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Biomedical subjects

J C Thompson

Publications and source records attributed to J C Thompson.

At least 379 records · Page 21Linked to original sources
PubMed1983

Correlation of spontaneous respiration and neurologic damage in near-drowning.

Twenty-six near-drowning children were assessed for neurologic damage with the Glasgow Coma Score, and for spontaneous respirations after CPR. All children had a Glasgow Coma Score of 3 or 4; after resuscitation, 13 children had spontaneous respiration and 13 were apneic. The 13 children with spontaneous respiration suffered little or no residual neurologic impairment. Those children with apnea had severe neurologic impairment or died despite treatment. It appears that the present of spontaneous respirations correlated with surviving a near-drowning episode with minimal or no neurologic deficit and may be of benefit as a prognostic indicator.

Apnea↗
PubMed1983

Release of cholecystokinin in conscious dogs: correlation with simultaneous measurements of gallbladder pressure and pancreatic protein secretion.

We have used an antibody that cross-reacts with cholecystokinin-33/39 to measure cholecystokinin release into plasma; this release was correlated with simultaneous measurements of gallbladder pressure and pancreatic protein secretion in response to intestinal administration of fat. Nine conscious dogs were prepared with chronic gastric, pancreatic, and gallbladder fistulas. Plasma cholecystokinin, gallbladder pressure, and pancreatic protein output were measured simultaneously before, and at intervals during, a 2-h intraduodenal infusion of sodium oleate. This infusion resulted in significant (p less than 0.05) elevations of plasma cholecystokinin (from 64 +/- 7 to 181 +/- 27 pg/ml), in gallbladder pressure (from 13 +/- 1 to 27 +/- 3 cmH2O), and in pancreatic protein output (from 65 +/- 7 to 148 +/- 21 mg/15 min); all measurements are from the basal state to 120 min after the onset of duodenal perfusion. Plasma concentrations of cholecystokinin were significantly correlated with gallbladder pressure (r = 0.91, p less than 0.05) and pancreatic protein output (r = 0.84, p less than 0.05). These data provide evidence that release of endogenous cholecystokinin, as measured by radioimmunoassay, can be correlated with the classic biologic actions ascribed to cholecystokinin.

Animals↗
PubMed1983

Correlation of release and actions of cholecystokinin in dogs before and after vagotomy.

Pancreatic secretion of enzymes and gallbladder contraction in response to intestinal stimulants are thought to be mediated through the vagus nerve and by means of release of cholecystokinin (CCK). The effect of truncal vagotomy on the release of CCK, pancreatic protein secretion, and gallbladder pressure (all stimulated by intraduodenal instillation of oleate) was studied in five dogs. Each dog was prepared with chronic pancreatic and gastric fistulas and catheter cholecystostomies. Simultaneous measurements were made of plasma CCK (by radioimmunoassay), pancreatic protein secretion, and gallbladder pressure (by perfused catheter technique) before and during intraduodenal administration of oleate. Before truncal vagotomy, intraduodenal oleate caused increases in plasma CCK (from 82 +/- 6 to 208 +/- 32 pg/ml), pancreatic protein secretion (from 83 +/- 8 to 165 +/- 15 mg/15 min), and gallbladder pressure (from 11 +/- 2 to 27 +/- 2 cm H2O) (all measured from basal state to 120 minutes). Truncal vagotomy caused a 45% decrease in the output of pancreatic protein in response to oleate and completely abolished the increase in gallbladder pressure, but it caused no change in release of CCK. The correlations between plasma CCK and pancreatic protein secretion before truncal vagotomy (r = 0.86) and after truncal vagotomy (r = 0.77) were highly significant. The correlation between plasma CCK and gallbladder pressure was highly significant before (r = 0.91) but not after (r = 0.42) truncal vagotomy. This study demonstrates that truncal vagotomy inhibits pancreatic protein secretion and gallbladder pressure in response to fat but does not interfere with release of CCK. The effects may be due to interruption of vagus-mediated reflexes between the intestine and the pancreas and gallbladder. The good correlation between plasma concentrations of CCK and both pancreatic protein secretion and gallbladder pressure provides evidence that the radioimmunoassay measures biologically active CCK.

