[Self-fixed endoprosthesis for biliary tract drainage without surgery].
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Biomedical subjects
Publications and source records attributed to K Thor.
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The effects of neurotensin on colonic motility were investigated in 6 healthy volunteers (rectosigmoid area) and 7 patients (ascending colon and at the splenic flexure). Neurotensin (12 pmol/kg X min) infused intravenously for 30 min increased the duration of the contractions to 76% in the ascending colon and 46% in the rectosigmoid area. In the postinfusion period, the values were 42% and 67%, respectively. The motor activity did not change significantly at the splenic flexure. During the infusion period, the motility index increased from 870 to 4500 in the ascending colon and from 332 to 1700 in the rectosigmoid area. In the rectosigmoid area, however, a statistically significant increase was recorded first after cessation of the infusion. All subjects reported increased sensation of intestinal movement after intravenous infusion of neurotensin, and the patients discharged a median volume of 600 ml of bowel contents 20 min after cessation of the infusion. The data show that neurotensin causes an increase in colonic motility in the ascending colon of patients and also, after a latent period, in the rectosigmoid area of healthy subjects.
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In patients with obstructive jaundice, biliary decompression can be achieved by an endoprosthesis inserted by a percutaneous transhepatic approach. The prosthesis sometimes becomes dislodged and thus additional percutaneous transhepatic procedures may be required. To avoid this problem, a nondislodgeable endoprosthesis has been developed. The prosthesis is constructed with a layer of biocompatible material (hydrogel) on its surface. The hydrogel is located in grooves around the endoprosthesis and has the ability to absorb liquid, which increases its size. By placing the rings of hydrogel on either side of the obstruction, dislodgement of the prosthesis can be prevented. The nondislodgeable endoprosthesis has been inserted into 11 patients with biliary obstructions due to malignant strictures. No dislodgement has occurred and the established internal drainage reduced serum bilirubin levels without any major complications.
Endoscopic injection sclerotherapy (ST) has gained wide acceptance as emergency and definitive treatment of bleeding oesophageal varices. The long-term effects of serial ST on oesophageal motility were studied in 19 patients with cirrhosis and prior variceal bleeding. A control group of 14 patients with compensated cirrhosis has been conservatively treated for major variceal haemorrhage a median of 5 months previously. In the ST group, eradication of the varices by serial ST had been completed a median of 7 months prior to manometry. The manometric results did not differ between the controls and 11 ST patients without dysphagia (SA). In eight ST patients with dysphagia (SB), the percentage of deglutitive peristaltic contractions (DPC) in the lower oesophagus was less than in the controls (31.4 vs. 98.6%) and in the SA patients (84%). Nonpropulsive contractions instead dominated in the lower oesophagus, but were frequent also in the upper part, resembling the motility pattern seen in patients with sclerodermal involvement of the oesophagus. When seven SB patients were reinvestigated after a median of 11.5 months (without further ST), the DPC value had increased to 74.2% and the dysphagia had decreased. The lower oesophageal sphincter pressure did not differ between the controls and the subgroups of ST patients.
Even if it is more than 250 years since the first description of a lumbar hernia occurred in the literature the diagnosis is still rare. This disease is discussed in the light of a case history with a primary lumbar hernia from the Grunfelt-Lesshaft triangle. The diagnosis is usually not difficult to establish although certain differential diagnosis has to be considered. The treatment is surgical either as in the present case with a simple closure or when larger defects in the transversalis fascia are present with more extensive surgery.
The aim of the present study in man was to investigate the influence of cigarette smoking on basal plasma concentrations of neurotensin-like immunoreactivity (p-NTLI), as well as on fat-induced elevation of p-NTLI levels. On three separate occasions, habitual tobacco smokers either ingested fat (55 ml Intralipid 20%) or smoked three cigarettes, or ingested fat and smoked. The subjects were fasted overnight and told no to smoke during the fasting period. Smoking of one cigarette at one hour intervals (0, 60, and 120 min) did not change the p-NTLI levels (n = 6). Ingestion of fat caused a significant increase (n = 16) and when these two procedures were combined (n = 16), the mean integrated p-NTLI response (nM0-180 min) was 56% larger than the response after fat ingestion alone. The results show that cigarette smoking potentiates the fat-induced elevation of p-NTLI levels, whereas cigarette smoking per se has no effect.
The physiological significance of neurotensin, with respect to gut motility in man, may be to mediate postprandial, fat-induced changes in the motility pattern of the gastrointestinal tract. There is strong experimental evidence that this effect of neurotensin is endocrine-mediated. The role of neurotensin as a paracrine hormone, neurotransmitter or neurocrine hormone remains to be determined.
