The effect of spinal anesthesia that is performed in sitting or right lateral position on post-spinal headache and intraocular pressure during elective cesarean section.

Background: Although spinal anesthesia can be applied in different patient positions, the most frequently used positions are sitting and lateral positions. It is known that different patient positions during spinal anesthesia have effects on hemodynamic parameters, postdural puncture headache, and intraocular pressure. Aim: The study aimed to determine the effect of spinal anesthesia performed in either sitting or right lateral position on postspinal headache and intraocular pressure during elective cesarean section. Patients and Methods: The study was a randomized controlled study of 104 eligible pregnant women scheduled to undergo elective cesarean section. The women were randomized into two groups. Spinal anesthesia was performed either in the sitting (Group S, n = 53) or the right lateral position (Group L, n = 51). Heart rate and blood pressure were recorded throughout the operation. The participants were informed and monitored for postspinal headaches. Intraocular pressure before and after the operation was measured with Icare PRO. The obtained data were statistically compared between the two groups. Results: There was no difference between the groups in terms of demographic data. Postdural puncture headache was observed in five patients in Group S and one patient in Group L (P =0.04). There was no difference between the groups in terms of intraocular pressure (P >.05). Heart rate was not significantly different between the groups; however, there was a significant difference in average blood pressure in 1, 5, 30, and 40 minutes (P <.05). The number of trials administered to patients for spinal anesthesia was significantly higher in Group L (P =0.01). Conclusion: Spinal anesthesia performed in the sitting position for cesarean section caused a higher postspinal headache than in the right lateral position, but the position did not affect intraocular pressure.

Medical ozone treatment on prevention of epidural fibrosis in the rat model.

Background/Aim: Epidural fibrosis is one of the problems that can be seen after spinal surgery. The aim of this study was to investigate the possible preventive role of medical ozone (O) treatment on epidural fibrosis. Materials and Methods: Twenty-four Sprague Dawley rats were randomly split into four groups: control (C), O, laminectomy (L), and L+O groups. Animals in the C group were sacrificed at the beginning of the experiment. The L and L+O groups had L procedure, while O treatment was supplied for the O and O+L groups. After 42 days of follow-up, for histological evaluation and biochemical measurements, the ratio of epidural fibrosis and catalase (CAT) with malondialdehyde (MDA) levels in serum, respectively, were analyzed in terms of statistical differences. Results: Histologically, a distinct difference was o bserved in the epidural space after O treatment. A significant difference in epidural fibrosis areas is found to be between the O, L, and O+L groups (P < 0,0001). There was no statistically significant difference between CAT and MDA levels that were obtained by spectrophotometric analysis. Conclusion: Histological results suggest that medical O treatment after L can be used as an alternative method to prevent epidural fibrosis. Further studies with wide cohorts and interval measures are required to detail the effects of doses.

Comparison of propofol-fentanyl and propofol-ketamine for sedoanalgesia in percutaneous endoscopic gastrostomy procedures.

Background: Percutaneous endoscopic gastrostomy (PEG) procedures are performed under sedation in critically ill patients who cannot be fed orally. Aim: We compared the efficacy and safety of propofol-fentanyl and propofol-ketamine for deep sedation in patients undergoing PEG. Retrospective Study. Materials and Methods: The study was conducted from 1 January 2013 to 31 December 2018 in Adiyaman University. The patients given propofol-fentanyl (0.5-1.2 mg/kg and 0.2-1 µg/kg, respectively) for sedo-analgesia were designated Group F, and those who received propofol-ketamine (0.2-0.6 mg/kg and 0.5-1 mg/kg, respectively) were placed in Group K. The demographic and hemodynamic characteristics, recovery times, perioperative complications, and need for additional doses were recorded. Results: Seventy-one patients who underwent PEG were analyzed. The age, sex, American Society of Anesthesiologists (ASA) score, comorbidities, duration of anesthesia, and duration of the PEG procedure were similar in the two groups. Recovery time was longer in Group K. The total propofol dose was 64 mg in Group F and 35 mg in Group K. Additional doses of propofol were administered to 12 patients in Group F, compared to none in Group K. The mean blood pressure values were higher in Group K at all-time points. The perioperative complication rate was higher in Group F. Desaturation was observed in 9 (22.5%) patients in Group F and in 3 (9.6%) patients in Group K. Hypotension was observed in 4 (10%) patients in Group F. Conclusion: Propofol-ketamine should be preferred for sedoanalgesia during PEG procedures because of the lower dose of propofol, more stable blood pressure, and greater peripheral oxygen saturation. In addition, we believe ketamine-propofol is safer based on its low complication rate.

