Cutoff volume of dietary fiber to ameliorate constipation in children.

OBJECTIVE: To evaluate the proper ingested volume of dietary fiber for relieving constipation in children. STUDY DESIGN: During a 3-year period, we prospectively evaluated the correlation of intake volume of dietary fiber with improvement of constipation in children. Patients were categorized into younger (3-7 years) and older (8-14 years) children. The evaluation period lasted 12 weeks. A good improvement was defined as the child exhibiting at least 60% relief of the constipation symptoms during the observation period. Freedom from constipation was observed during the last 4 weeks. RESULTS: The study population consisted of 422 patients (213 younger, 209 older), with a mean age of 7.89 +/- 4.71 years. Baseline daily dietary fiber intake of the younger and older groups was 5.97 +/- 2.35 g and 9.83 +/- 3.51 g, respectively. 227 cases (53.8 %) showed improvement of constipation, and 49.1 % of the patients had relief of constipation. Greater intake of dietary fiber was positively associated with good improvement of constipation in both groups (P = .002, and P < .001). Cutoff volumes of daily dietary fiber intake in the relief of constipation were 10 g in the younger group and 14.5 g in the older group. CONCLUSION: The cutoff of dietary fiber intake needed to relieve constipation increased with age, achievable in a 12-week intervention.

Are voltage-dependent ion channels involved in the endothelial cell control of vasomotor tone?

In the microcirculation, longitudinal conduction of vasomotor responses provides an essential means of coordinating flow distribution among vessels in a complex network. Spread of current along the vessel axis can display a regenerative component, which leads to propagation of vasomotor signals over many millimeters; the ionic basis for the regenerative response is unknown. We examined the responses to 10 s of focal electrical stimulation (30 Hz, 2 ms, 30 V) of mouse cremaster arterioles to test the hypothesis that voltage-dependent Na(+) (Na(v)) and Ca(2+) channels might be activated in long-distance signaling in microvessels. Electrical stimulation evoked a vasoconstriction at the site of stimulation and a spreading, nondecremental conducted dilation. Endothelial damage (air bubble) blocked conduction of the vasodilation, indicating an involvement of the endothelium. The Na(v) channel blocker bupivacaine also blocked conduction, and TTX attenuated it. The Na(v) channel activator veratridine induced an endothelium-dependent dilation. The Na(v) channel isoforms Na(v)1.2, Na(v)1.6, and Na(v)1.9 were detected in the endothelial cells of cremaster arterioles by immunocytochemistry. These findings are consistent with the involvement of Na(v) channels in the conducted response. BAPTA buffering of endothelial cell Ca(2+) delayed and reduced the conducted dilation, which was almost eliminated by Ni(2+), amiloride, or deletion of alpha(1H) T-type Ca(2+) (Ca(v)3.2) channels. Blockade of endothelial nitric oxide synthase or Ca(2+)-activated K(+) channels also inhibited the conducted vasodilation. Our findings indicate that an electrically induced signal can propagate along the vessel axis via the endothelium and can induce sequential activation of Na(v) and Ca(v)3.2 channels. The resultant Ca(2+) influx activates endothelial nitric oxide synthase and Ca(2+)-activated K(+) channels, triggering vasodilation.