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Biomedical subjects

W J Dodds

Publications and source records attributed to W J Dodds.

At least 145 records · Page 8Linked to original sources
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↗
PubMed1987

Salivary response to esophageal acid in normal subjects and patients with reflux esophagitis.

We studied the effect of esophageal acid perfusion on salivation in patients with reflux esophagitis and in normal subjects. Serial 10-min saliva collections were obtained by expectoration during perfusion of the esophagus with water, and then 0.1 N HCl (pH 1.2) for 50 min or 0.01 N HCl (pH 2.1) for 120 min. Within 1-5 min of beginning 0.1 N HCl perfusion, all 8 patients with esophagitis developed heartburn accompanied by an increase in saliva flow. By the time the severity of heartburn required discontinuation of HCl perfusion (10-40 min), saliva flow had increased nearly fourfold. With 0.1 N HCl perfusion, 8 of 10 volunteers developed mild heartburn after 22 +/- 3 min (mean +/- SE), whereas 0.01 N HCl induced heartburn in 6 of 10 volunteers after 57 +/- 12 min of perfusion. Saliva flow increased concurrently with the onset of heartburn and doubled in those volunteers who developed heartburn. Saliva flow did not change in those volunteers who were without heartburn. We conclude that esophageal acid perfusion unaccompanied by heartburn does not affect salivation. However, saliva flow increases concurrently with the onset of heartburn, a phenomenon called "water brash" when clinically evident. The increased saliva flow that accompanies heartburn may act as an endogenous antacid that serves as a protective response to symptomatic gastroesophageal reflux.

Acids↗
PubMed1987

Dysfunction of the belch reflex. A cause of incapacitating chest pain.

We report a 25-yr-old woman who suffered incapacitating chest pain caused by upper esophageal sphincter (UES) dysfunction. She presented with a long history of severe episodic chest pain associated with gurgling noises in her chest and was unable to belch despite feeling a need to do so during pain episodes. Fluoroscopic and manometric studies confirmed that the patient's chest pain and gurgling noise were associated with dysfunction of the belch reflex. Although reflux of gas from the stomach into the esophageal body occurred normally, the extreme esophageal distention resulting from the gas reflux failed to trigger UES relaxation. Consequently, there was no venting of gas across the UES. The gurgling noise was caused by the gastroesophageal reflux of gas and the pain was associated with profound esophageal distention. A manometric study of the UES revealed absent or incomplete UES relaxation in response to abrupt esophageal distention by gastroesophageal gas reflux, so that the nadir of UES pressure always exceeded esophageal body pressure. The distended esophagus was repeatedly cleared by secondary peristalsis. To our knowledge this is the first description of chest pain caused by dysfunction of the belch reflex. We speculate that the mechanism described in this patient may account for a subgroup of patients with "chest pain of esophageal origin."

Adult↗
PubMed1987

Animal models for the evolution of thrombotic disease.

Naturally occurring hemorrhagic and thrombotic diseases of animals closely parallel their human counterparts. While such models may be particularly useful in studying the pathogenesis of human disease, it is usually more realistic to depend upon experimentally induced disease models. The species selected for use is therefore of major importance in providing meaningful extrapolation to humans, as are the experimental design and type of procedure (in vitro, ex vivo, in vivo). Regardless of the test system used when in vitro procedures are employed, these must be translated eventually to the in vivo situation. Information about the normal aging process of different species is important here and should influence selection of the species and test system. The ideal situation may not be feasible or pertain because of cost, availability, size, and investigator familiarity, or lack thereof, with the most suitable species or model.

Animals↗
PubMed1987

Electrical control activity of the lower esophageal sphincter in unanesthetized opossums.

We recorded lower esophageal sphincter (LES) pressure and myoelectrical activity concurrently from the esophagus, LES, stomach, and proximal small intestine in unanesthetized opossums. LES electrical activity was characterized by almost continuous, spikelike oscillations at 15-40/min, which were accompanied by minicontractions 5-15 mmHg in amplitude. Basal LES pressure, however, did not depend on electrical oscillations. The LES exhibited cyclic changes in pressure and electrical activity synchronous with gastric contractions associated with the migrating myoelectric complex (MMC). During phase I, the LES pressure was stable and its electrical activity showed continuous low-amplitude (less than 0.3 mV) oscillations at a rate of 20 +/- 2 per min. During phases II and III of MMC-related gastric activity, the LES developed strong phasic contractions, while the electrical oscillations grouped into clusters with an increased rate (32 +/- 1 per min) and amplitude (0.4-0.8 mV), each cluster corresponding to a phasic contraction. Feeding, pentobarbital, and cholinergic blockade abolished MMC-related LES activity and resulted in a steady rate of LES electrical oscillations. LES relaxation induced by swallows or esophageal balloon distention abolished the LES electrical oscillations. Increases in LES pressure induced by pharmacological and hormonal stimulation correlated with concurrent increases in the rate of electrical oscillations. We conclude that the opossum LES has a unique pattern of electrical activity that differs from the electrical activity recorded from smooth muscle elsewhere in the gastrointestinal tract. This electrical activity is a form of control wave associated with a minicontraction. Phasic LES contractions during the intestinal MMC cycle may result from an increase in the rate and amplitude of the LES electrical control waves and fusion of minicontractions.