Sacral neuromodulation: long-term outcome and quality of life in patients with faecal incontinence.

AIM: Since 1994 sacral neuromodulation (SNM) has increasingly been used for the treatment of faecal incontinence, but no long-term data in a large group of patients have so far been published. We report long-term outcome and quality of life in the first 50 patients treated by permanent SNM for faecal incontinence. METHOD: We began to use SNM in 2000. Data from the first 50 patients with faecal incontinence who underwent permanent SNM are presented. Efficacy was assessed using a bowel diary and the Quality of Life score was assessed by the Faecal Incontinence Quality of Life questionnaire (FIQOL) and the standard short form health survey questionnaire (SF-36). RESULTS: Over a median follow up of 7.1 (5.6-8.7) years, forty-two (84%) patients had an improvement in continence of over 50%. Median incontinent episodes and days of incontinence per week decreased significantly during follow up (P<0.002). Improvement was seen in all four categories of the FIQOL scale and in some domains of the SF-36 QOL questionnaire. There were no statistically significant changes in the median resting and squeeze anal canal pressures. CONCLUSION: Initial improvement in continence with SNM was sustained in the majority of patients, with an overall success rate of 80% after a permanent implant at 7 years.

Sacral nerve modulation and other treatments in patients with faecal incontinence after unsuccessful pelvic floor rehabilitation: a prospective study.

OBJECTIVES: Sacral nerve modulation (SNM) is a minimally invasive technique for the treatment of faecal incontinence. This study investigates the results of SNM after negative outcome of a standardized pelvic floor rehabilitation (PFR) programme for the treatment of faecal incontinence. METHOD: A prospective cohort study was performed between December 2001 and August 2007. Consecutive patients who visited the outpatient department for faecal incontinence were included in a multicentre study and treated with standardized PFR. Those with an unsuccessful result who were eligible for SNM were included in the present study. Failures at test stimulation or SNM received another treatment. Clinical outcome, Vaizey scores and Hirschsprung's disease/anorectal malformation quality-of-life (EQ-5D and HAQL) were assessed during follow-up in patients with SNM and in patients with other treatments (OT). Adverse events (AE) were documented. RESULTS: Thirty-five patients (mean age 59.7 years; 31 females) were included. Twenty-one had a successful test stimulation and 19 patients proceeded to a SNM implant. Incontinence episodes per week decreased significantly from 11.1 +/- 11.7 to 1.9 +/- 2.6 during test stimulation (P < 0.0001) and SNM over 24.1 months follow-up. The overall success rate was 49% (17/35). The patients with unsuccessful test stimulation or SNM received OT. The Vaizey score improved in both SNM (18.2 +/- 3.5 vs 13.7 +/- 4.8; P = 0.004) and other treatment (18.2 +/- 3.5 vs 13.9 +/- 6.9; P = 0.019). The HAQL scale improved significantly during SNM in all subscales (P < 0.005), but not in the other treatment group. Eight AE occurred during test stimulation (23%) and six AE after permanent implantation (26%). CONCLUSION: Sacral nerve modulation improves disease specific quality of life significantly compared with other treatment.

Sacral neuromodulation: does it affect the rectoanal angle in patients with fecal incontinence?

