On the pathogenesis of gastroesophageal reflux: the concept of gastroesophageal dyssynergia

OBJECTIVES: The cause of lower esophageal sphincter incompetence in gastroesophageal reflux disease is not clearly understood. We investigated the hypothesis that the esophagogastric junction incompetence results from failure of the gastric distention to produce the lower esophageal sphincter and crural diaphragm contraction caused by a disordered reflex action. METHODS: The study was performed in 19 subjects (mean age, 42.6 +/- 7.2 years; 11 men and 8 women) who had reflux esophagitis and hiatus hernia and were scheduled for a fundoplication operation. Eight control volunteers (mean age, 41.8 +/- 6.9; 5 men and 3 women) who had huge supraumbilical ventral hernia but no reflux esophagitis or hiatus hernia were studied during operative hernia repair. The electromyographic activity and pressure response of the lower esophageal sphincter and crural diaphragm to separate esophageal and gastric distention were recorded. RESULTS: In the control subjects (volunteers) esophageal distention caused diminished electromyographic activity of the crural diaphragm and lower esophageal sphincter with decreased esophagogastric junction pressure, whereas gastric distention increased the electromyographic activity of the crural diaphragm and lower esophageal sphincter with increased esophagogastric junction pressure. In the patients the crural diaphragm and lower esophageal sphincter showed diminished resting electromyographic activity, with either no response or a paradoxical response to esophageal or gastric distention. CONCLUSION: The current study has demonstrated that the lower esophageal sphincter and crural diaphragm in patients with gastroesophageal reflux disease exhibited a diminished resting electric activity and either did not respond or reacted paradoxically to esophageal and gastric distention, constituting what we call esophagosphincteric and gastroesophageal paradox or dyssynergia. The cause of lower esophageal sphincter and crural diaphragm dysfunction is not known; a neurogenic cause was proposed. Further studies are required to investigate this point.     

The effect of external urethral sphincter contraction on the cavernosus muscles and its role in the sexual act

Objectives/Aim A study of the effect of external urethral sphincter contraction on ischio-/bulbo-cavernosus muscles could not be traced in the literature. We investigated the hypothesis that external urethral sphincter contraction induces cavernosus muscles’ contraction. Methods Twenty-one healthy volunteers (age 37.6 ± 9.7 SD years, 12 men, nine women) were studied. The electromyographic response of the ischio- and bulbo-cavernosus muscles to external urethral sphincter stimulation was recorded before and after anesthetization of the external urethral sphincter, and the ischio- and bulbo-cavernosus muscles; the response was also recorded using normal saline instead of lidocaine. Results Upon external urethral sphincter stimulation (five square pulses, 1 ms duration, 53.8 ± 10.2 mA threshold), both cavernosus muscles exhibited increased electromyographic activity with a mean amplitude of 386.2 ± 44.9 μV for the ischio-cavernosus and 318.4 ± 36.6 μV for the bulbo-cavernosus muscle. The mean latency read 16.8 ± 1.3 ms for the ischio-cavernosus muscle and 15.7 ± 1.2 ms for the bulbo-cavernosus muscle. Neither the ischio- nor the bulbo-cavernosus muscle responded to stimulation of the anesthetized external urethral sphincter, but both responded after saline administration. Likewise, the anesthetized ischio- and bulbo-cavernosus muscles showed no response to external urethral sphincter stimulation but responded after saline had been injected. Conclusions Increased electromyographic activity of the two cavernosus muscles on external urethral sphincter stimulation presumably denotes contraction of these two muscles and that this action is probably reflex, mediated through the ‘sphinctero-cavernosus-reflex’. Cavernosus muscles’ contraction assists in the erectile and ejaculatory mechanisms. It is suggested that this reflex be included as an investigative tool in the diagnosis of erectile and ejaculatory disorders, provided further studies are performed.     

