PubMed Health⌕ Search

Biomedical subjects

W J Dodds

Publications and source records attributed to W J Dodds.

At least 73 records · Page 4Linked to original sources
PubMed1991

Abnormal esophageal motility. An analysis of concurrent radiographic and manometric findings.

The findings of concurrent esophageal videofluoroscopy and manometry in 15 patients with major disturbances of esophageal motor function were evaluated and the data were analyzed from a fluid mechanical perspective. Each of 153 fluoroscopic barium swallow sequences was analyzed on a swallow-by-swallow basis. Two distinct pressure domains were identified: intrabolus pressure and pressure within a bolus-free contracting esophageal segment. Analyses in terms of these pressure domains showed specific and consistent correlations between the radiographic and manometric findings. Radiography was insensitive to contractions occurring in esophageal segments devoid of bolus fluid, whereas manometry was insensitive to contractions that did not occlude the lumen. It is concluded that using fluid mechanical principles of bolus transport allows meaningful comparison of esophageal motility as recorded by radiography and intraluminal manometry. However, the inherent limitations in the range of physical phenomena recorded by each modality make these techniques complementary for evaluating esophageal motor function.

Adult↗
PubMed1990

Clinical and laboratory features of a severe form of von Willebrand disease in Shetland sheepdogs.

Ten clinically affected Shetland Sheepdogs were evaluated to define their severe bleeding diathesis and were determined to have von Willebrand factor antigen (vWF:Ag) values less than 0.1% by ELISA assay. The virtual absence of vWF protein by ELISA assay and on multimeric analysis was diagnostic of either homozygosity or probable double heterozygosity for the canine von Willebrand disease (vWD) gene. Clinically affected dogs have type-III vWD and are the offspring of 2 heterozygous parents carrying type-I vWD. Twenty-three percent (1,428 dogs) of the more than 6,000 Shetland Sheepdogs screened for vWD at our facility since 1982 tested within the heterozygous carrier range for the common type-I form of this inherited disorder. Veterinarians and breeders should be aware of the potential for bleeding associated with elective and medical procedures in Shetland Sheepdogs and should use caution when breeding carriers of vWD because of the risk of producing clinically affected offspring with severe type-III vWD.

Animals↗
PubMed1990

Effect of exercise, DDAVP, and epinephrine on the factor VIII:C/von Willebrand factor complex in normal dogs and von Willebrand factor deficient Doberman pinscher dogs.

Endothelial cells in biopsied blood vessels from von Willebrand factor (vWf)-deficient Doberman pinscher dogs contain immunologically detectable vWf. These dogs and normal dogs were treated with DDAVP (0.6 microgram/kg) and epinephrine (0.5 microgram/kg/min for 30 minutes) and were exercised, using 5 different exercise protocols, (3-4 m/s for 5-40 minutes at 0-5% grade) to determine if treatments reported to increase plasma factor VIII:C/vWf complex in humans would elevate canine plasma vWf. Following the two most strenuous exercise conditions--30 and 40 minutes--plasma von Willebrand factor antigen (vWf:Ag) increased in normal dogs by 30% and 70%, respectively. Factor VIII:C was increased 47% by the most strenuous exercise conditions. The vWf-deficient dogs would not exercise beyond 30 minutes and neither vWf:Ag nor factor VIII:C activity increased. Following DDAVP, plasma vWf:Ag increased in the normal dogs by 47% and factor VIII:C activity was increased by 48%. Factor VIII:C activity increased by 30% in the vWf-deficient dogs, but there was only a slight change in vWf:Ag. Bleeding time decreased in 5 of 6 vWf-deficient dogs. In the normal dogs vWf:Ag increased by 14% after epinephrine infusion, but factor VIII:C activity did not change; neither parameter was altered in the vWf-deficient dogs. While the factor VIII:C/vWf:Ag complex was increased in the normal dog by exercise and DDAVP, the increase is not as pronounced as has been reported for humans. It is not known whether the poor response of the vWf-deficient dog is due to low levels of vWf in their endothelium or to a release defect.

Animals↗
PubMed1990

Manometric characteristics of glossopalatal sphincter.

