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The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and pepsin secretion in conscious dogs with gastric fistula. Infusion of histamine stimulated dose-dependently the acid secretion, whereas pepsin secretion was decreased by the high doses of histamine. Somatostatin inhibited dose-dependently the stimulated acid secretion but only with a maximum of 40%. The pepsin secretion was inhibited by somatostatin dose-dependently and with a higher potency. The acid inhibition was of a competitive type and prostaglandin-independent.

The purpose of the present study was to evaluate the effect of serotonin on bethanechol-stimulated gastric acid secretion and antral motility in conscious dogs with gastric fistula. Bethanechol stimulated the acid secretion dose-dependently and maintained the frequency and strength of the antral contractions at a high level. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was stimulated. The acid inhibition was blocked by propranolol, and dose-response analysis showed inhibition of a non-competitive type. This study thereby shows that serotonin inhibits bethanechol-stimulated gastric acid secretion similarly to salmefamol (β2-adrenergic agonist)-that is, dose-dependently and non-competitively. Serotonin has been proposed to be a mediator of the β-adrenergic influence on gastric function in vivo, but the counteracting effect of propranolol and the stimulatory effect of serotonin on motility contradict this hypothesis.

A direct numerical simulation of fully developed turbulent plane Couette flow has been performed. Unsteady large-scale structures, which contributed to the instantaneous energy level, were observed. These evolving and drifting vortical structures vanished after time-averaging, and the resulting mean velocity and streamwise turbulence intensity compared favourably with recent laboratory data.

The effect of somatostatin on pepsin secretion was determined in six dogs with gastric fistulas during stimulation with bethanechol. Somatostatin inhibited dose-dependently the stimulated pepsin secretion, with a dose of 0.3 mUg/kg/h being 35% inhibitory during stimulation with bethanechol, 80mUg/kg/h. Continuous infusion of somatostatin for 3 h did not cause any signs of tachyphylaxis. Withdrawal of somatostatin produced a return to the control level. The dose-response kinetics with five doses of bethanechol with and without somatostatin showed inhibition of a noncompetitive type. The effects of somatostatin were not altered by using adrenergic, dopaminergic, or serotonergic blocking drugs.

The effect of serotonin on pentagastrin-stimulated gastric pepsin secretion in dogs was evaluated with regard to dose-response kinetics and receptor mediation. The pepsin secretion showed a dual response to exogenous serotonin. The high and low doses of serotonin stimulated, whereas the doses in between inhibited. The inhibition was of a non-competitive type and could be significantly counteracted by β-adrenergic blocking drugs. This study supports the concept that the serotonin effect on gastric functions is mediated via sympathetic nerves releasing noradrenaline.

The effects of serotonin on pentagastrin- and bethanechol-stimulated gastric mucosal blood flow (GMBF) and acid secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method to estimate the mucosal blood flow. Serotonin inhibited the acid secretion, with a counteracting effect of propranolol and methysergide. Serotonin inhibited the pentagastrin- and bethanechol-stimulated GMBF after 15 min of infusion. The ratio between GMBF and acid secretion was increased during serotonin infusion, which suggests primary and independent changes in both variables. Propranolol and methysergide counteracted the serotonin inhibition of the GMBF. It may be concluded from this study that the acid-inhibitory effect of serotonin is not mediated by changes in the GMBF. The actions of serotonin on acid secretion and GMBF are mediated by specific receptors.

The effect of serotonin on bethanechol-stimulated gastric pepsin secretion was evaluated with regard to dose-response kinetics and receptor mediation. A low dose of exogenous serotonin produced a stimulation (0.5 μg/kg/min), whereas inhibition was found for higher doses (5-10 μg/kg/min). The inhibition was non-competitive and could be significantly counteracted by (J-adrenergic blocking drugs. This study confirms results obtained during pentagastrin stimulation and supports the concept that serotonin acts via sympathetic nerves to release noradrenaline.

The purpose of the present study was to evaluate whether the inhibitory effects of β-adrenergic agonists on gastric secretory activity in vivo could be mediated through a local release of somatostatin. The gastric secretion was measured during continuous stimulation with pentagastrin (1 μg/kg/h). The infusion of isoprenaline (β1 + β2), salmefamol (β2), and somatostatin produced inhibitory effects on both acid and pepsin secretion. The reaction patterns were similar for isoprenaline and somatostatin, whereas salmefamol induced an inhibition of longer duration and with dissimilar dose-response kinetics. The gastric somatostatin release was significantly increased after infusion of both β-adrenergic agonists and somatostatin, with patterns similar to those obtained for the secretory inhibition. There was a significant correlation between the somatostatin release and the acid and pepsin secretion during infusion of the secretory inhibitors but not in the control state. This study shows that β-adrenergic agonists have inhibitory effects on gastric secretion in vivo similar to those of somatostatin. Both somatostatin and the β-adrenergic agonists stimulated the release of somatostatin from the gastric mucosa. β-Adrenergic antagonists were without effects. Somatostatin thereby fulfils the requirements for an endogenous mediator of the β-adrenergic inhibition.