Evaluation of acellular human dermis reinforcement of the crural closure in patients with difficult hiatal hernias

Background Biologic prosthetics may circumvent mesh-related complications at the esophageal hiatus by becoming remodeled by native cells. We present our experience with acellular human dermal matrix in the repair of difficult hiatal hernias (HH). Methods Records of 17 patients who underwent laparoscopic HH repair using acellular human dermis to buttress the crural closure were analyzed. Hernias were paraesophageal (PEH) in 12 patients, large type 1 in 1 patient, and recurrent after prior HH repair in 4 patients. Barium swallow (BAS) was obtained 6–12 months after surgery. (Data are presented as mean ± standard deviation.) Results Mean patient age was 65 ± 12 years and BMI was 31 ± 4. Mean gastroesophageal (GE) junction distance above the diaphragm in the PEHs was 4.9 ± 1.5 cm; 9 of 12 patients with PEH had more than 50% of the stomach in the chest. Mean operating time was 273 ± 48 min. Average hiatal defect size was 4.7 × 2.7 cm, with 4.2 ± 1.2 sutures used to close the crura. Nissen fundoplication was performed in all patients, esophageal lengthening in four patients, and anterior gastropexy in three patients. Mean hospital length of stay (LOS) was 2.3 ± 0.8 days. Mean followup was 14.4 ± 4.4 months. Postoperatively, only one (6%) patient had heartburn/regurgitation, one (6%) had mild dysphagia, and two (12%) take proton pump inhibitors. Followup BAS at 10.3 ± 4.9 months after surgery showed small recurrent hernias in two patients (12%), but only one was symptomatic. In addition, there was one symptomatic failure of a redo Nissen in an obese patient. Reoperative gastric bypass 15 months later showed an intact crural closure with a remodeled buttress site. Conclusions Acellular human dermal matrix may be an effective method to buttress the crural closure in patients with large hiatal hernias. Longer followup in larger numbers of patients is needed to assess the validity of this approach. Presented at the April 28, 2006 SAGES Meeting, Dallas, TX     

The cervicocavernosus reflex: Description of the reflex and its role in the sexual act

The paper studies the action and clinical significance of a reflex termed the ‘cervicocavernosus’ reflex. Twenty-two healthy women (mean age 39.7±10.2 SD years) entered the study. The cervix uteri was stimulated both mechanically and electrically by a needle electrode. The response of the bulbo- and ischiocavernosus muscles was recorded by a needle electrode inserted in each muscle. In 10 subjects, the cervix was anesthetized and the cavernosus muscles' response to stimulation of the anesthetized cervix was recorded. The vaginal pressure was measured at rest and on cervical stimulation by means of a balloontipped catheter introduced into the vagina. The mean vaginal pressure at rest was 5.2±1.8 SD cmH₂O and on cervical stimulation 38.8±10.6 cmH₂O. The cavernosus muscles showed no resting activity. Upon cervical stimulation, the muscles contracted with a mean amplitude of 286.4±55.6 SD μV for the bulbocavernosus muscle and 176.6±48.8 μV for the ischiocavernosus muscle; the mean latency of the reflex response was 59.2 ±10.6 SD ms. Stimulation of the anesthetized cervix did not evoke contraction of the muscles. The cervicocavernosus reflex could play a role in enhancing both clitoral and penile erection during the sexual act.     

A case of spontaneous rupture of the esophagus

Spontaneous rupture of the esophagus is rare. It's initial symptoms are so varied that we often have a hard time for making early diagnosis of esophageal rupture. In this case, emergency surgery was performed immediately after early diagnosis by chest CT. When the left thoracotomy was done, the upper portion of the stomach protruded with it's mucous membrane was reflected outward into the thoracic cavity above the diaphragm. When the reflected stomach was drawn back into the abdominal cavity for replacement, a ruptured wound of about 5 cm was observed on the left wall of the esophagus above the diaphragm. The stomach was seen protruded from this ruptured wound of the esophagus, with the mucous membrane reflected outward. No pathological abnormalities of esophagus itself was detected even after through investigation to search the cause for this clinically manifested weakness of the esophageal wall which eventually ruptured causing protrusion of the upper portion of the stomach into the thoracic cavity. The mechanism of this gastric protrusion is difficult to define. The most informative diagnostic investigation was the chest CT.     

