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Biomedical subjects

V Harris

Publications and source records attributed to V Harris.

At least 73 records · Page 4Linked to original sources
PubMed1980

Free somatostatin in the circulation: amounts and molecular sizes of somatostatin-like immunoreactivity in portal, aortic, and vena caval plasma of fasting and meal-stimulated dogs.

Somatostatin-like immunoreactivity (SLI) of plasma from the portal vein, aorta, and inferior vena cava and of lymph from the thoracic duct of both fasted and meal-stimulated dogs was measured and characterized with respect to molecular size. Significant portal vein-arterial and arteriovenous SLI gradients were present in fasting dogs, and they increased sharply after the intragastric infusion of liver extract and HCl. Chromatography of fasting plasma at pH 7.4 revealed all measurable SLI to be confined to the void volume fractions of a Bio-Gel P-6 column, although, after a 7-fold concentration of fractions coeluting with somatostatin, approximately 1600-daltion SLI was detected in the portal venous plasma. The rise in SLI after a meal was due primarily to an increase of approximately 1600-dalton SLI; approximately 1600-dalton SLI was detectable in unconcentrated portal venous and aortic plasma and in the peripheral venous plasma concentrated 7-fold. SLI levels in lymph were similar to those of basal venous plasma and did not increase with a meal. This first demonstration at a physiological pH of a approximately 1600-dalton SLI in the arterial circulation suggests that a free, readily available form of endogenous somatostatin is present in the canine circulation and could be playing a hormonal role.

Animals↗
PubMed1979

Roentgenographic findings in infants with meconium aspiration syndrome.

Aspiration of meconium produces respiratory distress of various severity and outcome. To evaluate whether the initial chest roentgenogram (0 to 8 hours of age) can be used to predict the outcome, an analysis of 80 cases with clinical and roentgenographic features of aspiration syndrome was undertaken. Infiltration was seen in 62, consolidation or atelectasis in 44, hyperinflation in 37, air leak in 25, pleural effusion in 16, and increased cardiothymic shadow in 16. Consolidation or atelectasis, most commonly associated with thick meconium aspiration, appeared to be the most significant determinant of poor outcome. Infants who had consolidation or atelectasis were more ill, had lower pH, higher fraction of inspired oxygen, higher alveolar-arterial oxygen gradients, and required longer duration of oxygen intake than those infants who had no consolidation or atelectasis. Thus, the initial chest roentgenogram can be used for predicting outcome in infants with meconium aspiration syndrome.

Humans↗
PubMed1979

Choledochal cyst with cholelithiasis: 15-yr follow-up.

A 15-yr-old boy, who had had surgery for a choledochal cyst in infancy, was worked up for recurrent right upper quandrant pair. Intravenous cholangiogram and ultrasound demonstrated a choledochal cyst with stones. Angiogram showed only a distorted branch of the gastro-duodenal artery. These findings were confirmed at surgery.

Adolescent↗
PubMed1979

Response of plasma somatostatin-like immunoreactivity to the administration of alloxan in dogs.

The present study was designed to examine the effects of intravenously injected alloxan (75 mg/kg) upon plasma somatostatin-like immunoreactivity (SLI), glucagon (IRG), insulin (IRI) and glucose levels in 6 dogs. Within 2 hours of the injection of alloxan, SLI and IRI levels decreased significantly below their respective baselines, while IRG and plasma glucose concentrations increased. At 8 hours SLI levels had increased significantly by 55 pg/ml, together with a rise in IRI and a decrease in IRG and glucose concentrations. After 24 hours, marked hyperglycemia and hyperglucagonemia had developed whereas SLI levels were not different from preinjection values.

Alloxan↗
PubMed1979

Pancreatic and gastric release of somatostatinlike immunoreactivity during intestinal phase of a meal.

The present study was designed to examine pancreatic and gastric D-cell function during the intestinal phase of a liver meal. The intraduodenal instillation of a 20% liver meal (5 ml/min) elicited a significant rise in the plasma levels of somatostatinlike immunoreactivity (SLI) in the pancreatic vein and inferior vena cava, together with the rise in glucagon and insulin levels. The rise in pancreatic vein SLI was not reduced after truncal vagotomy or during atropine infusion. In the stomach, the intestinal liver meal elicited a significant rise in antral but not fundic vein SLI levels. The rise in antral vein SLI was augmented after truncal vagotomy and abolished during atropine infusion, as was the rise in inferior vena caval SLI. In contrast to the protein meal, intravenous infusion of an amino acid mixture elicited a rise in pancreatic vein SLI but not antral or fundic vein SLI. It is concluded that during the intestinal phase of a protein meal, pancreatic and antral but not fundic SLI release is stimulated. The effects of truncal vagotomy and atropine infusion on these responses suggest a close interaction between the vagus and muscarinic cholinergic mechanisms and the D cells of the stomach and pancreas.

