Methysergide in migraine prophylaxis.
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Biomedical subjects
Publications and source records attributed to E Pedersen.
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Parasympathetic cholinergic stimulation is excitatory for bladder and colon--rectum, normal as well as uninhibited. This is documented by pharmacological and neuroanatomical studies in man. The bladder and the left half of colon and rectum have motor supply in common as demonstrated by surgical intervention on sacral nerves. More detailed studies can be performed by electrical stimulation of sacral roots or rootlets. Sympathectomy may cause alteration of voiding pattern, but often only temporarily, and generally with no alteration of defecation habits. The sympathetic innervation is sparse in the human bladder, but alpha- and beta-adrenergic receptors have been demonstrated. The alpha-adrenergic blocking agent thymoxamine is able to cause a shift in the cystometrogram to the right, and to relax the spastic pelvic sphincters by i.v. administration. Like other alpha-adrenergic blocking agents, it can relax the proximal part of the urethra. The effect of other stimulating and blocking adrenergic compounds are reported, but further studies are needed. No simultaneous reactions are generally recorded in the uninhibited bladder and rectum, and no correlation was found between the hyperactivity of the uninhibited neurogenic bladder and colon.
A re-designed and simplified respiratory disease questionnaire was self-completed by 245 coke oven workers who previously were interviewed using the Standardized Medical Research Council/National Heart and Lung Institute form. The self-completion survey yielded significantly greater numbers of positive responses to various questions; nearly twice as many men were classified as having chronic bronchitis based on responses to the self-administered questionnaire. The severity of symptoms correlated with various factors such as the worker's smoking history; family history of lung disease, and job history. We suggest that, when compared with an interview using the British Medical Research Council/National Heart and Lung Institute respiratory disease questionnaire, a simplified, self-completion form may serve as a less expensive, more sensitive, and equally uniform and selective epidemiological tool. Self-completion forms deserve the attention and study previously afforded the interview process.
BACKGROUND: In individuals with cirrhosis the normal inhibiting effect of glucose on urea synthesis is lost, probably because of very high concentrations of glucagon. In agreement, glucose does not prevent the inducing effect of glucagon on urea synthesis in normal humans. In contrast, the sugar alcohol, xylitol, prevents the increasing effect of glucagon in normal humans. We, therefore, examined the effect of xylitol on urea synthesis in individuals with cirrhosis and hyperglucagonemia. METHODS: Urea synthesis, calculated as urinary excretion rate corrected for accumulation in total body water and intestinal loss, was measured during infusion of alanine (2 mmol/[h x kg body wt]) and during infusion of alanine superimposed on infusion of xylitol (0.12 g/[h x kg body wt]) in 8 individuals with biopsy-proven alcoholic cirrhosis. The functional hepatic nitrogen clearance (FHNC), ie, urea synthesis expressed independent of changes in plasma amino acid concentration, was calculated as the slope of the linear relation between the urea synthesis rate and the plasma amino acid concentration. RESULTS: All individuals had elevated basal plasma glucagon concentration (261 +/- 61 ng/L; mean +/- SEM) and a markedly increased response to alanine infusion (1037 +/- 226 ng/L). This was not changed by xylitol. Neither the basal urea synthesis rate (13.2 +/- 2.5 mmol/h) nor the alanine-stimulated urea synthesis rate (76.8 +/- 3.64 mmol/h) was changed by xylitol. FHNC during the infusion of alanine alone was 10.5 +/- 0.9 L/h and did not change during the concomitant infusion of xylitol (10.1 +/- 1.1 L/h). CONCLUSIONS: Xylitol reduces neither urea synthesis nor FHNC. The data do not support an important role of xylitol as a nitrogen-sparing agent in cirrhosis.
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Chronic hypertension causes the lower and upper limits of CBF autoregulation to reset to higher blood pressure levels. In the present study we examined whether the theophylline derivative P-23, which had lowered blood pressure in SHR, would influence CBF autoregulation. P-23 (10 mg/kg po) was administered once daily for 4 weeks and tail systolic pressure was measured weekly in this P-23 group and in a control group of SHR. At the end of the treatment period, CBF autoregulation was studied. CBF was determined using the intracarotid 133Xe injection method in halothane/nitrous oxide anesthetised animals. The lower and upper limits of autoregulation were studied in two subgroups of rats by, either raising blood pressure (MAP) stepwise with norepinephrine or lowering MAP stepwise by controlled bleeding and measuring CBF at MAP intervals of 10 mmHg. In the P-23-treated group, blood pressure fell significantly but in the control group, blood pressure increased slightly. The lower part of the autoregulation curve was shifted towards lower pressure in the treated group and the lower limit of autoregulation was significantly different from that in the control. The upper limit of autoregulation was above 180 mmHg in both groups. The beneficial effect of P-23 on CBF autoregulation should be taken into consideration during chronic administration in clinical studies in man.
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