Thyroid function was studied in 17 unrelated patients with Pendred’s syndrome. Fourteen patients had been treated with L-thyroxine, which was withdrawn during the investigation. Eight of the patients had previously had a thyroid resection. Thirteen patients had goiter at the time of study. The serum total thyroxine and serum total triiodothyronine concentrations were normal in 8, of whom 3 had elevated serum TSH concentrations. In the remaining 9 cases the thyroxine levels were below normal with elevated TSH. Serum reverse triiodothyronine concentrations were decreased in 8 out of 11. Median serum thyroglobulin was 973 μg/l (range 10.9–3200 μg/1) and increased in 13. Three patients had slightly positive thyroglobulin antibodies and one with normal level was thyrodectomized. Thyroid stimulating antibodies as measured by adenylate cyclase stimulation (median 114%, range 85–137%) were slightly increased in 11. When measured as TSH binding inhibiting immunoglobulins none were positive. Thyroid microsomal antibodies were negative in all. All patients with a detectable 131I uptake (n = 15) showed a pathological iodide perchlorate discharge test (median 32%, range 16–46%). These findings indicate an organification defect with impaired hormone synthesis.

The purpose of this study was to elucidate the effect of a β1-adrenoceptor agonist on gastric acid secretion in conscious dogs with gastric fistula. Isoprenaline, a β1- and β2-agonist was used alone and in conjunction with selective blockade of β2- and β1- receptors. Isoprenaline dose-dependently inhibited the secretory volume and the acidity. The antisecretory effect of isoprenaline was significantly blocked by the β1-adrenoceptor blocker practolol and by the β1 β2-adrenoceptor blocker propranolol but not by H 35/25, a β2-adrenoceptor blocker. This indicates that isoprenaline acts on the acid secretion exclusively through β1-receptors. Dose-response experiments with five logarithmically increased doses of pentagastrin and one dose of isoprenaline showed unchanged calculated maximum response and an increase in half-maximum acid response. It is concluded that the inhibitory effect of isoprenaline on gastric acid secretion is of competitive or uncompetitive type.

Thyroid stimulating immunoglobulins were measured in 43 patients with Graves’ disease both before and at the end of longterm antithyroid treatment. Parallel determinations were performed of thyrotropin binding inhibiting immunoglobulins (TBII) and thyroid adenylate cyclase stimulating antibodies (TSAb). Before treatment 33 patients were TBII positive and 32 TSAb positive, and at the end of treatment 19 remained TBII positive and 14 TSAb positive. The frequency of relapse was about 70% in the positive patients and about 40% in the patients, who became negative in either test for thyroid stimulating immunoglobulins. By combination of the two assays 23 patients were positive in both before treatment. In these patients 5 relapsed of the 6 who remained positive for both, while none relapsed of the 5 patients, who became negative during treatment. In the remaining 12 patients either TBI I or TSAb became negative during treatment and 7 of these relapsed. It is concluded, that the combined measurement of TBII and TSAb in this study seemed superior to the separate determinations of either activity in predicting relapse after medical treatment of Graves’ disease, though this evaluation was only possible in part of the patients.

The effects of somatostatin on gastric mucosal blood flow (GMBF), acid secretion, and pepsin secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method for estimating the mucosal blood flow. Somatostatin inhibited the pentagastrin- and bethanechol-stimulated gastric acid and pepsin secretion and resulted in an absolute decrease in mucosal blood flow. The ratios between GMBF and secretion (acid and pepsin) were increased during somatostation infusion, which suggests a relative increase in mucosal blood flow and independent inhibition of gastric secretion. It may be concluded from this study that the acid- and pepsin-inhibitory effects of somatostatin are not mediated by changes in the GMBF.