When a liquid bolus is held in the mouth, the posterior tongue and soft palate pinch together to prevent premature spillage of the bolus into the oropharynx. We propose that this glossopalatal closure acts as a glossopalatal sphincter (GPS). In this investigation, we studied glossopalatal closure by obtaining concurrent manometric and radiographic recordings of barium swallows in healthy volunteers. Manometry was done by both a continuous pull through method and also by a stationary catheter technique using a ribbon catheter with multiple sideholes spaced at 1-cm intervals. The results showed that when the mouth was loaded with a fluid bolus, the closed glossopalatal segment generated an asymmetric high-pressure zone with greater pressures toward the tongue and palate than laterally. With swallowing, the glossopalatal sphincter high-pressure zone relaxed and the glossopalatal sphincter opened to allow barium to flow from the mouth into the oropharynx. We conclude that the glossopalatal sphincter functions as a physiological sphincter in that it (1) generates a sustained high-pressure zone and closure when a liquid bolus is held in the mouth and (2) relaxes and opens with swallowing.

Adolescent↗
PubMed1990

Cholecystokinin-induced contraction of opossum sphincter of Oddi. Mechanism of action.

In this study, we evaluated the mechanism of action whereby cholecystokinin increases spike-burst rate of the opossum sphincter of Oddi (SO). Each spike burst corresponds to a peristaltic SO contraction. Two types of animal preparations were evaluated: (1) awake chronic animal preparations and (2) anesthetized animals. A total of 19 chronic animals were prepared by implantation of electrodes on the SO, gastric antrum, duodenum, and jejunum. SO spike-burst rate was stimulated by intravenous infusion of CCK-OP (10 ng/kg/min), feeding, or intraduodenal infusion of fat-containing nutrient. Each stimulus was begun 20 min after cessation of phase III duodenal MMC activity and caused an increase in SO spike-burst rate from about 2 to 6/min that lasted for less than or equal to 1 hr. Such increases were antagonized substantially by hexamethonium, atropine, or methysergide. The CCK antagonist, L364718, antagonized the excitatory SO response to CCK-OP infusion or intraduodenal infusion of fat-containing nutrient (Isocal) but did not antagonize the response to feeding; CR1409 had no antagonistic effect on SO response to any of the three types of stimuli. In the acute studies in anesthetized animals, an intravenous bolus dose of CCK-OP (800 ng/kg) caused a substantial increase in SO spike-burst rate that was antagonized by CR1409 but not by atropine, hexamethonium, methysergide, L364718, or TTX.(ABSTRACT TRUNCATED AT 250 WORDS)

Ampulla of Vater↗
PubMed1990

Mechanism of cholecystokinin-induced contraction of the opossum gallbladder.

The present study evaluated the mechanism of cholecystokinin-induced gallbladder contraction in awake opossums. Each of 19 chronic animal preparations had an indwelling gallbladder cannula for monitoring changes in gallbladder volume and a jugular catheter for administration of cholecystokinin octapeptide and drugs. An intraduodenal catheter allowed intraduodenal infusion of Isocal (Mead Johnson Laboratories, Evansville, Ind.). Bipolar electrodes in the stomach, duodenum, and jejunum enabled monitoring of the duodenal migratory myoelectric complex cycle. One-hour infusions of cholecystokinin octapeptide (10 ng/kg/min), intraduodenal Isocal (0.4 ml/min), or feeding were started 20 min after cessation of phase 3 duodenal migratory myoelectric complex activity. Bolus intravenous doses of potential pharmacological antagonists were given 10 min before and 20 min after the onset of cholecystokinin octapeptide infusion, Isocal infusion, or feeding. Each test challenge induced about 60% gallbladder emptying at 30 min and 70% at 60 min. Cholecystokinin octapeptide-induced gallbladder emptying was converted to filling by hexamethonium and nearly abolished by atropine. Similar results were obtained for gallbladder emptying induced by feeding or duodenal infusion of Isocal. Phentolamine caused a modest decrease of cholecystokinin octapeptide-induced gallbladder contraction at 30 min, whereas postprandial or Isocal-induced gallbladder contraction was unaffected. Cholecystokinin octapeptide-induced gallbladder contraction was not affected by pirenzepine, 4-diphenylacetoxy-N-methylpiperidine methiodide, prazosin, pyrilamine, cimetidine, methysergide, naloxone, or propranolol. In acute studies of anesthetized animals, gallbladder contraction induced by a D100 intravenous bolus of cholecystokinin octapeptide (800 ng/kg) was not antagonized by hexamethonium, atropine, or tetrodotoxin. It is concluded (a) that cholecystokinin-induced physiologic contraction of the opossum gallbladder occurs through neural mechanisms rather than by a direct action of cholecystokinin on gallbladder smooth muscle, and (b) that studies using pharmacologic bolus doses of cholecystokinin octapeptide and tetrodotoxin indicate that cholecystokinin receptors exist on the gallbladder smooth muscle which do not seem to have any physiological role in gallbladder emptying.