The effect of (Gln4)-neurotensin on antroduodenal motor activity was investigated in 7 healthy volunteers. Motor activity was monitored by measuring the intraluminal pressure in the antrum and in the proximal and middle part of the duodenum. Intravenous infusion of (Gln4)-neurotensin (6 pmol X kg-1 X min-1) for 20 min significantly increased the number of contractions in the duodenum, from 13.8 +/- 1.1 to 33.2 +/- 3.0 contractions X 5 min-1, and changed the motility pattern in the duodenum to irregular pressure waves similar to those seen after the ingestion of food. The contractile activity (amplitude X number of contractions) in the antrum and duodenum changed significantly from 230 +/- 29 to 148 X 39 and from 288 +/- 21 to 556 X 62 mmHg X 5 min-1, respectively, despite the fact that the baseline pressure gradient was unchanged. The number of antral contractions migrating to the duodenum was significantly reduced from 3.3 +/- 0.4 to 0.1 +/- 0.1 contractions X 5 min-1 and their velocity was also significantly decreased, from 18.2 +/- 1.7 to 11.1 +/- 1.7 mm X sec-1. The concentration of p-NTLI rose from 39 +/- 11 pM to a maximum of 150 +/- 14 pM at 20 min; these latter levels are within the range found after a fatty meal. Thus, (Gln4)-neurotensin changes antroduodenal motility to a pattern seen after a meal. This suggests that neurotensin, or a neurotensin metabolite, may carry the information to the antroduodenal area to decrease the rate of gastric emptying after a fatty meal.
The mechanisms behind the reduction of lower esophageal sphincter (LES) pressure by (Gln4)-neurotensin were investigated in 17 healthy volunteers. LES pressure was measured with a continuous pull-through technique. Intravenous infusion of (Gln4)-neurotensin (6, 12 or 18 pmol X kg-1 X min-1) caused a significant, prompt and dose-related fall in LES pressure from a mean basal value of 35.2 +/- 3.4 mmHg to 29.2 +/- 3.0, 27.3 +/- 3.5 and 25.9 +/- 2.7 mmHg, respectively. Atropine (1 mg) administered as a single i.v. bolus injection did not change the mean pressure significantly. After atropine, the LES pressure response to 12 pmol X kg-1 X min-1 of (Gln4)-neurotensin was abolished. The increase in LES pressure following a bolus injection of pentagastrin (0.6 microgram X kg-1) was not inhibited by 12 pmol X kg-1 X min-1 of (Gln4)-neurotensin. The concentration of plasma neurotensin-like immunoreactivity (p-NTLI) in all experiments was lower than, or in the same order of magnitude as, that obtained postprandially. Thus, the data indicate that reduction of LES pressure by neurotensin may occur postprandially and that this effect seems to involve a cholinergic nervous pathway, rather than being due to a direct myogenic action.
Ingestion of fat causes a pronounced decrease in lower esophageal sphincter (LES) pressure. This may be due in part to effects of neurotensin (NT), which is released postprandially after the ingestion of fat. The aim of the present investigation was to establish whether the LES pressure decreases at physiological plasma concentrations of NT(1-13). In addition, we have compared the effects and metabolism of NT(1-13) and (Gln4)NT(1-13). The experiments were performed in 3 healthy male volunteers who had fasted for at least 11 hours prior to the study. NT(1-13) or (Gln4)NT(1-13) were infused intravenously at a dose of 12 pmoles X kg-1 X min-1. LES pressure was monitored by a continuous pull-through method with a perfused catheter. The concentrations of chromatographically identified tridecapeptides were determined using NH2 and COOH-terminal directed antisera. Already one min after the start of the infusions the LES pressure had decreased by 43% of the control value. At that time the plasma concentration of the neurotensin tridecapeptide was about 15 pM. NT(1-13) and (Gln4)NT(1-13) had similar half-lives in plasma (2.5 min). NT(1-8) and (Gln4)NT(1-8) were found to be the main metabolites of NT(1-13) and (Gln4)NT(1-13) respectively. The results indicate that the increase in the plasma concentration of NT(1-13) seen after the ingestion of food is sufficient for neurotensin to function as a hormone of the endocrine type. NT(1-13) and (Gln4)NT(1-13) have the same effects on LES pressure in humans and show the same pharmacokinetic characteristics.
The effect of (Gln4)-neurotensin on the motor activities of the duodenum and small proximal jejunum was investigated in 8 healthy volunteers who fasted for at least 8 h. Motor activity was monitored by measuring the intraluminal pressure at three levels. The proximal site for pressure recording was in the first part of the duodenum, the middle was at the angle of Treitz, and the distal was 25 cm further down. Under control conditions the median time between the migrating motility complexes was 106.3 min. (Gln4)(-Neurotensin, 3 or 6 pmol/kg . min, infused intravenously for 200 min inhibited the migrating motor complexes for 220.4 min (median time) and they were replaced by irregular pressure waves with a frequency of 4-7 waves/min. The plasma concentration of neurotensinlike immunoreactivity increased from 13 +/- 2.8 pM to 131 +/- 6 pM and 231 +/- 16 pM, respectively. Ingestion of fat (55 ml 20% Intralipid) inhibited the migrating motor complex for 196.1 min (median time) and the migrating motor complexes were replaced by irregular pressure waves. The data show that (Gln4)-neurotensin alters the motility pattern in the duodenum and proximal jejunum in man from a fasting- to a fed-type. They further support the contention that neurotensin may function as an endocrine hormone participating in the postprandial regulation of intestinal motility.
