In the hibernating (diapausing) Colorado potato beetle, Leptinotarsa decemlineata Say, the flight muscles show pronounced degeneration. The muscle fibrils are greatly reduced in diameter and the sarcosomes are virtually absent. Similar signs of degeneration could be produced by extirpation of the postcerebral complex of endocrine glands, the corpora cardiaca and corpora allata. Reimplantation of active postcerebral complexes resulted in a very rapid regeneration of the muscle fibrils and new formation of sareosomes.
To examine the role of nicotine in the augmentation of elastase-induced emphysema by cigarette smoke, animals that had been pretreated with porcine pancreatic elastase (PPE) were exposed to cigarette smokes that had a five-fold difference in their nicotine concentrations. Young adult female Long-Evans rats were divided into seven groups: (1) untreated controls; (2) low nicotine cigarette smoke exposure (Kentucky 2A1 reference cigarettes; 35.0 mg total particulate matter, 0.42 mg nicotine, and 0.38 mg nitrogen oxides per cigarette); (3) high nicotine cigarette smoke exposure (Kentucky 2R1 reference cigarettes; 38.8 mg total particulate matter, 2.2 mg nicotine, and 0.34 mg nitrogen oxides per cigarette; (4) PPE alone; (5) PPE + sham smoke exposure; (6) PPE + 2A1 smoke exposure; and (7) PPE + 2R1 smoke exposure. Three days after intratracheal administration of PPE (400 IU/kg), animals in the smoke-treated groups were exposed to 10 puffs of cigarette smoke daily, 7 days/wk for 14 wk. Sham-treated animals received room air in place of cigarette smoke. After the exposures, pulmonary function tests were performed under general anesthesia. Whole lungs were examined for gross pathologic changes, and samples of lung tissue were harvested for quantitative morphometry. Cigarette smoke exposure alone did not produce significant changes in pulmonary function or structure. On the other hand, treatment with elastase alone produced a constellation of pulmonary functional and structural changes that were pathognomonic of emphysema. Exposure to 2R1 but not 2A1 cigarette smoke significantly augmented the emphysematous changes produced by PPE.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Lung Injury (ALI) and the Acute Respiratory Distress Syndrome (ARDS) are severe respiratory diseases that have a very poor prognosis and have numerous causes. Despite a great deal of research and investigation since the initial description of ARDS 30 years ago many questions about the pathogenesis, treatment and outcome of the disease remain unanswered. Although there is evidence to suggest that outcome of ALI and ARDS is improving, the reasons why are unknown and there is not yet a well developed treatment for these diseases. Inhalation injury resulting from exposure to pyrolysis and combustion atmospheres is among the causes of ALI/ARDS. Little is known of the mechanisms of fire related inhalation injury that results in the development of ALI/ARDS. There is a paucity of information about fire atmosphere exposure response relationships for smoke-induced inhalation injury. Although there is considerable information about the pulmonary toxicity of many of the more common constituents of fire atmospheres, little is known about the pulmonary toxicity of mixtures of these constituents. Fire related pulmonary health risks are of particular concern to the Navy due to the limited opportunity to escape the inhalation hazards posed by shipboard fires. Consequently the Naval Medical Research Institute Detachment (Toxicology) has undertaken a research program to develop research models of combustion atmosphere induced ALI/ARDS which can be exploited to systematically address some of the questions surrounding fire related ALI/ARDS. ALI/ARDS has been the topic of a vast amount of research, numerous symposia, working groups and their published proceedings, book chapters, and books. Less information is available regarding experimental models of smoke induced lung damage, however the literature on the subject is extensive. Consequently this article is intended to provide the reader with a primer or cursory "overview" of ALI and ARDS from a toxicological perspective and should not be considered comprehensive.
Chloropentafluorobenzene (CPFB) has been identified as a can didate simulant for nonpersistent chemical warfare agents. Acute toxicity studies have shown that CPFB has limited adverse ef fects on laboratory animals. A 21-day inhalation study of rats and mice to 2.5, 0.8, and 0.25 mg CPFB/liter resulted in re duced weight gain in male and female rats exposed at the high concentration only and identified the liver as a potential target organ. This multiconcentration inhalation study was designed to detect a no-observable-effect level associated with repeated expo sure to CPFB. Male and female rats and mice were exposed to 250, 50, or 10 mg CPFB/m3 (0.25, 0.05, or 0.01 mg CPFB/li ter) for 13 weeks. No treatment-related effects on body weight, clinical chemistries, mortality, absolute or relative organ weight or histopathology were noted.
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