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Copyright of Der Radiologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der Radiologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The effects on specific airway conductance (sGaw) of placebo, betaxolol and propranolol following the inhalation of salbutamol were studied in 8 healthy volunteers by whole body plethysmography. Each subject received placebo and single oral doses of betaxolol 40 mg and 80 mg, and propranolol 160 mg, and 320 mg. sGaw was measured before dosing and after 2 h, just before salbutamol was inhaled. It was then measured again after 15 min and 0.5, 1, 2, 3, 4 and 6 h. sGaw 2 h after the beta-blockers did not differ from the value whilst on placebo. The peak response to salbutamol after placebo and both doses of betaxolol was almost identical, whereas it was significantly reduced after propranolol. The AUC of the response to salbutamol over 6 h showed a reduction of 11% after betaxolol and of 19% after propranolol ( p<0.01 between β-blockers). The results indicate that, after betaxolol and in contrast to propranolol, a proportion of the bronchial β-receptor population remains available to a β-agonist. [ABSTRACT FROM AUTHOR]

The effect of calculation stress on hemodynamic parameters and plasma adrenalin and noradrenalin was studied in two groups of 6 male subjects, before and during β-Blockade. One group received propranolol 15 mg i. v. and the other received mepindolol sulphate 0,5 mg i. v. There was an increase in heart rate, cardiac output and blood pressure during mental stress. A significant increase in plasma adrenalin but not in noradrenalin occurred at the same time. The stress-induced rise in HR but not that in blood pressure could be prevented by β-receptor blockade with proprandolol and mepindolol sulfate. The peripheral resistance (PR) and diastolic blood pressure in stress were even higher after propranolol than in the control study. Propranolol had no effect on the increased adrenalin concentration during stress, but it was prevented by mepindolol sulfate. There was no correlation between the increase in HR and that in adrenalin during stress, but the HR in stress and the HR reaction to infused isoproterenol were highly correlated. [ABSTRACT FROM AUTHOR]

Copyright of Pneumonologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Clinical experiences in 23 cases of bronchial adenoma, 15 men and 8 women, are reported. These patients were admitted to a pneumophtisiology department between 1949 and 1970. Twenty-two adenomas were carcinoid and one cylindromatous. In 12 cases the correct histological diagnosis was established preoperatively by bronchoscopy and biopsy. Eighteen tumours were central and 5 peripheral. Twenty-one patients presented because of symptoms existing for an average of 2,9 years, 2 patients were symptomless. Twenty patients underwent surgery and resection proved possible in 19 of these cases. Stress is laid on the importance of preoperative histological diagnosis for the indication and scope of resection. [ABSTRACT FROM AUTHOR]

Aims To investigate the effect of the angiotensin converting enzyme inhibitor, benazepril, on pulmonary function. Methods We investigated the influence of benazepril, on lung function and the interaction with inhaled salbutamol (0.1 to 6.6 mg) and histamine (0.03 to 30.69 g l−1 ) in normal subjects. Benazepril 20 mg, salbutamol 8 mg, propranolol 160 mg, and placebo were given orally once daily over 10 days. Results On day 8, there was no difference in the area under the salbutamol dose-response curves between benazepril, placebo and oral salbutamol (P >0.05), propranolol shifted the curves to the right (P<0.05). On day 10, histamine challenge resulted in following PD35sGaw values (geometric mean and 95% CI): with placebo 1.02 (0.95-1.09) g l−1, benazepril 1.04 (0.99-1.08), salbutamol 1.19 (1.13-1.25), propranolol 0.57 (0.50-0.65). Conclusions Benazepril had no influence on baseline lung function, caused no interaction with inhaled salbutamol and the bronchial response to histamine was similar to placebo. However, our findings in normal subjects cannot be extrapolated automatically to asthmatics. [ABSTRACT FROM AUTHOR]