BACKGROUND: In the past decade numerous studies have been published on the successful treatment of fecal incontinence with sacral neuromodulation (SNM). The underlying mechanism of action for lower bowel motility disorders has been unclear. In the present study, the effect of SNM on the rectoanal angle in patients with fecal incontinence was investigated. PATIENTS AND METHODS: In 12 consecutive patients who qualified for SNM an X-defecography study was performed before SNM and at 6 months after permanent implant. Three single lateral rectal views were taken: one during rest, one during squeeze, and one during Valsalva's maneuver, after which the patient was asked to evacuate as rapidly and completely as possible during lateral fluoroscopy. At 6 months two further defecography studies were performed, one during stimulation with the pacemaker on and one with the pacemaker off. RESULTS: The defecography studies showed that the rectoanal angle decreased during rest, squeeze, and Valsalva's maneuver. A slight increase in rectoanal angle was seen during defecation. However, the differences did not reach statistical significance. Sacral neuromodulation improved fecal continence significantly in all patients at 6 months. Median incontinence episodes per week decreased from 6.2 to 1.0 (P = 0.001), and incontinent days per week decreased from 3.7 to 1.0 (P = 0.001) with SNM. There were no significant changes in the median resting and squeeze anal canal pressures, 46.5 versus 49.7 mmHg and 67.1 versus 72.3 mmHg, respectively. Median stimulation amplitude at follow-up was 2.7 V (range: 0.9-5.3 V). CONCLUSIONS: Rectoanal angle did not decrease significantly in patients with fecal incontinence during SNM.

Is a morphologically intact anal sphincter necessary for success with sacral nerve modulation in patients with faecal incontinence?

OBJECTIVE: Sacral nerve modulation (SNM) for the treatment of faecal incontinence was originally performed in patients with an intact anal sphincter or after repair of a sphincter defect. There is evidence that SNM can be performed in patients with faecal incontinence and an anal sphincter defect. METHOD: Two groups of patients were analysed retrospectively to determine whether SNM is as effective in patients with faecal incontinence associated with an anal sphincter defect as in those with a morphologically intact anal sphincter following anal repair (AR). Patients in group A had had an AR resulting in an intact anal sphincter ring. Group B included patients with a sphincter defect which was not primarily repaired. Both groups underwent SNM. All patients had undergone a test stimulation percutaneous nerve evaluation (PNE) followed by a subchronic test over 3 weeks. If the PNE was successful, a permanent SNM electrode was implanted. Follow-up visits for the successfully permanent implanted patients were scheduled at 1, 3, 6 and 12 months and annually thereafter. RESULTS: Group A consisted of 20 (19 women) patients. Eighteen (90%) had a positive subchronic test stimulation. Twelve patients had a successful SNM implant during middle-term follow-up. Group B consisted of 20 women. The size of the defect in the anal sphincter varied between 17% and 33% of the anal circumference. Fourteen (70%) had a positive subchronic test stimulation. Twelve patients had a successful SNM implant during middle-term follow-up. In both groups, the mean number of incontinence episodes decreased significantly with SNM (test vs baseline: P = 0.0001, P = 0.0002). There was no significant difference in resting and squeeze pressures during SNM in group A, but in group B squeeze pressure had increased significantly at 24 months. Comparison of patient characteristics and outcome between groups A and B revealed no statistical differences. CONCLUSION: A morphologically intact anal sphincter is not a prerequisite for success in the treatment of faecal incontinence with SNM. An anal sphincter defect of <33% of the circumference can be effectively treated primarily with SNM without repair.

Effects of econazole on receptor-operated and depolarization-induced contractions in rat isolated aorta.

In our previous study, econazole caused a decrease in serum nitrite levels in septic mice in vivo, but it enhanced the mortality rate. The aim of the study was to investigate the in vitro effects of econazole on receptor-operated and depolarization-induced contractions on endothelium-intact and -denuded rat isolated aorta. Econazole (0.1, 1 and 10 microM) significantly inhibited receptor-operated (phenylephrine, Phe) and depolarization (KCl)-induced contractions of endothelium-intact or -denuded rings in a noncompetitive and concentration-dependent manner. Removal of endothelium changed the pD'2 values only for KCl-induced responses. The pD'2 values of L-type calcium channel blocker nifedipine were significantly higher than the econazole on Phe concentration-response curves in endothelium-intact and -denuded rings. Econazole caused a biphasic response in precontracted by Phe or KCl in endothelium-intact and -denuded rings, first a transient contraction following sustained relaxation. Removal of endothelium did not affect the contractile responses induced by Phe. The contractile responses induced by 10 microM econazole in the KCl-precontracted rings were antagonized by the treatment of alpha-adrenergic receptor antagonist, phentolamine (10 microM). Deendothelization was significantly increased the IC50 values of econazole obtained from Phe- and KCl-precontractions. The relaxations induced by 10 microM econazole in endothelium-intact rings precontracted with Phe or KCl were not changed by NO synthase inhibitor, L-N(G)-nitroarginine (100 microM). The IC50 values of econazole were significantly higher than nifedipine in endothelium-intact and -denuded rings. These results suggest that econazole is a noncompetitive antagonist on alpha1-adrenoceptor-mediated and depolarization-induced contractions in rat isolated aorta by inhibiting Ca2+ entry through L-type calcium channels, and the endothelium seems to modulate vascular responses induced by this agent. The vascular effects of econazole may limit the usage of this agent in septic shock.

