I Although the majority of deaths resulting from exposure to sulfur mustard (HD) have been due to pulmonary dysfunction, there are no detailed accounts of the pathogenesis of HDinduced lesions in the respiratory tract. Accordingly, we investigated the early changes within the trachea and lungs of rats following inhalation exposure to HD. Anesthetized rats were exposed by intratracheal intubation to vaporized H D (0.35 mg in 100 wl absolute ethanol) or ethanol alone for 50 min. Animals were euthanatized at 0, 1, 4, 6, 12, 18, and 24 li postexposure (PE), and their respiratory tracts were prepared for histological and ultrastructural examination. In rats exposed to HD, multifocal, petechial hemorrhages were grossly evident on tlie pleural surface of the lung at 6 h PE. Atelectasis and edema of the accessory lobe occurred at 12-18 h PE. Histologically, lesions in the respiratory tract were confined primarify to the trachea, bronchi and targer bronchioles. It, HD-exposed rats, there was a progressive depletion of the bronchiolar-associated lymphoid tissue (BALTI, with necrosis of the lymphoid cells as early as 12 h PE. Necrosis and sloughing of the tracheal and bronchial epithelia at 6-12 h PE was followed by the formation of fibrinous pseudomembranes within the bronchi. Necrosis and separation of airway epithelia occurred at the mucosaUsubmucosal interface. Pseudomembranes formed almost exclusively in deepitlielialized areas overlying tlie BALT. Cartilaginous lesions, characterized by necrosis of individual chondrocytes, were evident at I2 li PE. Pulmonary edema and occasional alveolar hemorrhage occurred from I8 to 24 li PE. Small bronchioles and alveoli were relatively unaffected, and only a few inflammatory cells were observed at any time.
The effects of midazolam (MDZ), diazepam (DZ) and scopolamine (SCP) therapies on soman-induced electrocorticogram (ECoG) and biceps femoris electromyogram (EMG) activities and brain lesions were assessed in male rats. Animals received pyridostigmine (26 micrograms/kg, im) 30 min before soman (87.1 micrograms/kg, im) followed by therapy consisting of atropine (1.5 mg/kg) admixed with 2-PAM (25 mg/kg, im) 1 min later; MDZ (0.5 mg/kg), DZ (1.77 mg/kg) or SCP (0.43 mg/kg) was administered im at 1 min after the onset of convulsions (CVs). Typically, within 5 min after soman the ECoG profile changed to a full-blown, spike-and-dome epileptiform (SDE) pattern followed by CVs and increased amplitude of EMG activity. Treatment with SCP restored ECoG and EMG profiles by 30 min. At 2 hr after exposure only 1 animal demonstrated a slight abnormality in ECoG activity which was normal at 24 hr. Similarly, DZ and MDZ restored EcoG and EMG profiles by 30 min; however, in contrast to SCP, 83% of the animals demonstrated reappearance of SDE 2 hrs after soman. SCP therapy also enabled rats to move about in their cages by 30 min post treatment. In contrast, DZ- and MDZ-treated rats remained incapacitated as late as 2 hr post-exposure. Animals were euthanized at 24 hr, and the extent of soman-induced brain lesions was determined by light microscopic analysis. When present, brain lesions were minimal in SCP-treated rats. The mean brain lesion scores across all experimental conditions ranked as follows: soman control > MDZ > DZ > or = SCP = saline control. These observations suggest that SCP may be highly effective in severe soman intoxication.
Sonographic grading of ICEF is feasible and reliable. The presence of fetal ICEF in a population otherwise at low risk for aneuploidy seems to warrant the performance of fetal chromosomal analysis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.