Sympathetic outflow to brown adipose tissue (BAT) contributes to both thermoregulation and energy expenditure in rats through regulation of BAT thermogenesis. Acute cold exposure in mature animals augments BAT thermogenesis; however, the enhanced BAT thermogenic response returns to normal shortly after cessation of the cold exposure. In this study, we sought to determine whether cold exposure in early neonatal life could induce enhanced responses in the sympathetic outflow to BAT and whether this altered sympathetic regulation would be sustained after the cold stimulus was removed. BAT sympathetic nerve activity (SNA) was recorded in urethane-chloraloseanesthetized, artificially ventilated rats that were raised from birth in either 18 or 30°C environments and then, at 8 weeks of age, were maintained in 23°C for at least 4 weeks. An acute hypothermic stimulus, disinhibition of a brainstem thermogenic network in the raphe pallidus, or electrical stimulation in this raphe site produced increases in BAT SNA that were twice as great in rats reared at 18°C as in those reared at 30°C. The norepinephrine content of the interscapular BAT (IBAT) and the number of sympathetic ganglion cells projecting to interscapular BAT were 70% greater in the 18°C-reared rats. We conclude that neonatal exposure to a cold environment induces a permanent developmental alteration in the capacity for sympathetic stimulation of BAT thermogenesis that may be mediated, in part, by a greater number of sympathetic ganglion cells innervating BAT in coldreared animals.
The kinetics of the decomposition of ammonium perchlorate (AP) in the presence of rare earth oxides, yttrium oxide (Y2Oa) and lanthanum oxide (La2Oa) as catalysts have been investigated. The Prout-Tompkins and contracting-cube equations have been found to fit the isothermal thermogravimetry data of eatalysed AP decomposition. Gases evolved during catalytic decomposition of AP were analysed by infrared spectroscopy by matrix isolation technique. The mechanism of the catfflysed thermal decomposition of AP has also been disseussed in terms of an electron transfer process.Ammonium perchlorate (AP) has been found to play a key role in the combustion of composite solid propellants. The thermal decomposition of AP has been studied over an usually wide range of temperature [1]. Ammonium perchlorate is stable at room temperature but decomposes to a measurable extent at temperature exceeding 150 ~ It has also been observed that the decomposition and burning properties of AP can largely be improved by using various catalysts [2,3]. As a result chromium oxide, zinc oxide, copper oxide, copper chromite etc., find use in propellants. The effect of catalysts on the combustion of composite propellants has also been dealt with by many authors [4,5]. Solymosi has reviewed the effect of different oxides and salts on the slow and fast decomposition of AP [2]. The Prout-Tompkins, Avrami-Erofeyev and the contracting-cube equations have been found to fit the data. Furthermore, kinetic parameters for the catalytic AP decomposition in the acceleratory as well as deceleratory periods have also been reported b~, some workers [6,7].We have studied the kinetics of the thermal decomposition of AP in the presence and absence of catalysts. Rare earth oxides, yttrium oxide (Y 203) and lanthanum oxide (La~O3) were used as catalysts. The Prout-Tompkins and contracting-cube (n ~ 3) equatiOns were found to fit the TG data for the catalysed thermal decomposition of AP. Also, an attempt is made to identify the gases evolved at different terriperatures during the decomposition in the presence and absence of catalysts by inl~rarrd spectroscopy.
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.