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Biomedical subjects

R C Arndorfer

Publications and source records attributed to R C Arndorfer.

At least 19 recordsLinked to original sources
PubMed1992

Esophagoglottal closure reflex: a mechanism of airway protection.

Abrupt esophageal distention occurs commonly during gastroesophageal reflux, thereby generating a circumstance favorable to esophagopharyngeal regurgitation and laryngeal aspiration of gastric refluxate. The aims of the present study were to examine the glottal response to esophageal distention by air and regional esophageal distention by a balloon. Fifteen healthy volunteers (age, 25 +/- 5 years) were studied while they were in an upright position. Using concurrent videoendoscopy and manometry, glottal and upper esophageal sphincter (UES) responses to abrupt esophageal distention by air injection (10-60 mL) and balloon distention (1.5, 2.0, and 2.5 cm) were recorded simultaneously. In addition, 6 subjects were studied with concurrent synchronized videofluoroscopy. Results showed that esophageal distention by air at a threshold volume of 10-60 mL caused vocal cord closure. The UES response to this threshold volume was variable. Volumes larger than the threshold value caused complete UES relaxation and belching. In addition to vocal cord closure, belching was accompanied by anterior movement of the glottis. On videofluoroscopy, the hyoid bone moved anteriorly in association with belching, but not with vocal cord closure without belching. Proximal esophageal distention by the balloon also provoked vocal cord closure. This response was less consistent for balloon distention in the middle and distal esophagus. It is concluded that (a) esophageal distention by either air or a balloon evokes a glottal closure mechanism, thereby suggesting the existence of an esophagoglottal reflex; (b) this reflex is elicited most easily by distention of the proximal esophagus; (c) glottal and UES responses to esophageal distention are independent from each other; and (d) the esophagoglottal closure reflex may play an important role in preventing laryngeal aspiration of acid due to gastroesophageal reflux accompanied by acid regurgitation into the pharynx.

Adult↗
PubMed1992

Manometric characteristics of cervical dysphagia in a patient with the Kearns-Sayre syndrome.

The manometric findings of deglutitive pharyngoesophageal function in a patient with the Kearns-Sayre syndrome and cervical dysphagia are described. These findings indicate that striated muscles of the pharynx, upper esophageal sphincter (UES), and proximal esophagus are involved. Near absence of pharyngeal peristalsis, abnormally low UES resting pressure, and absence of proximal esophageal peristalsis characterize the manometric findings in this patient. It is conceivable that in mild cases, a combination of various degrees of severity of the above findings may exist.

Adult↗
PubMed1991

Gastrointestinal motor effects of erythromycin in humans.

The effects of an antibacterially effective IV dose of erythromycin on gastrointestinal motor activity were investigated in eight normal healthy human volunteers in the fasted state and the fed state. Motor activity was recorded by a multilumen manometric tube. Data were analyzed visually and by a computer method. Blood samples were obtained for erythromycin and motilin assays. In the gastric antrum, erythromycin significantly increased the total duration, amplitude, and area under contractions from 0 to 60 minutes and frequency of contractions from 0 to 30 minutes from the start of its infusion in the fasted state. A similar response in the fed state occurred mostly from 0 to 30 minutes after the start of erythromycin infusion. By contrast, erythromycin inhibited the frequency and decreased the duration of small intestinal contractions in the fed state but had no effect in the fasted state. The gastric motor response was related to the plasma concentration of erythromycin, but not to plasma motilin. Erythromycin significantly shortened the duration of migrating motor complex disruption by a meal. Erythromycin also induced symptoms of upper abdominal pain, bloating, and nausea. Abdominal pain was related to strong antral contractions in both fasted and fed states; bloating occurred only in the fed state. Nausea occurred in both fasted and fed states, but it was not related to any specific pattern of motor activity. It is concluded that the strong antral contractions induced by erythromycin may accelerate the rate of gastric emptying, but they may also be responsible for causing the sensations of upper abdominal pain and bloating. The motor response to erythromycin is less during the fed than during the fasted state. The strong antral contractions induced by erythromycin are not mediated by the release of motilin.

Abdominal Pain↗
PubMed1991

Myogenic oscillatory mechanism for opossum esophageal smooth muscle contractions.