The lowest effective intracuff pressure of the esophagus obstruction tube to prevent reflux of gastric contents: a study on rabbits

Purpose

To determine the lowest effective cuff pressure of the esophageal obstruction tube to prevent reflux of gastric contents in rabbits.

Methods

Twenty-two New Zealand white rabbits (2.0–2.5 kg) were anesthetized. An esophageal obstruction tube, an esophageal observation tube, and a gastric tube were inserted into the esophagus and stomach, respectively. Normal saline containing methylene blue was injected into the stomach for an animal model of gastric contents reflux. Possible saline reflux was observed through the esophageal observation tube. It was considered “regurgitation” when the saline flowed out, and “no regurgitation” when the saline did not. When a “regurgitation” result was obtained in a particular rabbit, the intracuff pressure was increased by 10 cm H₂O in the following rabbit and vice versa. The trial was not terminated until six crossover points were observed from “no regurgitation” to “regurgitation.” A probit regression model was used to analyze the effective intracuff pressure of the esophagus obstruction tube after 50 % and 95 % of the rabbits showed no reflux.

Results

The lowest effective intracuff pressure to prevent reflux of gastric contents in 50 % of rabbits from the Dixon up-down method was 61.67 ± 8.16 cm H₂O. The intracuff pressures at which there was 50 % and 95 % probability of lack of gastric contents reflux from a probit regression model were 61.95 and 74.39 cm H₂O, respectively.

Conclusion

The insertion of an esophageal obstruction tube before endotracheal intubation can be an acceptable method for preventing the reflux of gastric contents in most rabbits under light anesthesia.     

Effects of aminophylline on regional diaphragmatic shortening after thoracotomy in the awake lamb.

Aminophylline has been reported to augment diaphragmatic contraction, although this remains a controversial finding. We studied the effect of aminophylline on regional diaphragmatic shortening, changes in transdiaphragmatic pressure (delta Pdi), and integrated regional electromyographic (EMG) activity of the diaphragm (Edi) after a right thoracotomy in nine lambs using sonomicrometry, esophageal and gastric balloons, and EMG. Sonomicrometer crystals and EMG leads were implanted into the costal and crural regions of the diaphragm through a right thoracotomy, and a tracheostomy was performed. The animals were studied while awake within 4 days after surgery. Fractional costal and crural diaphragmatic shortening was measured using the sonomicrometer; delta Pdi was calculated from esophageal and gastric pressures. Respiratory variables were measured through the tracheostomy. Data were collected during quiet breathing and during CO2 rebreathing. After control measurements, aminophylline (10 mg/kg) was administered intravenously, producing a serum concentration of 17.7 +/- 1.5 micrograms/ml. Aminophylline did not augment shortening, increase delta Pdi, or overcome postoperative diaphragmatic inhibition acutely in the awake sheep after a right lateral thoracotomy. A small decrease of end-tidal CO2, from 5.2% to 4.9%, was measured at rest during aminophylline infusion, but Edi was unchanged. Although during CO2 rebreathing diaphragmatic shortening increased, the addition of aminophylline did not further augment shortening. Our data in awake lambs suggest that aminophylline does not improve diaphragmatic contraction in the acute postoperative period.     

Rectourethral reflex: description of a reflex and its clinical significance. A preliminary report.