Anesthesia↗
PubMed1987

Sonographic evaluation of resting gallbladder volume and postprandial emptying in patients with gallstones.

We investigated fasting gallbladder volume and gallbladder emptying in response to a fatty meal in 20 patients with asymptomatic gallstones and compared the results with findings from healthy controls. Compared with control subjects without gallstones, the majority of patients with gallstones exhibited a higher resting gallbladder volume, less fractional emptying after a fatty meal, and a higher postmeal residual volume. These abnormalities all appeared to stem from an abnormally high resting gallbladder volume. Whether the increased gallbladder volume and decreased postprandial fractional emptying in the gallstone patients represents a primary or secondary abnormality remains to be determined. The results suggest that in some patients decreased gallbladder contractility may contribute to gallstone development or proliferation.

Adult↗
PubMed1986

Evidence for regulatory control of canine platelet phosphodiesterase.

Forskolin, epinephrine, and prostaglandin I2 were used to examine the adenylate cyclase-phosphodiesterase system of intact thrombopathic and normal canine platelets. The results provide indirect support for the hypothesis that the elevation of intraplatelet c-AMP in this unique hereditary defect is due to impaired phosphodiesterase activity. The inhibitory (Nj) and stimulatory (Ns) components of adenylate cyclase appeared functionally intact. Cytosolic fractions of normal and thrombopathic platelets had similar cAMP hydrolytic activities. The failure of intact forskolin-stimulated thrombopathic platelets to return elevated cAMP to non-stimulated levels after 15 min, despite significant phosphodiesterase activity in cytosolic fractions, implies that the platelet isoenzymes are under regulatory control.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1986

Impaired cAMP metabolism associated with abnormal function of thrombopathic canine platelets.

The effects of forskolin and 1-Methyl-3-isobutyl-xanthine on thrombopathic platelet function and cyclic AMP accumulation were examined. The concentration of forskolin required to inhibit gamma-thrombin- induced platelet aggregation and secretion by 50% was significantly lower for thrombopathic than for normal platelets. This inhibition was accompanied by a marked elevation of cyclic AMP. 1-Methyl-3-isobutyl-xanthine, alone or in combination with forskolin, augmented both the cyclic AMP accumulation and the inhibition of platelet function. These results demonstrate that cyclic AMP metabolism is abnormal in thrombopathic platelets and imply that cyclic AMP-phosphodiesterase activity is impaired.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Prekallikrein deficiency in a dog.

A 15-year-old male dog with chronic hematuria was found to have prolonged activated partial thromboplastin time. Results of plasma coagulation assays indicated a deficiency of prekallikrein, a plasma protein that modulates the rate of activation of factors XI and XII in the intrinsic clotting system. Patients with prekallikrein deficiency rarely have manifestations of hemorrhage. The hematuria was the result of a renal transitional cell carcinoma.

Animals↗
PubMed1986

Conformational changes in von Willebrand's factor protein: effects on the binding of factor VIII-coagulant.

The effects of conformational changes in purified canine von Willebrand's factor (VWF) were investigated to explore the relationship between its factor VIII-related antigen (VIII:AG) and ristocetin cofactor (RCoF) properties and the factor VIII-coagulant (VIII:C) binding site(s). Binding of VIII:C from canine von Willebrand's disease (VWD) plasma by VWF was used to measure the combining reaction of these proteins. The VWF was denatured to varying degrees by exposure to temperature and pH extremes, low ionic strength, and 6 M urea. Various treatments resulted in three types of change: elimination of RCoF, VIIIR:Ag, and VIII:C binding, removal of RCoF activity alone; or elimination of RCoF and retarded elution of VIII:Ag and VIII:C. As long as VIIIR:Ag reactivity was maintained, binding of VIII:C could be demonstrated; but in the absence of VIIIR:Ag, neither RCoF activity nor VIII:C binding remained. These results suggest that VIII:C binding and RCoF sites are separate on VWF and that interaction between VIII:C and VWF is possible even after significant structural changes occur in VWF. Furthermore, RCoF is more vulnerable to denaturation than the antigenic site. The spectrum of conformational changes that affect the properties of VWF may parallel the various recognized subtypes of VWD.

Animals↗
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↗
PubMed1986

Assessing the specificity of anti-canine-factor VIII-related antigen.

Antibodies to canine factor VIII-related antigen should be monospecific to accurately study this protein's location in tissue and its structure. Because no uniformly accepted standard for monospecificity exists for anti-factor VIII-related antigen, we have compared the sensitivities of three common evaluation techniques--immunodiffusion, immunoelectrophoresis, and crossed immunoelectrophoresis. Unabsorbed rabbit anti-canine factor VIII-related antigen appeared monospecific against whole plasma by all three methods; however, multiple specificities were recognized against a plasma cryoconcentrate. These results demonstrate the insensitivity of the techniques under certain conditions, which can lead to erroneous interpretation of data.

Animals↗