We evaluated the control of phasic contractions in opossum esophageal circular smooth muscle by determining the contractile response in vitro to agents that cause membrane depolarization and excitation by different mechanisms. Transverse muscle strips taken from different sites along the length of the smooth muscle esophagus were exposed to progressively increasing concentrations of tetraethylammonium (1-30 mM), K+ (4.6-30 mM), or bethanechol (10(-6) to 10(-2) M). In normally inactive esophageal circular smooth muscle, tetraethylammonium and high K+ concentration elicited phasic contractions that were not blocked by atropine and tetrodotoxin. Bethanechol, an M2 muscarinic receptor agonist that acts selectively on smooth muscle, elicited phasic contractions that were not blocked by tetrodotoxin. We conclude that a latent myogenic oscillatory mechanism for control of phasic contractions exists in esophageal circular smooth muscle and that it may be activated by nonspecific excitation of the smooth muscle membrane. We suggest that this myogenic oscillatory mechanism is likely excited and modulated by nerves.

Animals↗
PubMed1990

Coordination of deglutitive glottic closure with oropharyngeal swallowing.

The goals of this study were to quantify the temporal relationship between swallow-induced glottic closure and (a) signals of swallow initiation, such as hyoid bone movement, tongue base movement, and mylohyoid electrical activity; (b) pharyngeal peristalsis; (c) laryngeal elevation; (d) vestibular closure; and (e) oropharyngeal barium bolus transit. Eight normal subjects (age 20-30 yr) were studied by concurrent transnasal video laryngoscopy, pharyngeal intraluminal manometry, and submental surface electromyography. The manometric, electromyographic, and both video recordings were synchronized with one another using a specially designed event marker. Dry, 5-ml water, and 5-ml barium swallows were recorded. Frame-by-frame analysis of the video endoscopic recordings showed that deglutitive laryngeal kinetics consisted of vocal cord adduction associated with transverse approximation of the arytenoids followed by vertical approximation of arytenoids to the base of the epiglottis followed by laryngeal ascent and epiglottic descent. Onset of swallow-induced vocal cord adduction preceded the onset of hyoid bone movement, base of the tongue movement, and submental surface myoelectric activity by 0.33 +/- 0.04 (SE) s, 0.31 +/- 0.04 s, and 0.38 +/- 0.04 s, respectively. Onset of vocal cord adduction also preceded the initiation of peristalsis in the nasopharynx and its propagation to oropharynx and upper esophageal sphincter by 0.64 +/- 0.05 s, 0.82 +/- 0.05 s, and 1.08 +/- 0.04 s, respectively. The time between the onset of vocal cord adduction and their return to full opening was 2.2 +/- 0.09 s. It was concluded that (a) among events evaluated, vocal cord adduction is the initial event during the swallowing sequence; (b) laryngeal kinetics during deglutition have distinctive features, and their close coordination with other swallowing events suggests that they are an essential feature of the swallowing program; and (c) abnormal laryngeal kinetics or lack of coordination between the glottic closure mechanism and oropharyngeal bolus transport may have an important role in swallow-induced aspiration.

Adult↗
PubMed1990

Oesophageal acidification does not increase lower oesophageal sphincter pressure.

We studied the effect of distal oesophageal acidification on lower oesophageal sphincter (LOS) pressure in normal human volunteers and in cats. The distal oesophagus was acidified by intraluminal injection of 0.1N HCl (pH 1.2). The LOS pressure was recorded by a sleeve device while pharyngeal and oesophageal pressures were monitored by nonperfused, water filled catheters. In normal human subjects, distal oesophageal acidification did not elicit a change in LOS pressure. In anaesthetised cats, injection of acid into the distal oesophagus elicited immediate LOS relaxation followed by a secondary peristaltic sequence. With propagation of the peristaltic sequence into the LOS, the LOS pressure abruptly increased 20-100 mmHg and gradually returned to the preinjection value over 15-180 s. In the one instance in which we were able to acidify the distal oesophagus without evoking secondary peristalsis, the LOS pressure did not change. Injection of saline into the distal oesophagus evoked a response in the LOS and oesophageal body that was indistinguishable from that seen with acid. We conclude that contrary to common belief, distal oesophageal acidification itself does not affect LOS pressure in man or the cat.

Adult↗
PubMed1989

Spatial and temporal patterns of human jejunal contractions.