Interleukin 6 has been suggested as second mediator of the effects of interleukin 1 in some cell systems. Interleukin 1 has previously been shown to inhibit the function of human thyrocytes in secondary cultures. We have therefore studied the influence of interleukin 6 (10−1−5·107U/l) on the function of thyroid cells. Recombinant interleukin 6 slightly inhibited the production of cAMP, but failed to influence the production of thyroglobulin or the DNA content. Endotoxins (lipopolysaccharides from Salmonella abortus equi or Yersinia enterocolitica) had only a slightly inhibitory effect on thyroid cell functions, and the effect of interleukin 6 could not by itself be explained by endotoxin contamination. The effect of interleukin 6 did not mimick effects on thyroid cells afforded by recombinant interleukin 1α and 1β. Furthermore, antibodies to interleukin 6 were not able to inhibit the interleukin 1β-induced inhibition of thyroid cell functions. In conclusion, it is unlikely that interleukin 6 by itself mediates the biological effects of interleukin 1 on human thyroid cells.

The purpose of the study was to evaluate the frequency of thyroid stimulating immunoglobulins and their possible effect in vivoin patients with rheumatoid arthritis. Thyroid stimulating antibodies (TSAb) were present in 17 (68%) of 25 patients with rheumatoid arthritis, whereas only 2 (8%) had thyrotropin binding inhibiting immunoglobulins (TBII). The groups with and without TSAb were comparable with regard to sex, age, anti-inflammatory drugs, serum thyroglobulin levels, antithyroglobulin and antimicrosomal antibodies, rheumatoid factor, as well as to the serum levels of thyroxine and 3, 5, 3′-triiodothyronine. A possible stimulating effect of TSAb in vivowas evaluated by an ultrasensitive immunoradiometric assay for TSH. Both groups had normal serum TSH levels, and no significant difference was found between the two groups suggesting that the demonstration of TSAb in vitrois not always associated with a stimulation of the thyroid gland in vivo.

The effects of serotonin on histamine-stimulated gastric acid and pepsin secretion were evaluated in conscious dogs with a gastric fistula. Histamine stimulated the acid secretion dose-dependently, whereas pepsin secretion was decreased by the high doses of histamine. The acid secretion was inhibited slightly by serotonin, with a maximum of 42% with a dose of 10 μg/kg/min. The pepsin secretion was only decreased non-significantly by serotonin, 10-15 μg/kg/min. The acid inhibition was counteracted by β-adrenergic antagonists (propranolol, atenolol) and methysergide (serotonergic antagonist). The dose-response analysis showed inhibition of a competitive type. In conclusion, serotonin inhibits histamine-stimulated gastric acid secretion via serotonergic receptors and β-adrenoceptors, whereas pepsin secretion is unaffected.

A new commercial method for measurement of anti-thyroid peroxidase (anti-TPO DYNOtest, Henning, Berlin) was evaluated in normal subjects and in patients with autoimmune thyroid and non-thyroid diseases, and compared to an immune fluorescence method for measurement of anti-microsomal antibodies (MicAb), and a radioimmunological method for quantifying thyroglobulin antibodies (TgAb). The majority of normal subjects had anti-TPO levels below 52 U/ml and patients with Hashimoto's thyroiditis had levels above 200 U/ml, with a good correlation to MicAb. In other autoimmune thyroid diseases the correlation was less pronounced. In non-thyroid autoimmune diseases MicAb showed falsely positive reactions in the presence of other autoantibodies, e. g. mitochondrial antibodies. The present study indicates that the anti-TPO method should probably replace measurements of MicAb for routine clinical use, thus providing a sensitive, precise, antigen specific method with the ability to reveal quantitative fluctuations. The study also indicates that TgAb could be abolished in routine diagnosis of autoimmune thyroid diseases and be reserved for special clinical situations, research purposes as well as measurement in sera before evaluation of serum thyroglobulin levels.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula by using miniature strain-gauge transducers. Infusion of pentagastrin changed the contractile activity to a digestive state. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors. The stimulated antral motility was inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone and by cis-flupenthixol. which blocks both peripheral and central dopaminergic receptors. The effect of dopamine was not significantly altered by the β1-adrenoceptor blocker practolol, the α-adrenoceptor blocker phentolamine, or the α- β-adrenoceptor blocker labetalol. Consequently, this study indicates that dopamine acts on gastric antral motility through dopaminergic receptors. β-adrenergic receptors, which are active in the impairment of gastric acid secretion, seem not to be involved in the motility response.