Temporal variation in serum nitrite levels in rats and mice.

Although considerable evidence implicates involvement of nitric oxide (NO) in circadian regulation, little is known about possible 24 h variations in basal NO metabolism. In this study, daily variations in serum nitrite levels were studied in locally bred mice and rats during the months of September and October. The serum was separated from blood samples obtained at six different times of the day and night (1 h, 5 h, 9 h, 13 h, 17 h, and 21 h after lights off [HALO] from male albino mice and rats). As an index of in vivo NO generation, serum nitrite levels (determined by the diazotization method) in rats exhibited significant temporal fluctuation (unpaired Student t test), with the concentration highest at 5 HALO and 21 HALO and lowest at 9 HALO. No such temporal variation was detected in mice in these studies conducted on locally bred animals in the autumn.

Circadian-rhythm-dependent effects of L-NG-nitroarginine methyl ester (L-NAME) on morphine-induced analgesia.

Circadian changes in the interactions between L-NG-nitroarginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, and morphine-induced antinociception were investigated by the mouse hot-plate test. Both the basal pain sensitivity and morphine-induced analgesia undergo significant 24 h variations. L-NAME (40 mg/kg, i.p.) alone did not show any antinociceptive activity, but potentiated morphine-induced analgesia when combined with morphine at all injection times. In terms of percentage absolute potentiation (%AP), L-NAME dramatically augmented the analgesic effect of morphine in the late dark period at 19 hours after lights on (HALO). It is concluded that nitric oxide (NO) is involved in the modulation of the analgesic effect of morphine; thus, the L-NAME and morphine combination might be beneficial in alleviating pain.

[Sacral neuromodulation is effective in the treatment of fecal incontinence with intact sphincter muscles; a prospective study]. / Sacrale neuromodulatie effectief bij fecale incontinentie en intacte kringspieren; een prospectieve studie.

OBJECTIVE: To evaluate the therapeutic effect of sacral neuromodulation on faecal incontinence in patients with structurally intact sphincters. DESIGN: Prospective. METHOD: In the period April 1st, 2000 to November 30th, 2001, patients with faecal incontinence and structurally intact sphincters were included, with or without previous surgery, in whom medicinal treatment and biofeedback therapy gave no improvement. Incontinence was defined as involuntary loss of stool at least once a week, which was objectified by completion of a 3-week bowel habit diary. Patients underwent 3 weeks of trial stimulation during which they also kept a diary. The trial stimulation was considered successful if the diary showed a > or = 50% improvement in continence. RESULTS: 38 patients (31 women) with an average age of 54 years (range: 26-73) underwent trial stimulation. Trail stimulation was carried out using a permanent electrode in 6 patients and using peripheral neural evaluation in the remaining 32 patients. Two patients did not respond to peripheral neural evaluation. Upon assessment after the trial stimulation period. continence was found to have improved by > or = 50% in 31 (82%) patients. The number of incontinence episodes decreased by an average of 86% (range: 50-100). In 27 patients an implantable pulse generator was implanted for continuous stimulation. During the average follow-up of 6 months the effect remained satisfactory. Anal manometry during stimulation showed no increase of sphincter pressures. CONCLUSION: Sacral neuromodulation was of therapeutic value in most of the patients treated for faecal incontinence without sphincter damage.

Second-line treatment for faecal incontinence.