The present communication studies the technique and clinical significance of a new reflex which I called 'rectourethral reflex'. The study comprised 29 subjects with normal anorectal and urinary functions. The procedure consisted of inflating the rectum with a balloon connected to the distal part of a catheter. The electromyographic activity of the external urethral sphincter was recorded using a concentric needle electrode inserted into the muscle. The procedure was repeated in 10 patients after muscle infiltration with Xylocaine or saline. Rectal distension evoked external urethral sphincter contraction in all the subjects. The amplitude of motor action potentials increased with increasing rectal distension. Anesthetized muscles did not respond, while saline-infiltrated muscles responded. The latency of the reflex decreased with increasing volume of rectal inflation. The reflex harmonizes the relation between defecation and micturition. It guards against involuntary micturition when the rectal detrusor is distended. Changes in amplitude and latency of the reflex may be significant in assessing rectourinary disorders. The reflex could thus be used as an investigative tool in the diagnosis of such disorders.     

Mechanism of ejection during ejaculation: identification of a urethrocavernosus reflex

The ejaculatory mechanism involves 2 reflexes: the "glans-vasal," which seems to bring the semen to the posterior urethra (emission phase of ejaculation), and the "urethromuscular" which ejects it to the exterior (ejection phase). This study investigated the mechanism of bulbocavernosus muscle (BCM) contraction, once the seminal fluid reaches the bulbous urethra. The study included 14 healthy male volunteers (mean age 37 +/- 10.2 SD years). To test the response of the BCM to urethral distension, a 10F balloon-tipped catheter was introduced into the prostatic urethra and filled with saline in increments of 0.25 mL: a needle electrode recorded the response. The balloon was then withdrawn to lie in the membranous. bulbous, and pendulous urethra and the test was repeated at each site. The latency of the muscle response was calculated. The BCM response to each of the anesthetized bulbous urethra and anesthetized BCM was recorded. Distension of the prostatic, membraneous, or pendulous urethra effected no BCM EMG response. Bulbous urethral distension with 0.25 mL of saline also produced no muscle response, whereas distension with 0.5 mL and up to 1.5 mL caused increased EMG activity of the BCM. The muscle response augmented with the increase of the distending volume. The mean latency was 10 +/- 1.3 ms and showed no significant change (p > .05) with the different distending volumes. Neither the anesthetized bulbous urethra nor the anesthetized BCM responded to bulbous urethral distension. The BCM contraction upon distension of the bulbous urethra is probably reflex and mediated through the urethrocavernosus reflex. Small-volume distension did not effect BCM contraction. The latter presumably propels the semen from the posterior to the pendulous urethra. It is suggested that the urethrocavernosus reflex be included in current andrologic investigations for patients with ejaculatory disorders.     

Effects of esophageal shortening on the gastroesophageal barrier: an experimental study on the causes of reflux in esophageal atresia

BACKGROUND/PURPOSE: Gastroesophageal reflux (GER) is frequently recognized after surgical repair of esophageal atresia. The aim of this study was to test the hypothesis that one or more components of the gastroesophageal pressure barrier are weakened by esophageal anastomosis under tension. METHODS: Lower esophageal sphincter pressure (LESP), crural sling pressure (CSP), and the length of the intraabdominal segment of the esophagus (LIAE) were measured by pull-through perfusion manometry in 20 rats before and after resection of 15 mm of the cervical esophagus, and in eight rats before and after esophageal transection (control group). RESULTS: This manouver decreased the LESP from 44.9+/-17.4 to 30.9+/-12.3 mm Hg and the LIAE from 17.9+/-2.8 to 15.8+/-2.4 mm (P < .05) in experimental animals, whereas they did not significantly change in controls. CSP did not change significantly. CONCLUSIONS: Anastomosis of the esophagus under tension in this model decreases significantly the lower esophageal sphincter tone and length of the intraabdominal esophagus, but it does not change the crural sling pressure. Postoperative reflux in patients operated on for esophageal atresia might be in part, caused by this mechanism.     

Intrathecal Morphine Reduces the Visceromotor Response to Acute Uterine Cervical Distension in an Estrogen-independent Manner

Background: Acute uterine cervical distension (UCD) forms the basis for obstetric and some gynecologic pain. Systemic morphine inhibits the visceromotor response to UCD in rats by an action in the central nervous system, but the effect of morphine is blocked by exposure to estrogen. The purpose of the present study was to determine whether this estrogen blockade of the action of morphine reflects a spinal mechanism.

