[A case of mucoepidermoid carcinoma of the parotid gland with differential diagnosis].
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Biomedical subjects
Publications and source records attributed to T Yamamura.
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The effects of increasing doses of halothane, thiamylal, and ketamine on central sympathetic tone (ST) and vagal tone (VT) in cats were studied. Compound action potentials were recorded simultaneously from the cervical sympathetic trunk and the vagus nerve. After full-wave rectification, they were integrated for continuous monitoring of the tonic levels of activity. ST and VT changed characteristically with different anesthetics. Halothane depressed ST and VT equally to approximately 70%, 60%, and 30% of the control level (70% N2O in O2) at end-tidal halothane concentrations of 0.5%, 1.0%, and 2.0%, respectively. When thiamylal was given intravenously at incremental doses (3, 6, 9, and 12 mg/kg), ST was markedly reduced to 10% of the control level. The reduction in VT was relatively small and the autonomic balance shifted in the vagodominant direction. Intravenous ketamine (2, 4, 6, and 8 mg/kg) changed neither ST nor VT significantly. Halothane and thiamylal markedly reduced central sympathetic and vagal outflows that play a role in peripheral homeostatic regulation. We suggest that these two anesthetics effect attenuated or altered autonomic regulation. Ketamine produced little change in central autonomic outflow.
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In order to elucidate the relationship between the release of gastric inhibitory polypeptide (GIP) and insulin, we compared plasma GIP and insulin concentration responses to meal ingestion in normal subjects and patients with various surgical modifications of the food pathway. Nine patients with Billroth I partial gastrectomy (BI), 7 patients with Billroth II partial gastrectomy (BII), and 6 patients with total gastrectomy (TG) were tested. In BI patients the increase in blood glucose was similar to that in normal subjects, but the response was significantly greater in BII and TG patients. In TG patients blood glucose rose significantly higher in response to a standard meal than in all other groups. In BI patients the mean peak GIP level after meal ingestion was significantly higher than in normal subjects. In BII and TG patients an extremely exaggerated GIP response after the meal was observed. The insulin response to feeding was increased only in the BII and TG patients. Since the insulin response was enhanced only when both the glucose and GIP responses were magnified, we conclude that endogenous GIP is a glucose-dependent insulinotropic factor. In addition, from the fact that meal-stimulated GIP release is most marked in patients with total gastrectomy, we conclude that the direct contact of food with the GIP-producing cells is a strong mechanical or chemical stimulus for GIP release.
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Intravenous glucose infusion was performed in six dogs with and without truncal vagotomy, and plasma pancreatic polypeptide (PP) responses were compared before and after truncal vagotomy. Following truncal vagotomy, basal PP levels decreased significantly from 286 +/- 64 pg/ml (mean +/- S.E.) to 94 +/- 14 pg/ml (P less than 0.05). Basal plasma insulin and blood glucose levels also tended to be lower, but not significantly. During the infusion of glucose, blood glucose concentrations rose rapidly in both groups and after 15 min reached peak values which were not significantly different from each other. In the vagotomized group the plasma insulin response to intravenous glucose infusion was significantly lower than in the control group. Following intravenous glucose loading, plasma PP concentrations decreased rapidly in both groups, but the PP level in the vagotomized group was suppressed only to 77 +/- 4% of the basal level whereas in the control group it decreased by 45 +/- 8%, significantly lower than in the vagotomized group (P less than 0.01). These results suggest that basal PP is regulated by vagal tonus and that vagus controls, at least in part, suppression by intravenous glucose administration.
During studies on binding of low density lipoprotein (LDL) to fibroblasts from patients with the homozygous form of familial hypercholesterolemia (FH), a unique line was derived from subject M.N. This line could bind as much LDL as normal cells, or even more. However, like fibroblasts from other patients with the homozygous form of FH, it failed to show regulation of cholesterol synthesis. Analyses of the LDL receptors showed that this line could not mediate internalization of receptor-bound LDL. Studies on the fibroblasts of the parents of this subject showed that the inability to internalize LDL was hereditary and that the subject was a pure homozygote for this defect. The plausibility of this finding was supported by the fact that her parents were first cousins. The possible existence of a homozygous state of this defect was predicted by Goldstein et al. [Goldstein, J. L., Brown, M. S. & Stone, N. J. (1977) Cell 12, 629-41], but an actual case of the internalization defect in a pure homozygous form had not been found. There were no differences from normal cells in the nature of the LDL binding activity of this line, such as in its specificity, affinity, or Ca2+ requirement.
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