BACKGROUND: In the treatment of faecal incontinence, more than 30% of patients experience continuation of their problem. We discuss new therapeutic procedures for dealing with faecal incontinence. METHODS: Discussion of authors' own work in relation to the literature. RESULTS: First-line care includes diets, constipating drugs, biofeedback therapy, anal repair and operations for prolapse and fistulas. For the failures of these first-line treatments there is hope with second-line therapies. Creation of a neosphincter is possible with a dynamic graciloplasty (DGP) or an artificial bowel sphincter (ABS). A DGP is a conventional graciloplasty with the addition of implanted electrodes and a stimulator that transforms the muscle into an automatic contracting sphincter. ABS comprises an inflatable cuff around the anus that is filled from a pressure-regulating balloon. The cuff can be emptied with an implanted pump. CONCLUSIONS: DGP and ABS give good results in 56%-88% of cases. For patients with an anatomical intact but nonfunctioning sphincter there is a new treatment: sacral nerve stimulation. This gives continence in a high percentage of cases, but experience is rather limited. Second-line treatment for faecal incontinence is successful and should be considered in cases where initial therapies fail.

Sacral neuromodulation in patients with faecal incontinence: results of the first 100 permanent implantations.

OBJECTIVE: Faecal incontinence (FI) is a socially devastating problem. Sacral nerve modulation (SNM) has proven its place in the treatment of patients with FI. In this study, the first 100 definitive SNM implants in a single centre have been evaluated prospectively. METHOD: Patients treated between March 2000 and May 2005 were included. Faecal incontinence was defined as at least one episode of involuntary faecal loss per week confirmed by a 3-week bowel habit diary. Patients were eligible for implantation of a permanent SNM when showing at least a 50% reduction in incontinence episodes or days during ambulatory test stimulation. Preoperative workup consisted of an X-defaecography, pudendal nerve terminal motor latency measurement, endo-anal ultrasound and anal manometry. The follow-up visits for the permanent implanted patients were scheduled at 1, 3, 6 and 12 months and annually thereafter. The bowel habit diary and anal manometry were repeated postoperatively during the follow-up visits. RESULTS: A total of 134 patients were included and received a subchronic test stimulation. One hundred patients (74.6%) had a positive test stimulation and received a definitive SNM implantation. The permanent implantation group consisted of 89 women and 11 men. The mean age was 55 years (range 26-75). The mean follow-up was 25.5 months (range 2.5-63.2). The mean number of incontinence episodes decreased significantly during the test stimulation (baseline, 31.3; test, 4.4; P < 0.0001) and at follow-up (36 months postoperatively, 4.8; P < 0.0001). There was no significant change in the mean anal resting pressure. The squeeze pressures were significantly higher at 6 months (109.8 mmHg; P = 0.03), 12 months (114.1 mmHg; P = 0.02) and 24 months postoperatively (113.5 mmHg; P = 0.007). The first sensation, urge and maximum tolerable volume did not change significantly. Twenty-one patients were considered late failures and received further treatment. CONCLUSION: Sacral neuromodulation is an effective treatment for FI. The medium-term results were satisfying.

Sacral neuromodulation; does it affect colonic transit time in patients with faecal incontinence?

OBJECTIVE: Sacral neuromodulation (SNM) has been a successful treatment in urinary voiding disorders for years. A concomitant effect on bowel function was observed leading to the treatment of faecal incontinence with SNM. In this study we describe the effect of SNM on bowel frequency and (segmental) colonic transit time. PATIENTS AND METHODS: Fourteen patients with faecal incontinence who qualified for permanent SNM underwent a colon transit study before and one month after permanent implant. Patients completed a three-week bowel habits diary before and during stimulation. RESULTS: Median incontinence episodes and days per week before SNM were, 8.7 and 4.2, respectively, and both decreased significantly to 0.67 (P = 0001) and 0.5 (P = 0001) during trial screening and to 0.33 (P = 0001) and 0.33 (P = 0001) after permanent implant. The median number of bowel movements per week decreased from 14.7 (6.7-41.7) to 10.0 (3.7-22.7)(P = 0005) during trial screening and to 10.0 (6.0-24.3)(P = 0008) during permanent stimulation. Resting and squeeze pressures did not change significantly during stimulation. Segmental colonic transit time before and during stimulation for right colon, left colon and recto sigmoid were, respectively, 6 (0-25) vs 5 (0-16) hours, 2 (0-29) vs 4 (0-45) hours and 7 (28) vs 8 (0-23) hours. No significant changes were found in both segmental and total colonic transit time; 17 (1-65) vs 25 (0-67) hours. CONCLUSION: SNM in patients with fecal incontinence led to a significant decrease of bowel movements however (segmental) colonic transit time was not influenced.