The purpose of this study was to elucidate the effect of intravenously administered dopamine on dopamine receptors and adrenergic receptors in terms of its effect on gastric acid secretion, the kinetic mechanism, blood flow, and antral motility. Dopamine was used alone and in conjunction with selective blockade of α-, β-, and dopaminergic receptors. A significant inhibition of gastric acid secretion was found with the highest dose of dopamine used (40 μg/kg/min). The kinetic study showed characteristics of a non-competitive type. The anti-secretory effect of dopamine was significantly blocked by non-selective β-blockade or by selective β1-blockade but not by α- or dopaminergic receptor blockade. This suggests that the inhibitory effect of dopamine on gastric secretion is mediated by β1-receptors. There was no significant effect on gastric mucosal blood flow, but the ratio between blood flow and acid secretion was significantly elevated during dopamine infusion, indicating that the acid inhibition was not secondary to changes in blood flow. It is concluded that the dopamine inhibition of acid secretion is mediated by β1-receptors, unlike the effect on antral gastric motility, which is mediated by dopamine receptors.

The aim of the present study was to investigate the effect of dopamine on bethanechol-stimulated gastric acid secretion and mucosal blood flow. Dopamine was used alone and in conjunction with selective blockade of the α, β, and dopaminergic receptors. An increasing and dose-dependent stimulation of gastric acid secretion was found for dopamine at 1, 5, and 10 μg/kg/min. A significant inhibition of gastric acid secretion was found with the highest dose of dopamine (40 μg/kg/min). The stimulatory effect seems to be mediated by more than one receptor, whereas the inhibition by high dopamine doses could be explained by a β1stimulation. Dopamine (10 μg/kg/min) was found to increase the bethanechol-stimulated gastric mucosal blood flow. Phentolamine (α blockade) increased this dopamine-elevated blood flow further, with a significant increase in the ratio between blood flow and acid secretion, indicating a primary action of the α receptors on blood flow. Bethanechol stimulated the gastric acid secretion and blood flow in a parallel manner. It is concluded that α-receptor stimulation is the predominant directly acting factor in the regulation of gastric mucosal blood flow, whereas stimulation of β, muscarinic, and ‘gastrinergic’ receptors mainly occurs indirectly via changes in parietal cell function. The main effect of dopamine seems to be on gastric motility, whereas the effect on gastric acid secretion is of minor importance.

The purpose of this study was to elucidate the effect of the β-adrenoceptor stimulation by isoprenaline on cholinergic-stimulated gastric acid secretion and mucosal blood flow in conscious dogs with gastric fistula. Isoprenaline, a β1- and β2-agonist, was used alone and in conjunction with selective blockade of β2and β1receptors. A low dose of isoprenaline had no significant effect, whereas higher doses had a significant antisecretory effect. The antisecretory effect was significantly blocked by the β1-adrenoceptor blocker practolol but not by H 35/25. a β2-adrenoceptor blocker. The dose-response curve with five doses of bethanechol with and without isoprenaline was in accordance with a non-competitive inhibition. There was no significant effect on gastric mucosal blood flow, indicating that the acid inhibition was not secondary to changes in blood flow. The inhibitory effect of isoprenaline seems to be mediated by the β1receptors and with an action primarily on the ‘gastrinergic receptors’.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility with regard to both frequency and strength. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone. The α-adrenoceptor blocker phentolamine reduced the effect of dopamine to some extent, but the reduction was not of statistical significance. The dopamine-inhibited motility was not altered by the β1-adrenoceptor blocker practolol or the β1 β2-adrenoceptor blocker propranolol. This indicates that dopamine acts on gastric antral motility predominantly through dopaminergic receptors. β-Adrenergic receptors, which are active in the impairment of gastric acid secretion, do not seem to be involved in the motility response. Dose-response investigations with five increasing doses of bethanechol and one dose of dopamine showed inhibition of a non-competitive type.

The purpose of the present study was to evaluate the effect of isoprenaline on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility for both frequency and strength. Isoprenaline, a β1- and β2-agonist, was used alone and in conjuction with selective blockade of β1and β2receptors. The stimulated antral motility was dose-dependently inhibited by isoprenaline. The effect was significantly blocked by the β1 β2-adrenoceptor blocker propranolol and by using in conjunction the β1-adrenoceptor blocker practolol and the β2-adrenoceptor blocker H 35/25. H 35/25 and particularly practolol reduced the effect of isoprenaline to some extent, but the reduction was not of statistical significance. This indicates that isoprenaline acts on antral motility through both β2and β1receptors. Dose-response experiments with five logarithmically increasing doses of bethanechol and one dose of isoprenaline showed inhibition of a non-competitive type.