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

Effects of substance P and vasoactive intestinal polypeptide on contractile activity and epithelial transport in the ferret jejunum.

Previous studies in the ferret demonstrated that vagal nerve stimulation induced an atropine-resistant water secretion. Substance P and vasoactive intestinal polypeptide are possible mediators of this secretory response. The objectives of this study were to investigate the in vivo effects of substance P and vasoactive intestinal polypeptide on the jejunal musculature and epithelium. Substance P caused an increase in jejunal motility, water secretion, and transmural potential difference. Cholinergic blockade did not affect the substance P-induced contractions, but did reduce the increase in transmural potential difference, suggesting an inhibition of water secretion. Vasoactive intestinal polypeptide abolished motor activity; however, it induced an increase in transmural potential difference that was atropine and tetrodotoxin resistant. By immunohistochemical methods, immunoreactive vasoactive intestinal polypeptide and immunoreactive substance P were localized to both nerve cell bodies and nerve fibers in the ferret intestine. Determination of intestinal concentrations of vasoactive intestinal polypeptide and substance P in the ferret showed concentrations of these two neuropeptides that were similar to those in human intestine and demonstrated much higher concentrations of these substances in the muscular layer than in the epithelial layer. Our data demonstrate that in the ferret substance P excites and vasoactive intestinal polypeptide inhibits jejunal motor activity. However, both peptides increase water secretion. Our results suggest that in response to vagal stimulation, neuronally released substance P or vasoactive intestinal polypeptide may participate in the atropine-resistant water secretion.

Action Potentials↗
PubMed1990

Biomechanics of cricopharyngeal bars.

Patients with a prominent cricopharyngeal bar visible on radiography are generally considered to have spasm of the cricopharyngeus, which is the major muscle component of the upper esophageal sphincter. This condition has been termed "cricopharyngeal achalasia." The aim of this study was to determine the pathogenesis of cricopharyngeal bars. Concurrent videofluoroscopic and manometric examinations of the pharynx and upper esophageal sphincter were performed in a cohort of six patients with prominent cricopharyngeal bars and in eight control volunteers. In each subject, swallows of 2-30-mL barium boluses were recorded. The patients with cricopharyngeal bars showed (a) normal peristaltic contraction in the pharynx, (b) normal axial upper esophageal sphincter pressure and relaxation, (c) normal flow rate across the upper esophageal sphincter, and (d) normal duration of upper esophageal sphincter opening for different bolus volumes. The major abnormalities in the patients with cricopharyngeal bars were (a) reduced maximal dimensions of the upper esophageal sphincter during the transsphincteric flow of barium and (b) increased intrabolus pressure upstream to the upper esophageal sphincter. Thus, the increase in intrabolus pressure preserved normal transsphincteric flow rates even though the upper esophageal sphincter did not open normally. Overall, the constellation of findings in the patients studied suggests that the underlying pathogenesis of their cricopharyngeal bar was reduced muscle compliance wherein the relaxed cricopharyngeus did not distend normally during swallowing.

Adult↗
PubMed1990

The Engström Elsa anaesthetic machine. An electronic system for anaesthesia.

Six Engström Elsa anaesthetic machines have been in regular use for 18-24 months. The machine incorporates a number of new concepts for anaesthetic delivery and monitoring. At flows below 1000 ml/minute, each machine delivered 20% more than the indicated value; at higher flows, the indicated value was within 10% of the flow delivered. Minute volume, tidal volumes and oxygen concentrations were within the manufacturer's specifications. However, vaporizer and vapour monitor performance was outside the (SD) 5% accuracy claimed by the manufacturers. It was noted that the bistable valve requires user familiarity for the change from controlled to spontaneous ventilation to be accomplished with ease. It was also possible to misconnect the breathing system and so isolate the excess pressure escape valve and high-pressure alarm. Nevertheless, once familiarisation was achieved, the machines have proved easy to operate and are particularly satisfactory when used with low fresh gas flows.

