Impurity of lipaemic factor VIII preparations.
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Biomedical subjects
Publications and source records attributed to W J Dodds.
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The authors discuss the selection of contrast media for radiographic examination of patients with suspected esophageal disruptions, and offer their recommendations.
The oppossum sphincter of Oddi (SO) exhibits peristaltic spike bursts with accompanying contraction waves that originate proximally in the sphincter of Oddi and propagate toward the duodenum. In this study we recorded myoelectrical activity of the opossum SO and upper gastrointestinal tract in six conscious animals using chronically implanted electrodes. Biopolar electrodes were implanted in the gastric antrum, duodenum, SO segment, jejunum, and ileum. During fasting the frequency of SO spike bursts, scored as number per minute, showed a cyclic pattern consisting of four phases (A to D). Phase A had a low spike burst frequency of approximately 2/min that lasted approximately 20 min. In phase B, the spike burst frequency increased progressively during a 40-45 min interval culminating in a short interval of phase C activity characterized by a maximal spike burst frequency of approximately 5/min. During phase D, the spike bursts decreased over 15 min to merge with the low frequency of phase A and the cycle repeated. Cycle length of the interdigestive SO cycle, 87+/-11 SD min, was virtually identical with that of the interdigestive migrating myoelectric complex (MMC) of the upper gastrointestinal tract. The onset of phase C activity in the SO began 1-2 min before phase III of the MMC activity in the duodenum. Feeding abolished the cyclic pattern of spike burst activity in the SO as well as in the upper gastrointestinal tract. After feeding the SO spike bursts occurred at a frequency of 5-6/min for at least 3 h. We conclude that: (a) During fasting, the oppossum SO exhibits cyclic changes in its spike burst frequency; (b) Maximal spike burst frequency of the SO occurs virtually concurrent with passage of phase III MMC activity through the duodenum and; (c) Feeding abolishes the interdigestive cyclic spike burst pattern of the SO as well as that of the gastrointestinal tract.
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The human sphincter of Oddi (SO) exhibits phasic wave activity over a 4 to 6 mm segment. Approximately 60% of these waves occur in an antegrade direction, 14% are retrograde, and 26% occur simultaneously. Because cholecystokinin-octapeptide (CCK-OP) stimulates the flow of bile into the duodenum, its effect on SO phasic wave contractions and contraction sequences was evaluated at ERCP manometry. An infused triple-lumen catheter of 1.7 mm outer diameter with side orifices spaced 2 mm apart was stationed in the SO segment so that all three orifices recorded phasic pressure waves. We studied 31 patients with normal ductal anatomy and normal SO pressures. In 21 of these patients CCK-OP (20 ng/kg) was given intravenously after a 2- to 3-minute baseline recording was obtained. Pressure recordings were continued for up to 10 minutes following CCK-OP administration. CCK-OP caused a significant inhibition in the frequency and amplitude of SO phasic waves as well as a significant decrease in basal SO pressure. Before CCK-OP most phasic contractions were antegrade, and after CCK-OP the sequence pattern remained unchanged. We conclude that CCK-OP reduces or transiently abolishes SO phasic contractions but that it does not change their temporal sequence. In addition, CCK-OP produces a decrease in basal SO pressure. These findings suggest that the action of CCK-OP in humans is to inhibit SO phasic activity and reduce SO basal pressure to allow increased flow of bile.
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Blood was obtained from 10 clinically normal West Indian manatees. Many coagulation screening tests were performed on the blood as well as specific clotting factor assays. All clotting factors were present and their activities compared to those of the dog. The clotting factor activities of the intrinsic system of the manatee are much higher than those of the dog. Factor X activity is about the same as that of the dog. The clotting factor activities of the extrinsic system seems to be less than that of the the dog.
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A convenient, accurate, and reproducible method was developed and characterized to test the effects of particulate solids and soluble agents on native whole blood. The effects of citrate anticoagulation and of variation in flow and column parameters were characterized by ancillary experiments. The study utilized a relatively homogeneous strain of large rabbits that had received intravenous [C14]-serotonin as a platelet radiolabel. The assay induced a 4 min contact time of either the test sample or saline control with freshly drawn arterial blood and was followed by a series of hemostatic measurements, both before and after passage of the blood through a standard 1 g glass bead column. Changes induced by soluble (ADP, ellagic acid, aspirin) and particulate (collagen) agents in the reactivity of this blood to the subsequent challenge of a large area of reactive surface revealed reproducible quantitative effects on platelets and clotting. Generally comparable results were obtained with native whole human blood when the glass bead surface was adjusted (2 g) for the species difference in coagulability and platelet reactivity.