Animals↗
PubMed1979

Half-life of somatostatin-like immunoreactivity in canine plasma.

Previous estimates of the half-life of synthetic somatostatin have been based upon the disappearance rate of 125I-labeled Tyr1-somatostatin. In the present study, the half-life of infused synthetic somatostatin was determined by RIA and compared with the duration of its suppressive action upon plasma insulin and glucagon. After the end of a 2-h infusion of somatostatin (500 ng/min), the radioimmunologically measured half-life was 1.82 min. The reappearance half-times for insulin and glucagon were 1.4 and 6.7 min, respectively. These data show that calculations of the half-life of somatostatin-like immunoreactivity in plasma may differ from estimates based on the duration of its biological activities, which may differ from one another.

Animals↗
PubMed1979

Evidence for a role of splanchnic somatostatin in the homeostasis of ingested nutrients.

Somatostatin was infused via the portal vein at a rate of 50 ng/min in a group of eight conscious dogs beginning 30 min before and continuing for 6 h after the ingestion of an 800-g fat-protein meal. The fasting and postprandial levels of plasma somatostatin-like immunoreactivity (SLI), insulin, glucagon, and triglycerides were compared with those during an intraportal infusion of saline as a control. In both groups, SLI rose significantly within 15 min of the ingestion of the meal, but during somatostatin infusion, mean peripheral vein levels of SLI ranged from 30-85 pg/ml above those of the saline control experiments. The postprandial rise in plasma triglycerides was reduced significantly below the control values at all points between 75-270 min, and this reduction was the result of lowered chylomicron levels. Neither fasting nor postprandial insulin or glucagon levels were significantly reduced by the somatostatin infusion. Intraportally infused somatostain also reduced portal vein xylose levels after an intragastric xylose load. The results are compatible with, but do not prove, a physiological role for somatostatin in the homeostasis of ingested nutrients.

Animals↗
PubMed1979

Release of somatostatin-like immunoreactivity from the lower gut.

The present study describes the effect of the instillation of a nutrient-containing hyperosmolar volume load into the lower ileum upon plasma levels of somatostatin-like immunoreactivity. The baseline levels of SLI in the mesenteric vein were significantly higher than those in the inferior vena cava and rose significantly in both veins in response to the nutrient load. SLI levels in the venous effluent of the pancreas and stomach did not rise. Mesenteric vein SLI was similar in molecular size to the SLI in the gastric and pancreatic veins and to synthetic somatostatin. The results suggest that the lower gut may contribute to the basal circulating SLI levels and that it is released from the lower gut in response to a nutrient-containing hyperosmolar volume load.

Animals↗
PubMed1978

Pancreatic and gastric somatostatin release in response to intragastric and intraduodenal nutrients and HCl in the dog.

The effects of the instillation of glucose, fat, casein hydrolysate, and HCl into the gastrointestinal tract upon plasma levels of somatostatin-like immunoreactivity (SLI) in the venous effluent of the pancreas, fundus and antrum of the stomach, and in the inferior vena cava (IVC) were determined in normal laparotomized dogs. Fasting SLI levels in the effluent plasma from these sites were significantly greater than IVC levels. The intragastric administration of glucose elicited a prompt and significant rise in SLI levels in pancreatic, fundic and antral venous plasma, and in IVC plasma; intraduodenal glucose elicited smaller increments. After intragastric fat, a smaller, more gradual increase in the pancreatic and fundic effluents was observed, whereas the rise in antral SLI was minute, and IVC SLI did not rise significantly. Intraduodenal fat elicited a prompt increase in the pancreatic and antral vein SLI levels, and a small but significant increase in fundic and IVC plasma which suggests faster release of enteric factors that influence SLI secretion in the pancreas and antrum. Intragastric casein hydrolysate elicited a prompt increase in SLI in both the pancreatic and fundic veins, the latter being marked, but the antral SLI response was small; IVC SLI rose significantly within 15 min. Intragastric HCl provoked a prompt and marked rise in pancreaticoduodenal and antral vein SLI but no increase in fundic vein SLI; IVC SLI levels rose significantly within 20 min. Intraduodenal HCl elicited an even more prompt and marked pancreatic SLI response, and SLI rose significantly in both the fundic and antral venous effluents; IVC SLI also rose more promptly. In dogs with a gastric fistula that prevented intraduodenal entry of HCl, intragastric HCl elicited only a very small and transient rise in pancreaticoduodenal vein SLI, markedly stimulated the antral SLI response, but completely suppressed fundic venous SLI levels. The results indicate that all three nutrients stimulate SLI release from the pancreas and stomach. The greater SLI response to intragastric, as opposed to intraduodenal, glucose suggests that unidentified local factors are of importance. The responses to the intraduodenal instillation of HCl and fat suggest a role of enteric hormones in the release of SLI from the pancreas and fundus and antrum of the stomach. Additionally, there is evidence of direct effects of HCl upon gastric SLI release.

Animals↗