Methods: Virgin Sprague-Dawley rats received estrogen or placebo treatment for 1 week after ovariectomy. Rats were then anesthetized, and the electromyographic response in the rectus abdominis muscle to UCD was recorded in the absence and presence of cumulative dosing with intrathecal morphine.

Results: Estrogen treatment did not alter the stimulus- response relationship between UCD and reflex muscle contraction. Intrathecal morphine reduced the visceromotor reflex response to UCD in a dose-dependent manner that was unaffected by estrogen treatment.     

Effect of rectal distension on vesical motor activity in humans: the identification of the recto-vesicourethral reflex

OBJECTIVE: Rectal lesions have an effect on the urinary bladder and its sphincters. Patients with constipation sometimes complain of difficult micturition or of retention. Urinary retention may also occur after anorectal operations. We investigated the hypothesis that rectal distension affects vesical dilatation through a reflex action. METHODS: The study comprised 22 healthy volunteers (14 men, 8 women, age 42.3 +/- 10.3 SD years). The rectum was distended by rectal balloon inflated with air in increments of 50 mL. The vesical and posterior urethral pressures were recorded before and after individual anesthetization of the rectum, bladder, and posterior urethra. RESULTS: Fifty-milliliter rectal distension effected no vesicourethral pressure response (P > 0.05). At 100 and up to 300-mL distension, the vesical pressure decreased (P < 0.05), while the urethral pressure increased (P < 0.05). The response showed no significant difference upon increase of the distending volume. The mean latency was 16.8 +/- 2.4 milliseconds. Vesicourethral pressure did not respond to rectal distension when the bladder, urethra, or rectum was individually anesthetized. CONCLUSIONS: Rectal distension seems to induce diminished vesical, but increased urethral sphincter tone, an effect that is presumably mediated through a reflex that we call the "recto-vesicourethral reflex." This reflex is apparently evoked at defecation to abort simultaneous micturition. The clinical significance of the reflex needs to be established.     

Pelviureteral inhibitory reflex and ureteropelvic excitatory reflex: Role of the two reflexes in regulation of urine flow from the renal pelvis to the ureter

The mechanism by which the ureteropelvic junction (UPJ) regulates the passage of urine from the renal pelvis to the ureter, and prevents urinary backflow from the ureter to the renal pelvis, is not completely understood. The current communication studies this mechanism in 18 dogs. With the dogs under anesthesia, nephrostomy was done through which two catheters (one pressure and one balloon-tipped) were introduced into the UPJ and the renal pelvis, respectively. Renal pelvis distension with a balloon filled with 1 ml of saline effected a rise of renal pelvic pressure from a mean basal pressure of 4.8 ± 1.2 cm H₂O to 6.9 ± 2.3 cm H₂O (P < 0.05). The basal UPJ pressure of 12.6 ± 2.7 cm H₂O showed no significant change with 1 ml distention of the renal pelvic balloon (P > 0.05). Renal pelvic distension with 2, 3, and 4 ml caused a significant rise of renal pelvic pressure to 8.4 ± 2.7 (P < 0.05), 10.6 ± 2.2 (P < 0.01), and 11.8 ± 1.9 (P < 0.01) cm H₂O, respectively, and a significant drop of UPJ pressure to 4.8 ± 1.2, 4.7 ± 1.1, and 4.6 ± 1.2 cm H₂O (P < 0.01), respectively. Ureteric distension with a balloon filled with 0.5 ml of saline significantly raised the ureteric pressure from a mean basal value of 4.3 ± 1.4 cm H₂O to 14.7 ± 3.3 cm H₂O (P < 0.01) and the UPJ pressure to a mean of 20.8 ± 3.8 (P < 0.05). Ureteric distension with 1 and 1.5 ml of saline led to an elevation of ureteric and UPJ pressure which was not significantly different from that observed with distension with 0.5 ml (P > 0.05). In contrast, the UPJ showed no significant pressure change upon distension of the locally anesthetized renal pelvis or ureter, respectively. Likewise, the locally anesthetized UPJ exhibited no significant pressure response to renal pelvic or ureteric distension. The study demonstrates that urine might have to accumulate in the renal pelvis up to a certain volume and pressure so as to effect UPJ opening, which occurs at its maximum irrespective of the distending volume. UPJ opening upon renal pelvic distension postulates a reflex relationship which we call “pelviureteral inhibitory reflex.” This reflex is believed to regulate the passage of urine from the renal pelvis to the ureter. Ureteric distension closes the UPJ we call this reflex action the “ureteropelvic excitatory reflex” as it seems to prevent reflux of urine through the UPJ and thus protects the kidney. The concept that the UPJ acts as a physiologic sphincter is put forward. Neurourol. Urodynam. 16:315–325, 1997. © 1997 Wiley-Liss, Inc.     