Six adults with myotonic dystrophy underwent detailed radiological and manometric studies of pharyngoesophageal function. Four of the patients had no history of swallowing dysfunction, while two had very mild symptoms. All patients showed abnormalities of pharyngoesophageal function. Pharyngeal peristalsis was present but of low amplitude. Resting upper esophageal sphincter pressure was diminished, but the sphincter relaxed normally. Peristalsis in the esophageal body was invariably absent in the striated muscle segment of the esophagus and was either absent of decreased in amplitude in the smooth muscle segment. The lower esophageal sphincter was normal. Myotonia did not occur in the sphincters or the esophageal body. These findings suggest that pharyngoesophageal dysfunction is common in patients with myotonic dystrophy, even when clinical symptoms are absent. The abnormalities are probably related to muscle weakness rather than to myotonia in the pharyngeal and esophageal musculature.
In order to determine the spectrum of esophageal dysfunction in repaired esophageal atresia, 14 patients were evaluated with esophageal manometry, intraluminal pH recording, and radiology. Nine patients had no difficulty in swallowing but six had symptoms suggestive of gastroesophageal (GE) reflux. On pH recording, six had evidence of GE reflux. Basal sphincter pressure was 22 mm Hg in both reflux and nonreflux patients. No patient had manometric evidence of peristalsis in the proximal esophagus, but six had peristalsis in the distal esophagus. On radiology all had a normal peristaltic stripping wave in the cervical esophagus, and peristalsis was absent in the proximal thoracic esophagus in all patients but present in the distal esophagus in five of the 10 patients studied. Esophageal dysfunction is present in all patients with repaired esophageal atresia even when symptoms are absent.
Plasmas having no detectable factor VIII-related antigen but moderate factor VIII coagulant were obtained from two unrelated dogs homozygous for von Willebrand's disease and with the severe clinical expression of the disease. when these plasmas were gel-filtered in a buffer at physiologic ionic strength, the factor VIII coagulant eluted in the bed volume as a single well-defined peak. Addition of protease inhibitors, including diisopropylfluorophosphate, did not change the elution pattern. Each plasma was then combined individually with plasmas from six different mutants of canine haemophilia, all of which had normal factor VIII-related antigen but no detectable factor VIII coagulant. The factor VIII coagulant elution profile of these combined plasma resembled that of normal canine plasma. Slightly over half of the recovered factor VIII coagulant coeluted in the void volume with the factor VIII-related antigen; the rest eluted as a second, distinct peak of lower molecular weight. These results demonstrated that part of the factor VIII coagulant of the von Willebrand plasmas had bound to the factor VIII-related antigen of the haemophilic plasmas. This finding supports the theory that factor VIII exists as a macromolecular complex of nonidentical components in normal citrated plasma.
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In this study, we used a high-fidelity manometric recording system to quantitate the effects of atropine on lower esophageal sphincter (LES) pressure and primary peristalsis (1 degree P). A sleeve sensor recorded LES pressure, and seven recording orifices spaced at 3-cm intervals registered motor activity in the esophageal body. Five randomized manometric studies were done in each of five normal subjects. LES pressure and 1 degree P with wet swallows were recorded for 30 min before and 70 min after intravenous injection of saline or atropine, 3, 6, 12, and 24 micrograms/kg. We also studied the effect of atropine on LES pressure in five additional subjects, four dogs, four opossums, and six monkeys. In humans, saline and 3 micrograms/kg atropine caused no significant change in pulse rate, LES pressure, or the incidence of complete peristaltic sequences. The 6, 12, and 24 micrograms/kg atropine doses caused significant inhibition of LES pressure and the incidence of intact 1 degree P. Only the 12 and 24 micrograms/kg doses increased pulse rate. When 1 degree P occurred in the smooth muscle portion of the esophagus its appearance in the proximal portion of the smooth muscle segment was delayed for several seconds. The amplitude of 1 degree P was decreased 30-60% in the smooth muscle segment, but 1 degree P was not affected in the proximal striated muscle esophageal segment. Atropine reduced canine LES pressure substantially but caused no change in opossums or monkeys. We conclude that 1) basal LES tone in humans and dogs, unlike that of the opossum and monkey, is partially generated by cholinergic neural input, 2) cholinergic nerves elicit 1 degree P in human esophageal smooth muscle, and 3) species variation exists in esophageal responses to atropine.