The prevalence of micro- and macroalbuminuria was determined in Type 2 (non-insulin-dependent) diabetic patients, less than 76 years of age, attending a diabetic clinic during 1987. All eligible patients (n=557) were asked to collect a 24-h urine sample for quantitative albumin analysis. Urine collections were obtained in 296 males and 253 females (96%). Normoalbuminuria were defined as urinary albumin excretion≤30 mg/24 h (n=323), microalbuminuria as 31–299 mg/24 h (n=151), and macroalbuminuria as ≥300 mg/ 24 h (n=75). The prevalence of macroalbuminuria was significantly higher in males (20%) than in females (6%), while the prevalence of microalbuminuria was almost identical in males (26%) and females (29%). The prevalence of arterial hypertension increased with increased albuminuria, being 48%, 68%, and 85% in patients with normoalbuminuria, microalbuminuria, and macroalbuminuria respectively. Prevalence of proliferative retinopathy rose with increasing albuminuria, being 2%, 5% and 12% in patients with normoalbuminuria, microalbuminuria, and macroalbuminuria respectively. Prevalence of coronary heart disease, based on Minnesota coded electrocardiograms, was more frequent in patients with macroalbuminuria (46%) compared to patients with microalbuminuria (26%) and patients with normoalbuminuria (22%). Foot ulcers were more frequent in micro- and macroalbuminuric patients, being 13% and 25%, respectively, compared to 5% in patients with normoalbuminuria. This cross-sectional study has revealed a high prevalence of microalbuminuria (27%) and macroalbuminuria (14%) in Type 2 diabetic patients. Patients with raised urinary albumin excretion are characterized by obesity, elevated haemoglobin Alc, increased frequency of arterial hypertension, proliferative retinopathy, coronary heart disease and foot ulcers. Thus, these findings suggest that urinary excretion of albumin should be monitored routinely in patients with Type 2 diabetes.

The effects of human recombinant interleukin 1α (20 pg/1-2 μg/l) and 1β (200 pg/1-20 μg/l) on two systems of thyroid cells have been compared. The thyroglobulin and cAMP secretion and the DNA content of human thyroid cells cultured in monolayer and of continuously grown rat thyroid cells, Fischer rat thyroid cell line have been studied. The growth of the rat thyroid cell line was inhibited by interleukin 1β (20 ng/1-20 μg/l), but not by interleukin 1α. None of the cytokines changed the cAMP production of the rat thyroid cells. In contrast, both cAMP production and thyroglobulin secretion were inhibited dose-dependently by the cytokines in human thyroid cells in secondary cultures. These results caution the interpretation and extrapolation of changes induced by interleukin 1 from one cell system to the other.

The aim of the present study was, in paired experiments in dogs, to examine the effect of β-receptor blockade on gastric acid secretion and mucosal blood flow before and after parietal cell vagotomy (PCV). The secretory response to pentagastrin was reduced after vagotomy, β-Adrenergic blockade had no effect on pentagastrin-stimulated gastric acid secretion before PCV, but after PCV β blockade caused a modest increase in acid secretion, mediated mainly by the β2receptors. A similar trend was seen in man. A marked increase in mucosal blood flow occurred 30 min after propranolol and was followed by a late decrease. One may conclude that a modest β-adrenergic tone, which reduces secretion, becomes manifest after vagal denervation and that an increase in the ratio between mucosal blood flow and acid secretion was induced by the PCV. This increase cannot be explained as a β-receptor-mediated effect.

Two screenings with Hemoccult-II were performed in a randomized study, allocating 30,970 persons to screening and 30,968 as controls in a population of 140,000 between 45 and 74 years old on the island of Funen, Denmark. The test was completed in 20,672 initially and in 18,779 of these during rescreening 2 years later. Positive H-II tests were found in 215 and 159 persons during the two screenings, respectively. A total colonoscopy was performed in 187 and 144, and cancer was detected in 37 and 13 and adenomata in 86 and 76, respectively. Interval cancers had developed in 40 persons at the end of the second screening, and 39 non-responders had developed cancer. Cancer was diagnosed in 115 controls and an adenoma in 100 during the same period. Interval cancers presented as rectal cancers more frequently than those detected by screening. Early cancers were more frequent in the screening group, and, accordingly, more patients had curative and also less extensive surgery, with a low postoperative mortality. The total number of deaths from colorectal cancer was 37 in the screening group, including interval cancers and cancers in non-responders and persons who developed cancer before they could be invited, which suggests a reduction in mortality of 27% (51 deaths among controls, compared with 37). The reduction is as yet not statistically significant, and final evaluation must await at least one more screening, ending in 1990, and a follow-up of some years. Removal of more large adenomas during screening makes it possible that the incidence of cancer will decrease.

