Responses to human urotensin-II (hU-II) were investigated in human and rat pulmonary arteries. Rat pulmonary arteries: hU-II was a potent vasoconstrictor of main pulmonary arteries (2 ± 3 mm i.d.) (pEC 50 , 8.55+0.08, n=21) and was *4 fold more potent than endothelin-1 [ET-1] (P50.01), although its E max was considerably less (*2.5 fold, P50.001). The potency of hU-II increased 2.5 fold with endothelium removal (P50.05) and after raising vascular tone with ET-1 (P50.01). E max was enhanced *1.5 fold in the presence of N o -nitro-L-arginine methylester (L-NAME, 100 mM, P50.01) and *2 fold in vessels from pulmonary hypertensive rats exposed to 2 weeks chronic hypoxia (P50.05). hU-II did not constrict smaller pulmonary arteries. Human pulmonary arteries (*250 mm i.d.): in the presence of L-NAME, 3 out of 10 vessels contracted to hU-II and this contraction was highly variable. hU-II is, therefore, a potent vasoconstrictor of rat main pulmonary arteries and this response is increased by endothelial factors, vascular tone and onset of pulmonary hypertension. Inhibition of nitric oxide synthase uncovers contractile responses to hU-II in human pulmonary arteries.
Gum chewing for 20 min causes an increase in salivary flow rate and salivary pH. Most people chew gum for longer than 20 min, and our aim was to determine how whole mouth salivary flow rate and pH might adapt during prolonged gum chewing. Resting saliva was collected over 5 min; gum-stimulated saliva was collected at intervals during 90 min, chewing a single pellet (1.5 g) of mint-flavoured, sugar-free gum (n = 19). Subjects chewed at their own preferred rate and style. Both salivary flow rate and pH were increased above resting levels for the entire 90 min. The salivary flow was significantly greater (anovaP < 0.05) than resting flows up to 55-min chewing. The saliva pH remained significantly higher (P < 0.0001) than the resting pH even after 90-min chewing. When the experiment was repeated with the gum pellets replaced at 30 and 60 min (n = 9), similar increases in salivary flow rate and pH were found. In the latter experiment, there was no evidence of any cumulative effects on flow or pH. The persistent increase in salivary pH in particular could be beneficial to oral and dental health.
The morphology of the mandibular canal after loss of teeth has received little detailed attention. Improved documentation of this topic would allow better interpretation of dental radiographs and would enable those engaged in tooth implantation to better understand the nature of the tissue into which the prostheses are placed. In this study on mandibles from seven dissecting room cadavers panoramic radiographs usually showed the mandibular canal clearly, an incisive canal less so. The wall of the mandibular canal was similar in dentate and edentulous mandibles, and was highly perforated, as suggested by Cryer (Anderson et al., 1991). In edentulous specimens, it was composed mainly of cancellous bone with only occasional single osteons. The inferior alveolar nerve near the mandibular foramen was a large trunk, consisting of three to four nerve bundles with connective tissue sheaths. It became more loosely arranged toward the mental foramen. Medial to the mental foramen, the nerves were frequently in the form of small bundles in the marrow. Any incisive canal was ill-defined and neurovascular bundles, when present, ran through a labyrinth of intertrabecular spaces.
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