We recorded human jejunal motor activity by a 12-lumen manometric tube with recording sites 2 cm apart. The contractile activity in the fasted and the fed state was analyzed by computer to define the spatial and temporal patterns of contractions. Mean duration and area of single contractions during phase III activity were not different from those during phase II activity. By contrast, the frequency and amplitude of contractions, their propagation distance, and the percentage of contractions that propagated for greater than or equal to 2 cm were significantly greater during phase III than during phase II activity. The mean frequency and percentage of propagated contractions in the fed state were intermediate between those during phase II and phase III activity. Mean propagation distance of postprandial contractions was not different from that of phase II contractions. Most contractions in the fed state were uncoordinated at adjacent recording sites. Occasionally, large-amplitude and long-duration contractions, called individual migrating contractions, propagated over long distances and frequently over the entire 22-cm study segment. We conclude that there are some significant differences between the spatial and temporal patterns of contractions between the fed state and phase II and phase III activity. The largely disorganized phasic contractions in the fed state may cause mostly mixing of the ingested meal and its slow distal propagation, whereas the infrequent individual migrating contractions may rapidly propel intestinal contents over longer distances.

Adult↗
PubMed1988

Effects of morphine on the human sphincter of Oddi.

The effects of morphine on intraluminal pressures recorded from the sphincter of Oddi (SO) at endoscopic retrograde cholangiopancreatography in 19 patients who were without evidence of biliary or pancreatic disease were studied. Morphine was given in four successive doses of 2.5, 2.5, 5, and 10 micrograms/kg iv at five minute intervals. Morphine in subanalgesic doses increased the frequency of SO phasic pressure waves to a maximum of 10-12/min, caused the phasic waves to occur simultaneously along the sphincter segment, increased phasic wave amplitude from 72 (26) (SE) to 136 (31) mmHg, and increased SO basal pressure from 10 (1) to 29 (9) mmHg (p less than 0.05). The effects of morphine on the SO are mediated by more than one opioid receptor type, as naloxone competitively antagonised the increase in phasic wave frequency induced by morphine, but did not affect the increase in SO basal pressure elicited by morphine. When given after naloxone, morphine decreased phasic wave amplitude, an inhibitory effect that is normally masked by morphine's dominant naloxone sensitive excitatory effect. Mu receptors do not appear to be involved in control of spontaneous SO motor function, as naloxone alone did not affect SO motor activity. The excitatory effects of morphine on the SO are not mediated by cholinergic nerves, as they were not blocked by atropine. Cholinergic nerves, however, may have a role in regulating spontaneous SO motor function because atropine alone depressed phasic wave activity and basal pressure. Although morphine does cause 'spasm' of the human SO, its effects are more complex than is commonly believed.

Adult↗
PubMed1987

Chronic recurrent pancreatitis secondary to a submucosal ampullary tumor in a patient with neurofibromatosis.

We report a 45-year-old nonalcoholic patient with Von Recklinghausen's disease and chronic recurrent pancreatitis. On endoscopy, a benign-appearing submucosal tumor surrounded the papilla of Vater. Cannulation of the pancreatic duct showed a dilated ductal system with subsequent delayed drainage. Endoscopic manometry revealed elevated sphincter of Oddi pressures. Endoscopic sphincterotomy resulted in immediate normal drainage of the pancreatic duct and in subsequent clinical improvement.

Ampulla of Vater↗
PubMed1987

A method for continuous monitoring of upper esophageal sphincter pressure.

We tested a manometric assembly employing a sleeve sensor that is able to monitor anterior or posterior pressure in the human upper esophageal sphincter (UES) for prolonged intervals. When compared to rapid pull-through measurement of UES pressure obtained with conventional manometric assemblies, the sleeve sensor measured significantly lower UES pressures with less variability between subjects, thereby suggesting that the rapid pull-through maneuver stimulates the UES to contract. Concurrent recordings of UES pressure with a sleeve sensor and a side-hole sensor during a slow station pull-through yielded almost equal pressure values at the peak of the high-pressure zone (station zero), but the side-hole site recorded significantly lower pressures than the sleeve at stations 0.5 cm or more from the peak of the high-pressure zone. During 10 min of recording at station zero, the sleeve sensor recorded greater pressures than the side-hole sensor. This finding demonstrated the suceptibility of the side-hole sensor to axial movement relative to peak UES pressure. When stationary, both the sleeve sensor and the side-hole sensor recorded significantly lower UES pressure after 1-2 min of recording, again suggesting that movement of the recording assembly stimulates the UES to contract. Sleeve recordings of swallow-induced UES relaxations showed that UES relaxations induced by water swallows were slightly longer than those induced by dry swallows. Augmentations of UES pressure induced by balloon distension of the esophageal body were also recorded. We conclude that the sleeve sensor is a suitable method for investigating the normal physiology and pathophysiology of the UES in human subjects.

