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The effects of injections of a synthetic adrenocorticotropin (ACTH 1-17, Synchrodyn) on the rate of DNA labeling in the metaphyseal bone of CD2F1 mice were tested on a chronopharmacological dosing schedule. Groups of mice that had been conditioned to a 12-hr light/12-hr dark schedule were injected at one of six different timepoints, 4 hr apart, during a single 24-hr span with either a low (0.02 I.U./kg) or a high (20 I.U./kg) dose of ACTH 1-17. Control groups received injections of a placebo at corresponding timepoints. Subgroups of mice were injected with [3H]thymidine ([3H]Tdr) to follow the changes in DNA labeling in the proximal tibial metaphysis at 15 min and 2, 4, 8, 12 and 24 hr after ACTH 1-17 or placebo treatment. All mice were injected with the isotope 30 min before killing, except for those killed 15 min after Rx administration where the isotope had been injected 14 min before killing. The data were analyzed both by analysis of variance and by the cosinor method, the latter of which tests the fit of a 24-hr cosine curve to the data. The effect of ACTH 1-17 on the target cell population was dependent not only upon the dose but upon the time of administration. Both doses exerted time-dependent action, ranging from stimulation to inhibition of DNA labeling. Inhibition was noted when the ACTH 1-17 was administered at 2 hr after the beginning of the daily dark span when nocturnal animals become active. When administered at this circadian stage, the larger dose in particular was associated with an inhibition of DNA labeling lasting for 24 hr. The inhibitory effect was much shorter when the same dose was injected 4 hr earlier. Moreover, the large ACTH 1-17 dose had a stimulatory effect lasting for 24 hr when it was administered 2 hr after the onset of the daily light span, with a much shorter stimulation following administration of the large dose at 6 hr after the beginning of the daily dark span. A circadian stage-dependent stimulation or inhibition of DNA labeling at 2 or 14 hr after light onset, respectively, was thus complemented by an initial inhibition followed by stimulation and vice versa at 10 and 18 hr after light onset respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Many aspects of panic attacks, eg, palpitations, tremor, sweating, and an emotional sense of "fear," have been theorized to arise from sympathetic nervous system activation. However, most studies have not demonstrated clearly increased levels of catecholamines during an attack, which is contrary to this hypothesis. To explore another possible cause for the physiological changes known to occur during a panic attack, we assessed parasympathetic nervous system activity by measuring vagal tone during treatments known to produce panic symptoms: sodium lactate administration and hyperventilation. Our findings showed a marked reduction in vagal tone during both procedures. We postulate that withdrawal of parasympathetic activity may explain some of the physiological changes occurring in panic attacks and be contributing to the origin of panic.

This study reports the effects of simulation of certain aspects of hypogravity (via partial skeletal unloading) on the growth and maturation of the non-weight bearing mandibles of 41-d and 1-yr-old rats. Partial skeletal unloading was effected by elevating the hindquarters (PULEH), and this simulation was controlled with normally loaded animals fed either ad libitum or the average amount of food consumed by the the experimental group (group-mean fed). The chemical status of the mandibles after 10 d or 14 d PULEH closely resembled that of control rats. The younger PULEH rats and their group-mean fed controls demonstrated a trend toward impaired maturation of mineral and matrix moieties; yet the concentrations of calcium (Ca) and phosphorus (P) expressed as a ratio to collagen hydroxyproline content were normally distributed within a density gradient profile which separates the mineral and matrix moieties into various age-dependent fractions. These data demonstrate that 10 d or 14 d PULEH in young or old rats, respectively, is not sufficient to elicit the maturation deficit observed in the mandibles of rats flown for 18.5 d in the Soviet Biosatellite Cosmos-1129. Unless the duration of PULEH is critical, the cephalad fluid shift which is common to PULEH and spaceflight animals cannot be solely responsible for the flight-induced maturation deficit. Because the mandibles of the PULEH rats remain antigravity-postured, the results emphasize the importance of gravity unloading to the impairment of mandibular bone matrix/mineral maturation during spaceflight. Decreased gravity and, hence, gravity unloading cannot be mimicked in ground-based models of hypokinesia.

The effects of 14 days of total postcranial body immobilization (in plaster casts) on the mineralization rate and on the maturation of matrix and mineral moieties in the rhesus jaw were studied by tetracycline labeling and by density gradient methods, respectively. Immobilization did not alter the rates of periosteal and endosteal mineralization in the dense cortical bone from the lingular region of the jaw, but it did impair mineralization in osteonal bone. Osteons that continued to show radial closure did so at a normal rate. In the more trabecular cortex (premolar region) in young monkeys (3-6 kg body weight), immobilization impaired bone mineralization, as shown by lower ratios of calcium and inorganic phosphorus to hydroxyproline (Ca/HO-Pr;Pi/HO-Pr), and it reduced the rate at which the newly formed bone and mineral moieties matured. In older monkeys (6-10 kg body weight) immobilization did not alter Ca/HO-Pr and Pi/HO-Pr ratios or impair tissue maturation. These changes tended to normalize within 7 to 14 days after decasting.