Pyloro-oxyntic neurohumoral inhibitory reflex of acid secretion

Antral distension has previously been shown to activate a neurohumoral mechanism that inhibits acid secretion from the main stomach and from a denervated fundic pouch. Neither the antrum nor the central nervous system (CNS) appears to be the source of the inhibitory substance since, when only vagal communication between the antrum and the CNS is maintained, with vagal denervation of all other abdominal organs, antral distension no longer causes inhibition of acid secretion. The present study was designed to investigate whether intact vagal innervation to the oxyntic cell mucosa was a necessary pathway for this inhibitory mechanism. In four dogs with innervated antral pouch (AP) and gastric fistula (GF), the effect of antral distension with 0.1 M HCl at 40-cm pressure on a plateau of GF acid secretion in response to pentagastrin (4.0 μg kg^?1 hr^?1) was studied before and after proximal gastric vagotomy (PGV). The completeness of vagal denervation of the proximal stomach was shown by failure of acid response to insulin hypoglycemia after PGV. Prior to PGV, antral distension caused a significant inhibition of GF acid response to pentagastrin, with a maximal inhibition of 55% of the plateau of acid secretion. After PGV, antral distension was without inhibitory effect. These results indicate that the inhibitory action of antral distension is mediated by a pyloro-oxyntic reflex. Further, since antral distension inhibits a denervated pouch, the study suggests that this pyloro-oxyntic reflex might release a humoral inhibitor from the oxyntic mucosa.     

Effects of diltiazem on contractility and electromyographic activity of non-fatigued diaphragm in dogs

BACKGROUND: No data are available for diltiazem on muscle function (contractility and electomyographic activity) of non-fatigued diaphragm. METHODS: Eighteen pentobarbital-anesthetized dogs were divided into 3 groups of 6 each: Group I received no drug; Group II received small-dose of diltiazem (0.1 mg.kg-1.h-1); Group III received large-dose of diltiazem (0.5 mg.kg-1.h-1). Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi), the difference between esophageal and gastric pressures. Diaphragmatic electromyographic activity (Edi) was measured by means of electrodes placed at the anterior portion of the crural and costal parts of the diaphragm. After measuring baseline values of Pdi and Edi at 20 Hz and 100 Hz stimulation, the study drug was administered for 30 min. RESULTS: With infusion of diltiazem, Pdi and Edi to each stimulus did not change in Groups II and III. In Group I, these variables also showed no change. CONCLUSIONS: Diltiazem, at doses below 0.5 mg.kg-1.h-1, does not affect contractility and electromyographic activity of non-fatigued canine diaphragm.     