Animals↗
PubMed1982

Gastrinoma.

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Adolescent↗
PubMed1982

Correlation between release of cholecystokinin and contraction of the gallbladder in patients with gallstones.

The role of endogenously released cholecystokinin (CCK) in mediating gallblader (GB) contraction was evaluated in 12 normal volunteers and 24 patients with gallstones (11 additional gallstone patients were excluded because of failure of adequate ultrasonographic visualization). CCK concentrations before and after oral administration of fat (Lipomul((R))) were measured by a specific radioimmunoassay. CCK release was correlated with changes in GB volume determined simultaneously by ultrasonography. On the basis of gallbladder contraction and operative findings, gallstone patients were divided into "contractors" (14), "noncontractors" (6), and "hydrops" (4). Lipomul caused prompt release of CCK in normal volunteers and all groups of gallstone patients. The changes (basal to peak) in plasma CCK (pg/ml) for the different groups were as follows: normal volunteers (108 +/- 9 to 200 +/- 16), contractors (77 +/- 10 to 128 +/- 13), noncontractors (59 +/- 7 to 159 +/- 38), and hydrops (43 +/- 5 to 113 +/- 47). The total integrated output of CCK (0-60 min) was greater in normal volunteers (3975 +/- 762 pg-min/ml) than in contractors (1530 +/- 567 pg-min/ml). Lipomul caused similar GB contraction in normal volunteers and contractors (from basal volumes to maximal contraction); these changes were from 19.5 +/- 2.3 ml to 5.6 +/- 1.0 ml in normal volunteers, and from 19.6 +/- 3.2 to 5.2 +/- 1.0 in contractors. Plasma concentrations of CCK and GB volume were highly correlated in the 12 normal volunteers (r = -0.89, p < 0.01) and in the 14 contractors (r= -0.99, p < 0.01)), but the GB was significantly (p < 0.01) more sensitive to changes in plasma CCK in the gallstone contractors than in the normal volunteers. The authors suggest that there may be two groups of gallstone patients, noncontractors and contractors. Stasis may be important in the pathogenesis of gallstones in the noncontractors, whereas in contractors, the authors speculate that an abnormality in the CCK-gallbladder relationship (characterized by diminished CCK release and increased GB sensitivity to CCK) may be involved in the evolution of the disease.

Adult↗
PubMed1982

Effect of colectomy on cholecystokinin and gastrin release.

Studies were conducted to determine the effect of resection of the colon on the release of cholecystokinin (CCK) and gastrin. A standard food stimulation test was performed in five dogs. Peripheral blood samples were collected for future measurement of CCK and gastrin by specific radioimmunoassay. Each dog underwent subtotal colectomy with side-to-end ileoproctostomy. The food stimulation test was repeated at approximately weekly intervals for eight weeks after colectomy. Basal plasma CCK levels of 139 +/- 21 pg/ml before colectomy did not change after colectomy. Total amount CCK released after food was increased significantly at both four (5.94 +/- 0.78 ng min/ml) and eight (13.00 +/- 2.72 ng min/ml) weeks after colectomy in comparison with that observed prior to colectomy (2.94 +/- 0.54 ng min/ml). Basal serum gastrin levels of 28 +/- 9 pg/ml did not change significantly after colectomy. Total amount of gastrin released after food was increased significantly at both two (8651 +/- 2294 pg min/ml) and three (6940 +/- 1426 pg min/ml) weeks after operation, but at none of the later weeks. The precolectomy output, used for comparison, was 5608 +/- 1346 pg min/ml. It was concluded that resection of the colon leads to an increase in release of CCK and gastrin after food stimulation. This finding provides further evidence that the colon contains a factor that inhibits the release of CCK and gastrin, and that the colon functions as an endocrine organ.

Animals↗
PubMed1982

Removal of circulating gastrin and cholecystokinin into the lumen of the small intestine.