Adult↗
PubMed1987

Effect of sleep, spontaneous gastroesophageal reflux, and a meal on upper esophageal sphincter pressure in normal human volunteers.

Owing to the inherent difficulties of recording upper esophageal sphincter pressure, little is known about normal upper esophageal sphincter physiology. In this study we used a modified sleeve device to record upper esophageal sphincter pressure continuously in 8 normal volunteers. Intraesophageal pH and electroencephalogram activity were also recorded to document the occurrence of spontaneous gastroesophageal reflux and sleep. After an hour of baseline recording, the subjects ate a meal. Recording was then resumed for an additional 7 h during which period the subjects slept part of the time. The mean upper esophageal sphincter pressure was measured for each 10-min epoch. Electroencephalogram recordings were read blindly for the presence and stage of sleep. Periods of sleep were then correlated with the manometric tracings. Mean upper esophageal sphincter pressure during wakefulness, stage 1 sleep, and deeper sleep was 40 +/- 17 (SD), 20 +/- 17, and 8 +/- 3 mmHg, respectively. A significant change in upper esophageal sphincter pressure did not occur postprandially or during episodes of spontaneous gastroesophageal reflux. Upper esophageal sphincter pressure was observed to increase transiently with each inspiration during periods of restfulness and sleep, a response consistent with the hypothesis that one function of the upper esophageal sphincter is to exclude air from the esophagus during respiration. The demonstration that upper esophageal sphincter pressure falls markedly during sleep may have significance in that this diminishes the barrier to nocturnal regurgitation and potential aspiration.

Adult↗
PubMed1986

Upper esophageal sphincter function during belching.

We studied the mechanism of belching with specific attention to the upper esophageal sphincter (UES) in 14 normal volunteers. Belching occurred by the following sequence of events: lower esophageal sphincter relaxation; gastroesophageal gas reflux, recorded manometrically as a gastroesophageal common cavity phenomenon; UES relaxation; esophagopharyngeal gas reflux; and restoration of intraesophageal pressure to baseline by a peristaltic contraction. Upper esophageal sphincter relaxations comparable to those associated with belches were induced by abrupt esophageal distention with air boluses. In contrast, fluid boluses injected into the midesophageal body either had no effect on UES pressure or increased UES pressure. Thus, the UES responded to esophageal body distention in two distinct ways: abrupt relaxation in response to air boluses and pressure augmentation in response to fluid boluses. Mucosal anesthesia did not alter the UES response to esophageal boluses of gas or liquid thereby making it unlikely that these substances are differentiated by a mucosal receptor. Rapid distention of the proximal esophagus with a cylindrical balloon (15 cm long) elicited UES relaxation. These findings suggest that the rapidity and spatial pattern of esophageal distention, rather than discrimination of the type of material causing the distention, determines whether or not UES relaxation occurs.

Adult↗
PubMed1986

Esophageal peristaltic dysfunction in peptic esophagitis.

Esophageal exposure to acid is a major determinant in the pathogenesis of reflux esophagitis. In this study, we analyzed the esophageal peristaltic function of 177 patients and asymptomatic volunteers for abnormalities that could lead to prolonged esophageal acid clearance. The subjects were divided into five groups: normal volunteers, patient controls, patients with noninflammatory gastroesophageal reflux disease, patients with mild esophagitis, and ones with severe esophagitis. Manometric data were analyzed for the occurrence of failed primary peristalsis, for the occurrence of feeble peristalsis in the distal esophagus, and for hypotensive lower esophageal sphincter pressure. From an analysis of the data on control patients, peristaltic dysfunction was defined as the occurrence of either failed primary peristalsis or hypotensive peristalsis in the distal esophagus for over half of the test swallows. Peristaltic dysfunction was increasingly prevalent with increasing severity of peptic esophagitis, occurring in 25% of patients with mild esophagitis and 48% of patients with severe esophagitis. A correlation did not exist between the occurrence of peristaltic dysfunction and hypotensive lower esophageal sphincter pressure (less than or equal to 10 mmHg). We conclude that peristaltic dysfunction occurs in a substantial minority of patients with peptic esophagitis and could contribute to increased esophageal exposure to refluxed acid material.

Adult↗
PubMed1986

Integrity of cholinergic innervation to the lower esophageal sphincter in achalasia.