Effect of sacral neuromodulation on the rectum.

BACKGROUND: Sacral neuromodulation (SNM) is a new treatment for faecal incontinence. At present the exact underlying mechanism is still unclear. Modulation of the sacral reflex arcs might have an effect on rectal sensitivity, wall tension and compliance. METHODS: Fifteen consecutive patients with faecal incontinence who qualified for SNM underwent barostat measurements before and during neuromodulation. An 'infinitely' compliant plastic bag with a volume of 600 ml was placed in the rectum and connected to a computer-controlled barostat system. An isobaric phasic distension protocol was used. Patients were asked to report rectal filling sensations: first sensation (FS), earliest urge to defaecate (EUD) and an irresistible, painful urge to defaecate (maximum tolerated volume; MTV). Rectal wall tension and compliance were calculated. RESULTS: During isobaric phasic distension each patient experienced all rectal filling sensations at the time of stimulation. Median volume thresholds decreased significantly during stimulation, from 98.1 to 44.2 ml for FS (P = 0.003), from 132.3 to 82.8 ml for EUD (P = 0.001) and from 205.8 to 162.8 ml for MTV (P = 0.002). Pressure thresholds tended to be lower for all filling sensations, but only that to evoke MTV was reduced significantly by stimulation (37.3 versus 30.3 mmHg; P = 0.005). Median rectal wall tension for all filling sensations decreased significantly with stimulation. There was no significant difference between compliance before and during stimulation. CONCLUSION: SNM affects rectal sensory perception, but further research is required to clarify the mechanism.

Incidence of surgical site infections in pediatric patients: a 3-month prospective study in an academic pediatric surgical unit.

During a 3-month period 259 pediatric surgical procedures in 236 patients were followed for the development of surgical site infections (SSI): 17 sites became infected, an overall infection rate of 6.6%. The incidence in our study was therefore higher than expected. As expected, the infection rate increased according to wound contamination: dirty sites had a SSI rate of 30%. Emergency procedures, operation duration over 1 h, and inpatients showed a statistically significant higher risk of developing SSI. Although there were differences between males and females, individual surgeons, and the use of antibiotic prophylaxis, these differences were not statistically significant.

Effects of nitric oxide synthase inhibition in lipopolysaccharide-induced sepsis in mice.

In the present study, we have investigated the effects of nitric oxide (NO) synthase inhibition on mortality in lipopolysaccharide (LPS)-induced sepsis in mice. Serum nitrite levels peaked at 15 h after an injection of LPS (10 mg kg-1, i.p.). Aminoguanidine, a selective inducible NO synthase (iNOS) inhibitor, at a dose of 100 mg kg-1 significantly reduced the LPS-induced increase in nitrite levels and improved mortality. Econazole, iNOS inhibitor, calmodulin antagonist, 5-lipoxygenase and a specific thromboxane synthase inhibitor, at a 1 mg kg-1 dose significantly decreased the LPS-induced increase in nitrite levels, but increased mortality 4. 9-fold when compared to the LPS group (control). Indomethacin, a putative iNOS and non-selective cyclo-oxygenase (COX) inhibitor, of 1, 10 and 100 mg kg-1, dose dependently decreased the LPS-induced increase in nitrite levels. This decrease was significantly different from the control at 10 and 100 mg kg-1 dose levels. When indomethacin (100 mg kg-1) was combined with aminoguanidine (100 mg kg-1), LPS-induced nitrite levels were significantly attenuated. NO precursor, L-arginine, was added to this combination in order to test the inhibition of iNOS activity which resulted in no change in nitrite levels. An indomethacin and aminoguanidine combination increased mortality twofold when compared to the control. The addition of L-arginine to the combination enhanced the mortality rate to 1.5-fold. These results suggest that NO appears to play a role in the LPS-induced septic shock model in mice. The improvement in sepsis-induced mortality enhanced by aminoguanidine by the inhibition of iNOS but not with the other agents or combinations should be re-evaluated in order to make an appropriate choice of the therapeutic target. In addition, it may also suggest that other mediators, such as arachidonic acid products and cytokines play a role in septic shock pathogenesis as well. (c) 1998 The Italian Pharmacological Society.

