Some pubertal children are susceptible to orthostatic stress but little is known about mechanisms of circulatory adjustment to the posture change in children. We investigated beat-to-beat blood pressure (BP) and heart rate (HR) responses to active standing in 173 schoolchildren, 92 boys and 81 girls, aged 6-18 years (mean age: 13.4 years) using a non-invasive continuous monitoring system (Finapres 2300, Ohmeda). The subjects were divided into four age groups: prepubertal I (7-9 years), prepubertal II (10-12 years), pubertal (13-15 years) and young adult (16-18 years). Supine BP increased and HR decreased with age. At the onset of active standing two older groups showed a significantly larger initial drop than the prepubertal groups (-36 +/- 15 versus -15 +/- 16% reduction for systolic BP and -36 +/- 14 versus -20 +/- 19% for diastolic BP, respectively, p < 0.01). Moreover, the pubertal group had a significantly smaller vasoconstrictor index than prepubertals and two older groups had a significantly more prolonged BP recovery time. In keeping with this the pubertal group most frequently had hypotensive symptoms during active standing. The rise in HR at the peak was higher in two older groups than in prepubertals (34 +/- 9 versus 29 +/- 8 beats/min-1, respectively, p < 0.001), whereas the baroreflex index was almost identical for the four groups. The effect of body proportion on BP responses was not found. There was no significant difference in BP and HR changes in the later stage during 7 min of standing. These results indicated that pubertal children were more susceptible to orthostatic stress, probably due to abnormal BP responses in the initial phase of active standing, which seemed to reflect enhanced cardiopulmonary reflexes and diminished sympathetic activation associated with the age. Moreover, BP reduction at an initial drop of more than 60% or a recovery time of more than 25 s might be postulated to be an abnormal circulatory response.

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Aged mice exhibit an increase in their body weight (BW), which is associated with fat deposit increase. Epidermal growth factor (EGF) concentration in the submandibular gland also increases with aging. We examined the effects of elevated EGF on the adiposity of aged female mice. Studies were started in two groups of animals consisting of sham-operated (n = 10) and sialoadenectomized (n = 10, Sx; surgical removal of the submandibular glands) mice at 8 weeks of age. Body weight gain and food intake were measured throughout 78 weeks of age in these two groups. Body weight was significantly less in the Sx group throughout 78 weeks, while food intake was not changed by Sx after 12 weeks of age. To examine further if EGF plays a role in the induction of adiposity in aged female mice, sham-operated animals were given 100 microliters anti-EGF rabbit antiserum (anti-EGF group, n = 5) or normal rabbit serum (control group, n = 5) every 3 days, and Sx animals were given 5 micrograms/day EGF (Sx+EGF group, n = 5) or saline (Sx group, n = 5) from 78 weeks of age for 3 weeks. At 81 weeks of age, all animals of these four groups were killed, and carcass fat deposition and fat cell sizes were measured. Although the relative weights (weight ratio to BW) of the liver and kidney were not changed by Sx and anti-EGF treatment, the relative weights of mesenteric and subcutaneous fat tissues and adipocyte weights were significantly decreased in Sx and anti-EGF groups compared with the control group. Moreover, both acyl-CoA synthetase (ACS) and lipoprotein lipase (LPL) mRNA levels were significantly decreased by Sx or anti-EGF administration in mesenteric and subcutaneous fat tissues. On the other hand, EGF administration to Sx animals had no effect on BW, fat tissues and adipocyte weights, and ACS and LPL mRNA levels. The results, however, were consistent with the fact that adipose tissue EGF receptors were down regulated in Sx mice. These findings suggest that EGF may play a role in the induction of adiposity in aged female mice.

The acute toxicity of hydrofluoric acid (HFA) was investigated in a 24-h lethal dose study of intravenous infusion in rats. The lethal dose lowest (LDLo) and LD50 were 13.1 and 17.4 mg/kg, respectively. Harmful systemic effects were also studied 1 h after acute sublethal exposure to HFA. The maximum dose was set at 9.6 mg/kg (LD5). Rats were injected with HFA (1.6, 3.2, 6.4 or 9.6 mg/kg), saline, sodium fluoride (NaF) or HCl solution. NaF and HCl solution concentrations corresponded to the F- and H+ concentrations of 9.6 mg/kg HFA. Blood urea nitrogen (BUN) and Cr were significantly increased in response to HFA concentrations greater than 3.2mg/kg. Acute glomerular dysfunction also occurred at HFA concentrations greater than 3.2 mg/kg. HCO3- and base excess (BE) were significantly decreased in the 6.4 and 9.6 mg/kg groups. Ca2+ was significantly decreased, and K+ was increased in the 9.6 mg/kg group. BUN was significantly increased in the NaF and HFA groups and was increased in the HFA group compared with that in the NaF group. Cr was significantly increased in the HFA group only. HCO3- and BE were significantly decreased in the NaF and HFA groups and were increased in the HFA group compared with values in the NaF group. Ca2+ was significantly decreased in the NaF and HFA groups, and K+ was significantly increased in the NaF and HFA groups. F- exposure directly affected serum electrolytes. Mortality was thought to be due to cardiac arrhythmia resulting from hypocalcemia and hyperkalemia. Metabolic acidosis and renal failure were more severe in response to HFA exposure than in response to NaF exposure because of more free F-, which has strong cytotoxicity, in the HFA group than in the NaF group. Lethal effects of HFA are promoted by exposure routes such as inhalation that cause rapid absorption into the body. Even low exposure to HFA can cause acute renal dysfunction, electrolyte abnormalities and metabolic acidosis. These complications result in a poor prognosis.