antigen-induced IAR and LAR, and the distribution of LTC4 was examined by immunohistochemistry. IAR and LAR were induced by inhalation of aerosolized ovalbumin (OA) in conscious guinea pigs. The development of IAR and LAR following inhaled OA exposure was determined in sensitized guinea pigs by measurement of respiratory resistance using the oscillation method. LTC4 in lung tissue was measured by radioimmunoassay at six different stages (S1: non-treated group; S2: group before OA-challenge following sensitization; S3: IAR group; S4: group two hours after IAR; S5: LAR-positive group; S6: LAR-negative group). For immunohistochemistry, non-treated guinea pigs and the sensitized animals at the onset of LAR were used. Lung sections were stained with anti-LTC4 antibody by avidin biotin peroxidase complex method (ABC method). About 70% of the guinea pigs displayed IAR, followed by LAR that peaked at 6-20 hours after OA challenge. The LTC4 content in lung tissue was significantly increased (p less than 0.01) at the onset of IAR, but was significantly decreased (p less than 0.01) after two hours, and significantly increased (p less than 0.01) at the onset of LAR.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of hydrocortisone and aminophylline on plasma leukotriene C4 levels in patients during an asthmatic attack.

To study the role of leukotriene C4(LTC4) and the effect of hydrocortisone and aminophylline on plasma LTC4 levels in patients with asthmatic attacks, we measured LTC4 in plasma of 18 asthmatics during a wheezing attack and of 7 normal subjects. Blood samples were obtained before and after treatment with aminophylline and/or hydrocortisone injections. We extracted LTC4 using a Sep-Pak C18 cartridge for the measurement of LTC4 by radioimmunoassay. The plasma levels of immunoreactive LTC4 (i-LTC4) of the normal subjects were 142 +/- 25 pg/ml (n = 7), while those of nonatopic type asthmatic patients with wheezing attacks were 208 +/- 68 pg/ml (n = 15) (p less than 0.01). Before and after treatment with both hydrocortisone succinate (100 mg) and aminophylline (250 mg), 6 asthmatic patients with wheezing attacks had a mean plasma level of i-LTC4 181 +/- 24 and 132 +/- 18 pg/ml (p less than 0.01), respectively. On the other hand, the treatment with aminophylline 250 mg alone increased the i-LTC4 levels from 178 +/- 19 pg/mg to 213 +/- 16 pg/mg (n = 6)(p less than 0.05), while treatment with hydrocortisone succinate 100 mg decreased the i-LTC4 level 0.05 from 284 +/- 99 pg/ml to 249 +/- 85 pg/ml (n = 4)(p less than 0.05). In conclusion, the present study shows that the i-LTC4 level in venous blood of patients with asthmatic attacks is decreased significantly by treatment with hydrocortisone succinate.

Protective effects of superoxide dismutase on acute reperfusion injury of gerbil brain.

It has been postulated that oxygen-derived free radicals are produced in significant quantities upon reperfusion of ischemic brain and could cause brain edema and cell death. This study was undertaken in an attempt to examine the effect of recombinant human superoxide dismutase, a scavenger of superoxide radicals, on survival outcome and brain edema in gerbils undergoing 1-hour bilateral carotid occlusion and reperfusion. Superoxide dismutase was continuously infused over either 1 or 3 h of reperfusion. Neither low dose (100,000 U/kg bolus followed by 100,000 U/kg/h continuous infusion) nor high dose (100,000 U/kg bolus followed by 800,000 U/kg/h) recombinant human superoxide dismutase had an effect upon water and sodium content of whole brain at 1 h of reperfusion following 1 h of ischemia, but high-dose treatment effectively reduced brain water content at 3 h of reperfusion. All gerbils receiving high-dose treatment survived the 3 h of reperfusion, while 4 of the 7 gerbils in the control group died between 2 and 3 h of reperfusion (p less than 0.05). From this study, we conclude that prophylactic administration of superoxide dismutase can reduce the delayed vasogenic edema developing at 3 h of reperfusion and afford significant cerebroprotection in these models of transient global ischemia.