Effect of salicylates on gentamicin ototoxicity in humans

Reports showed a protective effect of salicylates, when given in low doses, against Gentamicin-induced ototoxicity in animals. The aim of the present study was to test this contention in humans. The study included 30 patients recruited from the chest department. Fifteen patients served as control and took Gentamicin, for 10 to 14 days. The study group included 15 patients taking the same dosage of Gentamicin in addition to aceryl salicylic acid. Audiologic evaluation was done in the form of pure tone audiometry, transient-evoked and distortion product [DP] oto-acoustic emission. The evaluation was done before the start of therapy and immediately after its cessation. In the study group, salicylates resulted in significant protection of outer hair cells against gentamicin-induced ototoxicity, which was manifested by the following: 1-Improved reproducibility of the transient emissions, although levels of emission decreased. 2-Increased DP peak levels. 3-Improved DP thresholds. 4-Increased DP levels-at-thresholds. The study recommended the use of salicylates as an adjuvant to Gentamicin to reduce the latter's ototoxic effects

Histological changes in the alveolar structure of the rat lung after exposure to hyperoxia

The study evaluated the effect of acute and subchronic exposure to normobaric hyperphysiologic concentrations of oxygen [O2] on the alveolar structure of rat lung. This study was carried out on thirty adult male albino rats divided equally into 5 groups. Group I: included unexposed rats, to be considered as control group, group II; included rats exposed to 95% O2 for 24 hours, group III rats were exposed as in group II and were left for recovery in room air for 2 weeks. Group IV: included rats exposed to 60% 02 for two weeks, group rats were exposed as in group IV, then left in room air for another two weeks. The alveolar structure of the rat lung for all groups was examined by light and transmission electron microscopy. The present work demonstrated that exposure to 95% 02 for 24 hours resulted in severe pulmonary congestion with extravasation of red blood cells, edema and alteration in alveolar structure, while recovery in room air for another 2 weeks did not result in repair of the alveolar structure. On the other hand, exposure to 60% O2 for 2 weeks resulted in focal affection of the alveoli with thickened inter-alveolar septum, intense cellular infiltration together with proliferation of type II pneumocyte and deposition of interstitial collagen fibers, while recovery in room air for another 2 weeks was associated with partial improvement in alveolar structure