Mechanical consequences of short gastric vessel division at the time of laparoscopic total fundoplication

Laparoscopic Nissen fundoplication is currently the most commonly practiced antireflux operation. Some adverse consequences of the operation remain in the form of mechanical side effects, labeled postfundoplication complaints, of which dysphagia and gas bloat seem to predominate. Measures have been suggested to counteract some of these and one frequently advocated has been division of the short gastric vessels to create a short-floppy wrap. The advantages of this are still debated, particularly in the long-term perspective. The aim of the present study was to evaluate the mechanical consequences of dividing all short gastric vessels at the time of a laparoscopic total fundoplication. Ninety-nine patients with chronic gastroesophageal reflux disease (GERD) were originally allocated on a random basis to have either all short gastric vessels divided or left intact at the time of a laparoscopic total fundoplication. A subsample of these patients, again selected at random, were recruited for a comprehensive manometric investigation 1 year after the operation. In this cohort, 12 patients had all short gastrics divided and in 12 patients, the wrap was done with intact vessels by use of the anterior portion of the fundus. Manometry was carried out by the use of a sleeve sensor to straddle the lower esophageal sphincter (LES), and gastric distension (750 ml air) was used to trigger transient LES relaxations (TLESR). The basal LES tone was similar in the two groups (14.2 ± 2.4 and 18.8 ± 4.3, mean ± SE), respectively. Accordingly, all other relevant manometric variables were equal when the two groups were compared, except for the total number of TLESRs (triggered by gastric distension by air) that were significantly higher (p < 0.02) in patients having their short gastric vessels intact. Consequently, numerically more common cavities were recorded in the latter group. Very similar outcomes in terms of motor function of the LES and esophageal body were observed after a total fundoplication irrespective of whether a complete division of all gastric vessels had been carried out or not. However, after gastric distension with air, more TLESRs were recorded in the latter group suggesting a better maintained ability to vent air from the stomach.     

Effect of Straining on the Lower Esophageal Sphincter: Identification of the “Straining-Esophageal Reflex” and Its Role in Gastroesophageal Competence Mechanism

The lower esophagus is intra-abdominal and exposed to intra-abdominal pressure (IAP) variations that may lead to gastroesophageal reflux (GER). We investigated the hypothesis that the lower esophageal sphincter (LES) undergoes phasic contraction on IAP increase, with a resulting inhibition of the stress GER. The study comprised 17 subjects (age 42.3 ± 8.7 SD yr, 10 men, 7 women) who were scheduled for surgical repair of abdominal hernia. The patients had no swallowing problems. The electromyographic (EMG) activity of the LES and pressure within the LES were recorded at rest and during increased IAP (coughing, straining). The recording was repeated after LES anesthetization or saline infiltration. The LES EMG at rest showed regular slow waves (SWs), superimposed on or followed by random action potentials (APs). Coughing or straining induced increase of the SWs parameters and also of the APs; although the increase with straining was less than with coughing, the difference was insignificant. Coughing or straining increased the LES pressure significantly (p<.05, p<.05, respectively). Ten minutes after LES anesthetization, coughing or straining did not produce significant LES EMG or pressure changes, while saline infiltration of LES caused LES response similar to preinjection. Thus, coughing and straining effected an increase of the LES EMG activity and pressure, an action presumably mediated through a reflex that we call the “straining-esophageal reflex.” This reflex seems to be evoked during increased intra-abdominal pressure and to effect LES contraction, thus, sharing with other factors in prevention of gastroesophageal reflux.     

Pharmacology of Opioid Inhibition to Noxious Uterine Cervical Distension

Background: Reflex abdominal muscle contraction elicited by colorectal distension in male rats is inhibited by [mu]- and [kappa]-opioid receptor agonists and sites of action and receptor subtypes have been probed. The authors examined the pharmacology of opioid agonist inhibition in visceral pain related to the uterine cervix, the source of labor pain.