This study was undertaken to investigate the mechanism by which the small intestine removes circulating gastrin and cholecystokinin (CCK). A 100-cm (acute study, 10 dogs) or a 50-cm (chronic study, 5 dogs) segment of midjejunum was excluded in all 15 dogs. The excluded loop was perfused with 0.1 M phosphate buffer (pH 7.4), which was constantly recirculated by a peristaltic pump. It the acute control study (5 dogs), gastrin concentrations in the intestinal perfusate were increased gradually to a level of 320 +/- 49 pg/ml at 90 min (i.e., 7.6 +/- 0.9 times higher than serum gastrin levels). In the antrectomy group (5 dogs), perfusate gastrin concentrations were greatly decreased after antrectomy, in consonance with the decrease in serum gastrin concentrations. In the chronic study (5 dogs), perfusate gastrin concentrations were significantly increased after food stimulation, in consonance with the increase in serum gastrin concentrations. CCK was also released into the bowel lumen in considerable amounts basally and after endogenous release. Although one cannot exclude the possibility that a considerable amount of gastrin or CCK in the lumen may originate from the bowel segment, this study shows that the small bowel removes gastrin and CCK from the circulation by their secretion into the bowel lumen. Loss of this mechanism might partially explain the rise in gastrin levels that is observed in some patients after extensive small bowel resections.

Animals↗
PubMed1982

Pancreatic protein secretion and gastrointestinal hormone release in response to parenteral amino acids and lipid in dogs.

Parenteral nutrition has been advocated for and used in clinical situations in which provision of calories without stimulation of pancreatic secretion is desired. A recent report, however, provided evidence for substantial stimulation of pancreatic secretion after parenteral administration of amino acids and fat. We have studied the effect of intravenous administration of crystalline amino acids and lipid on pancreatic protein secretion and release of gastrointestinal hormones in five dogs with chronic pancreatic fistulas. The amino acids were given as a 4.25% solution in 5% glucose at 2 gm/hr. Parenteral fat was administered as Intralipid 10% at 3.5 ml/kg/hr. Plasma concentrations of cholecystokinin (CCK) and pancreatic polypeptide (PP) and serum concentrations of gastrin, measured by radioimmunoassay, were determined before, and at intervals during, infusion of amino acids and fat. Pancreatic juice was collected simultaneously with blood sampling, and volume and protein output were measured. Basal concentrations of CCK, PP, and gastrin were not affected by intravenous infusion of amino acids. Pancreatic protein secretion and volume were also unaffected by parenteral amino acids. Parenteral infusion of fat resulted in a significant inhibition of integrated gastrin release but had no effect on plasma concentrations or integrated release of CCK or PP. Neither the volume nor protein output of pancreatic secretion was affected by intravenous fat administration. In summary, no stimulation of pancreatic secretion or release of CCK, PP, or gastrin occurred as a result of parenteral amino acid or fat administration. There is, therefore, no contraindication to the use of parenteral nutrition in situations in which it is desirable to keep the pancreas at rest.

Amino Acids↗
PubMed1982

Reduction of postprandial release of pancreatic polypeptide after development of pancreatic fibrosis.

We have measured the plasma pancreatic polypeptide response to a meal before and after the development of pancreatic fibrosis in dogs. Peripheral blood samples were collected in five dogs before and after a standard meal for measurement of pancreatic polypeptide by a specific radioimmunoassay. The next day, all of the pancreatic ducts were ligated in each dog, and one month after pancreatic ductal ligation, the food study was repeated. The dogs were sacrificed on the following day, and the pancreas of each dog was studied morphologically. Before pancreatic ductal ligation, plasma pancreatic polypeptide concentrations showed a biphasic response to a meal; a primary, rapid increase lasted 30 to 45 minutes, and a secondary, prolonged increase lasted for more than 180 minutes. One month after pancreatic ductal ligation, plasma concentrations of pancreatic polypeptide, at each time period during the initial 60 minutes after food, were significantly less than the corresponding sample before pancreatic ductal ligation. The total amount of pancreatic polypeptide released after a meal during the initial 60 minutes was diminished significantly by pancreatic ductal ligation. Neither plasma concentrations of pancreatic polypeptide nor the total amount of pancreatic polypeptide release after a meal showed a significant change during the last 180 minutes after food. Results of histologic observations showed destruction and fibrotic replacement of the acini of the pancreas after ligation of the pancreatic ducts. The islets were well preserved. Since the cells of origin of pancreatic polypeptide are distributed in both the acini and islets of the pancreas in dogs, we suggest that the primary, rapid phase of pancreatic polypeptide after a meal may be derived chiefly from cells in the acini, whereas the secondary phase of response may be derived chiefly from cells in the islets.