The human lower esophageal sphincter (LES) is believed to be innervated by nonadrenergic, noncholinergic inhibitory nerves, and cholinergic excitatory nerves. In idiopathic achalasia, LES relaxation is abnormal because the inhibitory nerves to the sphincter are either absent or functionally impaired. The integrity of cholinergic excitatory nerves to the LES, however, has not been thoroughly evaluated. In 27 patients with untreated idiopathic achalasia, and 21 healthy volunteers, we investigated the hypothesis that postganglionic cholinergic nerves to the LES are functionally intact in achalasia. The LES responses to atropine, edrophonium, methacholine, amyl nitrite, and pentagastrin were assessed. In 2 achalasia patients, patterns of fasting motor activity in the LES were investigated during overnight manometric studies. Resting LES pressure was significantly greater in the achalasia patients, 41 +/- 4 mmHg (mean +/- SE), than in the normal subjects, 20 +/- 2 mmHg. Atropine significantly reduced LES pressure in both groups by 30%-75%. Edrophonium increased LES pressure in the achalasia patients but had negligible effect on the normal subjects. The LES in achalasia patients exhibited an increased sensitivity to both methacholine and pentagastrin compared with the normal subjects. In both patients who underwent an overnight manometric study, the LES exhibited cyclic phasic contractile activity synchronous with gastric contractions during the migrating motor complex. We conclude that the study findings support the hypothesis that postganglionic cholinergic LES innervation in achalasia patients is either normal or only minimally impaired, in contrast to the marked impairment of the inhibitory nerves governing LES relaxation.

Adult↗
PubMed1985

Multipeaked esophageal peristaltic pressure waves in patients with diabetic neuropathy.

We evaluated esophageal function in 14 consecutive insulin-dependent diabetic patients who had evidence of peripheral and autonomic neuropathy, but no esophageal symptoms. One to three contraction waves immediately followed a primary peristaltic contraction wave. The majority of these multipeaked pressure complexes consisted of two peaks. Multipeaked contractions were observed with all peristaltic waves in 12 of the 14 diabetic patients and with most of the peristaltic complexes in the remaining 2 patients. Multipeaked peristaltic waves were present in 1 of 6 diabetic patients without neuropathy, in 1 of 100 consecutive nondiabetic patients referred for suspected esophageal disease, and in 1 of 10 healthy volunteers. Double-peaked peristaltic pressure complexes in the nondiabetic control subjects differed from those present in the insulin-dependent patients by their low incidence and by a tendency to be limited to the distal esophagus. Pharmacologic responses to edrophonium and atropine suggested a possible increased cholinergic tone as the basis of the multipeaked peristaltic waves in diabetics with autonomic neuropathy.

Adolescent↗
PubMed1979

Biliary and pancreatic duct pressures measured by ERCP manometry in patients with suspected papillary stenosis.

Papillary stenosis is an imprecisely defined clinical syndrome which eludes definitive diagnosis. In this study we evaluated 26 patients with suspected papillary stenosis by manometric examination of the sphincter of Oddi done during ERCP examination. Basal pressure in the sphincter of Oddi was elevated in 14 of the patients. Of these 14 patients, 10 underwent sphincterotomy and all experienced improvement in clinical symptoms after their surgery. We suggest that ERCP manometry is a useful procedure for identifying patients with papillary stenosis who may benefit from sphincterotomy.

Ampulla of Vater↗
PubMed1979

Depressant effect of sodium nitroprusside on the lower esophageal sphincter of the opossum.

In this study, we evaluated the effect of sodium nitroprusside (SNP), a vascular smooth-muscle relaxant, on lower esophageal sphincter (LES) pressure in the opossum. Resting LES pressure was monitored with a perfused sleeve sensor which allows accurate recording of LES pressure irrespective of axial LES motion. Intravenous pulse doses and infusion doses of SNP both caused significant decreases in both blood pressure and LES pressure. Les tone, however, was more sensitive to SNP than blood pressure. For example, an SNP pulse dose of 20 microgram/kg which lowered blood pressure only about 30% virtually abolished LES tone. A similar result was obtained for an SNP infusion dose of 10 microgram/kg/min. Tachyphylaxis to SNP did not occur for repeated pulse doses to 10 microgram/kg, but did develop during a 20-min infusion of 10 microgram/kg/min. The effect of SNP on LES pressure was not antagonized by propranolol, metiamide, haloperidol, atropine, phentolamine, or tetrodotoxin. We conclude that the potent depressant effect of SNP on LES tone is due to a direct action of the drug on sphincter smooth muscle.

Animals↗