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Alterations in the hypoxic ventilatory response with advancing age in awake rats

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This study seeks to determine the influence of aging on hypoxic ventilatory responsiveness. We addressed the issue by comparing the hypoxic ventilatory responses in three age-groups of conscious rats: 3, 12, and 24 months old animals. Ventilation was recorded in a whole body rodent plethysmograph. Minute ventilation (E), respiratory rate, and tidal volume were considered for analysis. The rats were subjected to two levels of acute hypoxia: 14 and 11% O2 in N2. Hypoxic exposures were separated by a 15 min recovery interval in air. The part of the study between the 12 and 24 months age interval was longitudinal in that the same animals were studied twice, whereas the youngest animals belonged to a separate breed. All data were normalized to body mass. All hypoxic responses were biphasic with the stimulatory peak at 0.5 min after onset of hypoxia. The results demonstrate that there were no appreciable differences in magnitude of the peak hypoxic E responses between 3 and 12 months old rats. The hypoxic E responses and also the hypoxic ventilatory gain were, however, enhanced in the senescent rats. In these rats, the increment in peak E from 14 to 11% hypoxia amounted to 364.1±95.8 ml.min-1.kg-1, which was more than double compared with 12 and 3 months old rats (P<0.02). We conclude that ventilatory responsiveness is not curtailed in senescent rats. The respiratory system is able to compensate for any age-related handicaps in the respiratory system to maintain a stimulatory response to ventilatory stress.
The capabilities of porcine adrenal cortex mitochondria to oxidize glycerol-3-phos- phate (GP) were studied. In comparison with bovine adrenal cortex mitochondria, porcine mitochondria oxidized GP about three times more actively (18.9 vs 6.1 nmol O2/min per mg protein in the presence of ADP) and the activity of mitochondrial glycerol-3-phosphate dehydrogenase was about four times higher (33.4 vs 8.2 nmol/min per mg protein). In porcine adrenal cortex mitochondria we found similar values for succinate and GP oxidation both in the absence and presence of ADP or deoxycorticosterone (DOC). Rotenone sensitivity of DOC stimulation of GP oxidation indicated that porcine adrenal cortex mitochondria are able to oxidize GP and thus to generate NADPH from GP, presumably via reverse electron transport followed by energy-dependent NADH-NADP transhydrogenation.
In the present study we investigated the possibility of central convergence of neural pathways coming from distant anatomical regions in modulating the cough response. We addressed this issue by inducing cough from the tracheo-bronchial region on the background of capsaicin-stimulated and mesocain-blocked nasal mucosa in 14 anesthetized guinea pigs. The control group consisted of 6 guinea pigs in which the active agents, capsaicin and mesocain, were substituted for by inert physiological saline. All animals were tracheostomized, and the larynx was disconnected from the proximal part of the trachea with preserved innervations, and all were subjected to the same protocol. Cough, induced by mechanical irritation of the tracheo-bronchial mucosa, was elicited three times: in the control condition, after intranasal capsaicin challenge, and after another capsaicin challenge preceded by intranasal instillation of a local anesthetic, mesocain. The main finding of the study was that the number of cough efforts per bout, assessed from positive deflections on the intrapleural pressure recordings, was significantly enhanced by intranasal capsaicin challenge and this effect was reversed by intranasal pretreatment with the anesthetic mesocain [2.1 ±0.2 (control) vs. 3.5 ±0.4 (capsaicin) vs. 2.2 ±0.2 (capsaicin after mesocain) (P<0.01)], with no appreciable changes in the magnitude of cough efforts. The cough response in the control group remained unchanged. We conclude that tracheo-bronchial cough may be modified by neural sensory input to the brain coming from nasal mucosa. Therefore, cough reflex is subject to central convergence of peripheral neural pathways originating at distant anatomical locations.
There is general agreement that oxidative stress may induce apoptotic and necrotic cell death. Recently it has been shown that NADH can be considered an important antioxidant as it reacts with peroxyl and alkoxyl radicals under in vitro conditions. Therefore, in the present study we hypothesized that an increase in intracellular NADH using specific substrates will protect RL-34 cells against cytotoxicity of 2’-azobis (2-amidinopropane) dihydrochloride (AAPH), which is a peroxyl radical generating compound. Cells treated for 24 hours with 6.0 mM AAPH were severely damaged: mitochondria were vacuolated, and the level of free radicals significantly increased. Both apoptotic and necrotic cells were detected (11.1% and 11.4%, respectively) even after 5 hours of treatment. Pretreatment of the cells with substrates which increase the intracellular level of NADH, such as lactate, beta-hydroxybutyrate, and ethanol, distinctly inhibited AAPH-induced reactive oxygen species (ROS) formation and cell death. On the other hand, acetoacetate (AcA), which decrease the intracellular level of NADH, had opposite effects. Interestingly, NADH-generating substrates augment, while AcA reduced superoxide radical formation induced by AAPH. These results may suggest that although NADH generating substrates may exert some deleterious effects within a cell by inducing reductive stress, they diminish alkoxyl or peroxyl radical cytotoxicity. The protection is associated with a decrease in ROS formation measured by dichlorofluorescein, but with an increase in superoxide radical formation. (Folia Morphol 2009; 68, 4: 247–255)
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