Electrophysiological and horseradish peroxidase (HRP) techniques have provided new insights into the organization of the sacral parasympathetic reflex pathways to the large intestine and urinary bladder. The innervation of the two organs arises from separate groups of sacral preganglionic cells: (1) a dorsal band of cells in laminae V and VI providing an input to the intestine; and (2) a lateral band of cells in lamina VII providing an input to the bladder. These two groups of cells were separated by an interband region containing tract cells and interneurons. Neurons in the interband region received a visceral afferent input and exhibited firing correlated with the activity of intestine and urinary bladder. It seems reasonable therefore to consider the interband region as a third component of the sacral parasympathetic nucleus. Anterograde transport of HRP revealed that visceral afferents from the intestine and bladder projected into the parasympathetic nucleus. Most of the projections were collaterals from afferent axons in Lissauer's tract that passed in lamina I laterally and medially around the dorsal horn. These afferent collaterals were located in close proximity to preganglionic perikarya and dendrites in laminae I, V and VI. The proximity of visceral afferents and efferents in the sacral cord probably reflects the existence of polysynaptic rather than monosynaptic connections since electrophysiological studies revealed that both the defecation and micturition reflexes occurred with very long central delays (45-70 msec). The reflex pathways mediating defecation and micturition in cats with an intact neuraxis were markedly different. Defecation was dependent upon a spinal reflex with unmyelinated (C-fiber) peripheral afferent and efferent limbs. On the other hand, micturition was mediated by a spinobulbospinal pathway with myelinated peripheral afferent (A-fiber) and efferent axons (B-fiber). Transection of the spinal cord at T12-L2 blocked the micturition reflex but only transiently depressed the defecation reflex. In chronic spinal cats the micturition reflex recovered 1-2 weeks after spinalization; however, in these animals bladder-to-bladder micturition reflexes were elicited by C-fiber rather than A-fiber afferents. The C-fiber afferent-evoked reflex was weak or undetectable in animals with an intact neuraxis. Transection of the spinal cord also changed the micturition reflex in neonatal kittens (age 5-28 days). In neonates with an intact neuraxis bladder-to-bladder reflexes occurred via a long latency spinobulbospinal pathway (325-430 msec). The long latency is attributable to the slow conduction velocity in immature unmyelinated peripheral and central axons. In chronic spinal kittens (3-7 days after spinalization) the long latency reflex was abolished and a shorter latency (90-150 msec) bladder reflex was unmasked. The emergence of this spinal pathway may reflect axonal sprouting and the formation of new reflex connections within the sacral parasympathetic nucleus.
(Gln4)-neurotensin was infused i.v. for 5 to 70 min at 3 different infusion rates (6, 12 and 18 pmol X kg-1 X min-1, respectively) in 19 male volunteers, aged 26-47. The plasma concentration of neurotensin-like immunoreactivity (NTLI), the lower esophageal sphincter (LES) pressure, blood pressure, heart rate. ECG and blood glucose concentration were measured. The volunteers did not report any subjective effects during the infusion. Following infusion periods of 30 min or more the volunteers often reported bowel movements starting 5 min or more after cessation of the infusion. Neither blood pressure nor heart rate changed significantly. No changes were noted in the continuous ECG or in the blood glucose concentration. Apparent steady state levels of about 300 pM NTLI were reached at about 40 min during infusion of 12 pmol X kg-1 X min-1 (Gln4)-neurotensin. In all volunteers the LES pressure was significantly reduced within 5 min of starting the infusion. In 6 volunteers 12 pmol X kg-1 X min-1 (Gln4)-neurotensin was infused i.v. for 5 min. The LES pressure decreased significantly (P less than 0.01) from 13.7 +/- 1.3 mmHg to 5.3 +/- 0.8 mmHg. The decrease in the LES pressure occurred at plasma NTLI concentrations of approximately 50 pM, i.e. at levels below those obtained in man after a meal or the ingestion of fat. The present data further support the hypothesis that in man plasma neurotensin, or a neurotensin metabolite is an endocrine hormone involved in the postprandial regulation of the motor functions of the gastrointestinal tract.
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Immunohistochemical and pharmacological studies were conducted to examine the origin and function of peptidergic nerves in the sacral autonomic system of the cat. Leucine-enkephalin (L-Enk) immunoreactivity was identified in nerve terminals in peripheral ganglia on the surface of the urinary bladder and in the parasympathetic nucleus in the sacral spinal cord. In colchicine-treated animals L-Enk was also detected in sacral preganglionic neurons (sPGN) identified by retrograde transport of a fluorescent dye. L-Enk terminals in bladder ganglia are believed to arise from sPGN since the terminals were eliminated by transection of the sacral ventral roots. Pharmacological studies indicated that exogenous as well as endogenously released enkephalins have an inhibitory action at both ganglionic and spinal sites in the sacral outflow to the urinary bladder. Peptides were also associated with afferents nerves in the sacral autonomic system. The distribution of substance P, VIP and cholecystokinin in the sacral dorsal horn paralleled the distribution of visceral afferent projections as demonstrated with HRP techniques. Dye labeling combined with immunohistochemistry revealed that some dorsal root ganglion cells projecting to the pelvic viscera contain substance P or VIP.