The role of L-arginine/nitric oxide pathway in the antinociceptive activity of pyridoxine in mouse.

In the present study the role of L-arginine/nitric oxide (NO)/cGMP pathway in the antinociceptive activity of pyridoxine in p-benzoquinone-induced abdominal constriction test in mouse was investigated. Pyridoxine (CAS 58-56-0) displayed dose-dependent antinociceptive activity at 0.0625-1 mg/kg (s.c.) doses. L-arginine (CAS 1119-34-2), a NO precursor, displayed a triphasic pattern as antinociception-nociception-antinociception (61.8 +/- 7.8, -36.5 +/- 12.7 and 17.0 +/- 4.3%, 5, 40 and 50 mg/kg, s.c., respectively). The antinociceptive effect of pyridoxine at ED50 dose (0.43 mg/kg, s.c.) (47.7 +/- 3.9%) was significantly decreased by L-arginine at 40 and 50 mg/kg doses (4.1 +/- 9.3 and 37.8 +/- 1.6%, respectively) while 5 mg/kg dose of L-arginine significantly potentiated the pyridoxine analgesia. On the other hand, pyridoxine reversed the L-arginine-induced nociception to antinociception (4.1 +/- 9.3%) and augmented the antinociceptive effect of L-arginine (37.8 +/- 1.6%). L-NG-nitroarginine methyl ester (CAS 51298-62-5), a NO synthase inhibitor, at 75 mg/kg, s.c. produced antinociception and significantly increased the antinociceptive effect of pyridoxine (63.7 +/- 1.2%). Methylene blue (CAS 61-73-4, MB), a guanylyl cyclase and/or NO synthase inhibitor, was antinociceptive and nociceptive at 5 and 40 mg/kg doses, respectively, 5 mg/kg dose of MB significantly increased the antinociceptive effect of pyridoxine, but did not change it at 40 mg/kg dose. On the other hand, pyridoxine significantly decreased the antinociceptive effect of MB and reversed the MB-induced nociception to antinociception. Combination of pyridoxine and morphine (CAS 57-27-2) (ED50: 0.13 mg/kg, s.c.) at 49.8 +/- 1.9% revealed a significant antinociceptive potentiation (69.1 +/- 1.8%). The findings of the present study emphasise the contribution of central and/or peripheral L-arginine/NO/cGMP nociceptive processes in pyridoxine-induced antinociception.

Dynamic graciloplasty for fecal incontinence.

Fecal incontinence is a socially incapacitating condition with associated high treatment costs. The most common cause of fecal incontinence is trauma during childbirth followed by surgical interventions. After unsuccessful conventional treatment, muscle transposition is the next treatment option. Two local muscles are used for this purpose: the gluteus and the gracilis muscles. With both muscles, long-term muscle contractions are difficult to maintain due to muscle fatigue. The gracilis muscle, however, is technically much easier to transfer and most activities of daily living and even sports are still possible. Experimental studies have shown that electrical stimulation of skeletal muscles can transform fatigue-prone muscles into fatigue-resistant muscles. In 1986, we started to perform graciloplasty procedures with intramuscular electrodes connected to an electrical stimulator. To date, 200 patients have been treated in our institution using dynamic graciloplasty. All patients had severe incontinence without control of liquid or solid feces, most of them had previously received unsuccessful treatment using other techniques. The mean age was 48 years, the average time that patients had been incontinent was 12.4 years, and the cause of incontinence were trauma (n = 99), congenital (n = 28), pudendopathy (n = 58), and low motor neurological lesions (n = 15). Of these patients, 76% were considered to have successful outcomes. Patients whose cause of incontinence was trauma or pudendopathy tended to respond better to this treatment than patients with anal atresia.