Methods: Ovariectomized female rats were anesthetized with halothane, and metal rods inserted in the uterine cervix through a small midline laparotomy. After a period of stabilization the cervix was distended by manual separation of the rods, using stimuli of 25-100 g, and reflex rectus abdominis electromyographic activity was recorded. After determining the stimulus response relationship, we tested inhibition of reflex activity by -U50,488 and morphine and their reversal with norbinaltorphimine, or with naltrexone and methyl-naltrexone, respectively.

Results: Cervical distension produced a stimulus-dependent increase in electromyographic activity, with a threshold of 25 g. Morphine and -U50,488 produced dose-dependent inhibition of the reflex activity. Log linear regression analysis demonstrated an ID50 of 0.03 for morphine, and of 0.05 mg/kg for -U50,488. These effects were reversed by naltrexone, but not by methylnaltrexone or norbinaltorphimine.     

Short esophagus or bad dissected esophagus? An experimental cadaveric study

Short esophagus is defined as the inability to reduce the gastroesophageal junction below the diaphragm. One of the factors responsible for this inability can be inadequate esophageal mobilization. We evaluated esophageal lengthening achieved by means of dissection in a cadaveric model. Fifty-one cadavers were dissected (27 transthoracically and 24 transhiatally). Abdominal esophageal length was assessed before and after dissection of the esophagus from the hiatus to the carina. In the transthoracic group, a mean of 1.7 ± 1.3 cm (range0.3 to 5.0cm) was gained with dissection. In the transhiatal group, a mean of 1.8 ± 0.8 cm (range 0 to 3.0 cm) was gained with dissection. In a comparison of results of transthoracic and transhiatal approaches, the difference was not statistically significant. We concluded that a significant increase in esophageal length was achieved after dissection; however, the access route (thorax or abdomen) did not influence the results.     

Partially covered esophageal stents cause bowel injury when used to treat complications of bariatric surgery

Background

We hypothesized that an esophageal nitinol stent that is mainly silicone-covered but partially uncovered may allow tissue ingrowth and decrease the migration rate seen with fully covered stents and still allow safe stent removal. The aim of this study was to evaluate the first human results of using partially covered stents for anastomotic complications of bariatric surgery.

Methods

This was a retrospective evaluation of all patients with staple-line complications after bariatric surgery who received a partly covered stent at a single tertiary-care bariatric center. The stents varied in length from 10 to 15 cm and in diameter from 18 to 23 mm.

Results

From April 2009 to April 2010, eight patients received partially covered stents on 14 separate occasions. The indications were gastrojejunal stricture in four, acute leak in two, acute leak followed by a later stricture in one, and a perforated anastomotic ulcer in one patient. Single stents were placed in 12 sessions and two overlapping stents in two sessions. At the time of stent deployment, one patient had the uncovered proximal end of the stent in the stomach, with all others in the distal esophagus. Immediate symptom improvement occurred in 12/14 stent placements. Oral nutrition was initiated for 10/14 stent treatments within 48 h. Stents were removed after 25 ± 10 days. Minor stent displacement occurred with 9/13 stents, with the proximal end of the stent moving into the stomach, though the site of pathology remained covered. The stents were difficult to remove when tissue ingrowth was present. One patient required laparoscopic removal and one required two endoscopy sessions for removal. At the time of removal of ten stents, where the proximal end was found in the stomach, four had gastric ulceration, three had gastric mucosa replaced by granulation tissue, and three had normal gastric mucosa. In four cases where the proximal portion of the stent stayed in the esophagus, the esophageal deployment zone had abnormalities: three with granulation tissue and one with denuding of the esophageal mucosa. The distal uncovered portion of the stent in the Roux limb never became embedded in the mucosa and caused minimal injury.

Conclusions

A partially covered stent was successful in keeping the site of the pathology covered and provided rapid symptom improvement and oral nutrition in most patients. The proximal end of the stent generally moved from the esophagus to the stomach, probably due to esophageal peristalsis. The proximal uncovered portion of the stent causes significant bowel mucosal injury and sometimes becomes embedded in the esophagus or the stomach, making removal difficult. We no longer use partially covered stents.