Animals↗
PubMed1982

Release of antral gastrin in response to an intestinal meal in dogs.

This study was designed to determine whether gastrin is released by the antrum in response to an intestinal meal in dogs. Two groups of anesthetized dogs were prepared with innervated antral pouches. The antrum and duodenum were separated by complete division at the pylorus to prevent duodenoantral reflux. The duodenum and proximal jejunum were perfused with 10% liver extract at 200 ml/hr. In one group of six dogs a significant elevation of antral vein gastrin levels was observed after 45 minutes. Gastrin levels in portal and peripheral blood were not significantly elevated. In another group of eight dogs, in which antral veins were not cannulated, a significant rise in peripheral gastrin concentration was noted after 60 minutes. We conclude that gastrin is released by the antrum during the intestinal phase of gastric acid secretion; significantly increased levels of gastrin are detected in both antral and peripheral venous blood. Duodenoantral reflux, as a possible cause of this release, is ruled out by complete surgical separation between duodenum and antrum.

Animals↗
PubMed1982

Development of a transplantable model of pancreatic duct adenocarcinoma.

We report here the first development of a continuous cell line in tissue culture of an animal pancreatic duct adenocarcinoma that is histologically similar to human pancreatic duct adenocarcinoma. A primary pancreatic duct adenocarcinoma, induced in a male Syrian golden hamster after 23 weeks of weekly subcutaneous injection of N-nitrobis (2-hydroxypropyl)amine, was minced and injected subcutaneously into three hamsters. After 8 weeks, a single tumor was apparent. Subsequent passages of fragments into the cheek pouches were performed at 3- to 4-week intervals. After five passages, minced fragments of a tumor were placed in tissue culture. Colonies appeared by 7 days; an epitheloid cell line, without fibroblasts, was established by 60 days. Single-cell suspensions, injected into hamster cheek pouches or subcutaneously, produced tumors in a dose-dependent fashion. Spent culture medium of tissue culture cells and saline extracts of freshly excised tumors contained pancreatic oncofetal antigen-like activity.

Adenocarcinoma↗
PubMed1981

Nasopharyngeal carcinoma--a retrospective review of patients less than thirty years of age: a report of Children's Cancer Study Group.

Data from 119 patients with nasopharyngeal carcinoma who were under 30 years of age were retrospectively analyzed by the investigators of the Children's Cancer Study Group. The overall five-year survival and relapse-free survival rates from diagnosis were 51 and 36%, respectively. When the tumor was confined to the nasopharynx (1 + T2, 41 patients), the five-year survival was 75%. No significant correlation was found between survival or local recurrence and the radiation dose to the primary site. The five-year survival from relapse was 37% for 21 reirradiated patients with local and/or regional relapse compared with 11% for 45 patients with other forms of relapse. It is concluded that the optimal radiation dose for tumor eradication in young patients is now known.

Adolescent↗
PubMed1981

Pancreatic polypeptide. A review.

Pancreatic polypeptide (PP), 36-amino acid peptide, may function as an important feedback inhibitor of pancreatic secretion after a meal. It arises from both islet and acinar cells of the pancreas. Release of PP by a meal, primarily protein, occurs in a biphasic manner. The first rapid release occurs as a result of vagal stimulation; the second, more prolonged rise (the so-called intestinal phase) occurs in response to hormonal stimulation, predominantly cholecystokinin. Plasma PP levels increase with age; PP levels are elevated above those of age-controlled normal subjects in diabetic patients and in some patients with pancreatic amine precursor uptake decarboxylase tumors. The value of plasma PP as a possible marker for pancreatic tumors is as yet unsettled but may be a valuable tool.

Animals↗