The effects of exogenous serotonin on pentagastrin-stimulated gastric acid secretion and antral motility were evaluated with regard to inhibition kinetics and receptor mediation. Conscious gastric fistula dogs were used. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was initially stimulated and thereafter inhibited. The inhibition of secretion was counteracted by different β-adrenergic blocking drugs and methysergide, whereas the inhibition of antral motility was blocked by methysergide and indomethacin. Dose-response analysis showed inhibition of non-competitive types. This study supports the concept of differences in the regulation of gastric acid secretion and motility, but further experiments with simultaneous registration are required.

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of bethanechol stimulated dose-dependently acid secretion, whereas the frequency and strength of antral motility was maintained at a high level. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using aL-adrenergic, bT-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with four doses of bethanechol with and without somatostatin showed inhibition of a non-competitive type for gastric acid secretion and of a competitive type for antral motility with regard to amplitude.

We have compared the anaesthetic and analgesic efficacy of levobupivacaine with that of racemic bupivacaine in 66 male patients undergoing ambulatory primary inguinal herniorrhaphy. Patients were allocated randomly in a double-blind manner to local infiltration anaesthesia (0.25%w/v 50 ml) with either racemic bupivacaine (n=33) or levobupivacaine (n=33). Scores for intraoperative pain and satisfaction with anaesthesia were recorded, togther with perception of postoperative pain and need for supplementary postoperative analgesic medications in the first 48 h after operation. Intraoperative satisfaction with the infiltration anaesthesia was similar, with median scores of 77 (levobupivacaine) and 80 (bupivacaine) (VAS; 100 mm=extremely satisfied). Time averaged postoperative pain scores (48 h) were 8 (levobupivacaine) and 10 (bupivacaine in the supine position, 13 (levobupivacaine) and 12 (bupivacaine) while rising from the supine position to sitting, and 9 (levobupivacaine) and 13 (bupivacaine) while walking (VAS; 100 mm=worst pain imaginable) (ns). There was no difference in the use of peroral postoperative analgesics between the two groups. We conclude that racaemic bupivacaine and its S-enantiomer levobupivacaine had similar efficacy when used as local infiltration anaesthesia in inguinal herniorrhaphy.
Key words: anaesthetics local, bupivacaine; pharmacokinetics, stereoisomers; surgery, herniorrhaphy

We have compared the anaesthetic and analgesic efficacy of levobupivacaine with that of racemic bupivacaine in 66 male patients undergoing ambulatory primary inguinal herniorrhaphy. Patients were allocated randomly in a double-blind manner to local infiltration anaesthesia (0.25% w/v 50 ml) with either racemic bupivacaine (n = 33) or levobupivacaine (n = 33). Scores for intraoperative pain and satisfaction with anaesthesia were recorded, together with perception of postoperative pain and need for supplementary postoperative analgesic medications in the first 48 h after operation. Intraoperative satisfaction with the infiltration anaesthesia was similar, with median scores of 77 (levobupivacaine) and 80 (bupivacaine) (VAS; 100 mm = extremely satisfied). Time averaged postoperative pain scores (48 h) were 8 (levobupivacaine) and 10 (bupivacaine) in the supine position, 13 (levobupivacaine) and 12 (bupivacaine) while rising from the supine position to sitting, and 9 (levobupivacaine) and 13 (bupivacaine) while walking (VAS; 100 mm = worst pain imaginable) (ns). There was no difference in the use of peroral postoperative analgesics between the two groups. We conclude that racemic bupivacaine and its S-enantiomer levobupivacaine had similar efficacy when used as local infiltration anaesthesia in inguinal herniorrhaphy.

As mixed tumors from accessory lacrimal gland tissue are relatively rare, we find that the case described below is worthy of publication, especially because of the localization and nature of the tumor and the pertinent histopathological considerations. REPORT OF CASE The patient was a man, aged 50, in good general health, with a hazelnut-sized tumor in the left inner canthal region. He stated that a similar growth had been removed from the same site 12 years previously. After the operation, the eye surgeon had told him that the tumor had not been removed in toto. Five years later, the growth recurred, and a tumor of the same size as the first was excised. Unfortunately, histological descriptions of the two tumors was not available. During the seven years which had passed since the removal of the second tumor, a nodule had gradually developed below the old scar.Ophthalmological examination revealed that