Anesthesiology↗
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↗
PubMed1990

Control of belching by the lower oesophageal sphincter.

The mechanism that controls venting of gas from the stomach into the oesophagus was studied manometrically in 14 healthy subjects. The stomach was distended abruptly with one litre of carbon dioxide. Gas reflux was characterised by an abrupt increase in basal oesophageal body pressure to intragastric pressure. Reflux of gas from the stomach into the oesophagus occurred during transient lower oesophageal sphincter relaxations that generally had a pattern distinctly different from swallow-induced lower oesophageal sphincter relaxation. Thus, at the onset of an episode of gas reflux lower oesophageal sphincter pressure had relaxed to 3 mmHg, or less, in 96% of instances. After gas loading of the stomach the prevalence of gas reflux was significantly less when the subjects were supine (1.2/10 min) than when they were sitting (6.8/10 min) (p less than 0.001). The lower oesophageal sphincter relaxations associated with most episodes of gas reflux had a distinctive pattern that resembled those of the lower oesophageal sphincter relaxations associated with acid gastro-oesophageal reflux.

Adult↗
PubMed1990

Effect of swallowed bolus variables on oral and pharyngeal phases of swallowing.

In this investigation, we studied the effects of bolus volume and viscosity on the quantitative features of the oral and pharyngeal phases of swallowing. Concurrent videofluoroscopic and manometric studies were done in 10 healthy volunteers who were imaged in lateral projection. Videofluorography was done at 30 frames/s while concurrent manometry was done with 5 intraluminal transducers that straddled the pharynx and upper esophageal sphincter (UES). Submental electromyography was recorded also. Swallows of 2-20 ml were recorded for low-viscosity liquid barium and high-viscosity paste barium. Analysis indicated that the major effect of increases in bolus volume was an earlier onset of anterior tongue base movement, superior palatal movement, anterior laryngeal movement, and UES opening. These events provide receptive adaptation for receiving a swallowed bolus. Earlier UES opening was associated with an increase in the duration of sphincter opening and sphincter diameter. The major effects of high bolus viscosity, unrelated to bolus volume, were to delay oral and pharyngeal bolus transit, increase the duration of pharyngeal peristaltic waves, and prolong and increase UES opening. Thus the specific effect of bolus viscosity per se differs substantially from that of bolus volume. We conclude that 1) specific variables of swallowing are affected significantly by the variables of the swallowed bolus, such as volume and viscosity; 2) overall, bolus volume and viscosity affect swallowing in a different manner; and 3) the study findings have implications about the neural control mechanisms that govern swallowing as well as about the diagnosis and treatment of patients with abnormal oral-pharyngeal swallowing.

Adult↗
PubMed1990

Fasting and postprandial hepatic bile flow in unanesthetized opossums.

In conscious opossums, we evaluated the relationship between hepatic bile flow and the intestinal motor function during fasting as well as after feeding. In six opossums, bipolar electrodes were implanted from the gastric antrum to the terminal ileum. After cholecystectomy, the common duct was ligated, and a catheter was tied into the proximal common duct for collecting hepatic bile. During subsequent studies, hepatic bile flow was measured, and bile was returned to the duodenum through an externalized duodenal catheter. Cyclic increases in bile flow during fasting did not show a close correlate with the duodenal migratory motor complex (MMC) cycle. Rather, bile flow showed peak values [0.11 +/- 0.02 (SE) ml/min] when phase III MMC activity reached the midileum. Hepatic bile flow correlated closely with the amount of bile acid secreted by the liver. When the bile acid pool was depleted by diverting bile from the intestine, hepatic secretion of bile fell to uniformly low values of approximately 0.04 ml/min that did not show cyclic variation. Hepatic bile flow after feeding increased to a maximal value of 0.12 +/- 0.01 ml/min at 90 min. We conclude that increases in hepatic bile flow during fasting and after meals are determined mainly by variations in intestinal motor activity that alter small bowel transit and thereby affect the enterohepatic circulation of bile acids.

Animals↗