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Biomedical subjects

I Lundquist

Publications and source records attributed to I Lundquist.

At least 145 records · Page 8Linked to original sources
PubMed1980

Vagal influences on the pancreatic response to intraluminal trypsin.

The significance of vagal influences on the pancreatic response to intraluminal trypsin was investigated in conscious rats surgically prepared with bile-pancreatic fistulae. Vagotomy as well as cholinergic blockage depressed the hypersecretion of protein in fistula rats. Contrary to in control rats intraduodenal trypsin infusion did not change the protein output after vagotomy or cholinergic blockage. Indirect vagal stimulation induced by insulin hypoglycemia did not further increase the protein output in rats with their bile-pancreatic juice deviated from the intestine. In these latter rats, however, intraduodenal infusion of trypsin markedly inhibited the protein secretion. The results suggest that vagal integrity is essential for the response of the pancreas to intraduodenal trypsin.

Animals↗
PubMed1980

Intestinal concentrations of pancreatic enzymes following pancreatic replacement therapy.

The activities of amylase, lipase, phospholipase, and trypsin in four commercially available preparations of pancreatin with different galenic and adjunctive protective properties were estimated in vitro, using human small-intestinal juice as the incubation medium. These preparations were administered to healthy subjects and to patients with severe pancreatic insufficiency, and their ability to increase the intestinal concentrations of pancreatic enzymes was evaluated. The relations between in vitro and in vivo activities were also studied. In vitro testing showed that the preparations contained high but varying activities of enzymes, with the greatest variations in lipase and trypsin. Pancreatin in the form of tablets, with or without protective measures against acid, did not cause any apparent increase in the activities of pancreatic enzymes in the upper part of the gut in patients with pancreatic insufficiency. Granulated pancreatin, on the other hand, brought about an increase in the activities of amylase, phospholipase, lipase, and trypsin. Relatively higher activities of the enzymes in granulated form reached the small intestine as compared with those of the tablets.

Amylases↗
PubMed1979

Insulin secretion and carbohydrate metabolism in the dystrophic mouse.

Dystrophic mice were investigated with regard to their regulation of blood glucose and insulin secretion in vivo. The following were also measured: tissue glycogen levels, activity of the glycogenolytic hydrolase, acid amyloglucosidase, and in vitro glucose utilization by liver, muscle and adipose tissue. Basal levels of blood glucose and plasma insulin of dystrophic mice were essentially within the same range as in the clinically unaffected littermate controls. Dystrophic mice had a decreased tolerance to glucose and glibenclamide; the secretion of insulin in response to these secretagogues was moderately reduced. Insulin release following beta-adrenergic stimulation, however, was increased in the dystrophic mice. Glycogen levels and acid amyloglucosidase activity were increased in dystrophic muscles but were normal in liver. Acid amyloglucosidase activity in pancreatic islets was lower in the dystrophic mouse. Glucose utilization in vitro appeared normal in liver tissue from dystrophic mice; in dystrophic muscle there was a threefold increase in 14CO2-production with no concomitant increase in either glycogen or 14C-incorporation into glycogen. 14CO2 production and 14C-incorporation into lipid and glycogen were increased in dystrophic adipose tissue. We suggest that the decreased glucose tolerance, and the reduced insulin response to glucose in the dystrophic mouse are compensated by an increased glucose utilization in muscle and adipose tissue and an increased beta-adrenergic-mediated secretion of insulin.

Adipose Tissue↗
PubMed1979

T-tubule endocytosis in dystrophic chicken muscle and its relation to muscle fiber degeneration.

Pectoralis muscles from normal and dystrophic chickens were investigated 2 h after an i.v. injection of horseradish peroxidase, by cytochemical and biochemical techniques to demonstrate peroxidase activity. Light microscopic examination of dystrophic muscles showed that peroxidase activity could be detected inside a population of fibers, in deliminated bodies often restricted to segments of the muscle fiber. Such bodies containing peroxidase were not observed in normal muscle fibers. Electron microscopy of dystrophic muscle fibers revealed that numerous vesicles containing peroxidase were frequently present in fiber regions with signs of cytoplasmic degradation. These vesicles, which occasionally were found to be coated, were 50--100 nm in size and appeared to be derived from t-tubules. Larger (up to 1.7 micrometers) inclusions containing peroxidase and delimited by a single membrane were also present at degenerating areas of dystrophic muscle fibers. These bodies seemed to be formed by fusion between several primary t-tubule vesicles and probably also lysosomes. Vacuoles containing the peroxidase were frequently encountered. Biochemical determination of horseradish peroxidase activity, performed after extensive washing of the muscle tissue, showed that dystrophic muscles contained about twice as much peroxidase as normal control muscles. It is suggested that endocytosis from t-tubules is an early and essential pathological phenomenon in dystrophic muscle fibers, which may be related to lysosomal function and muscle fiber degeneration

Animals↗
PubMed1979

Inhibitory effect of somatostatin on insulin secretion during alpha-adrenergic blockade in three different species.

It has recently been suggested from experiments in dogs that somatostatin suppresses insulin release via a stimulation of the inhibitory alpha-adrenoceptors of the pancreatic B-cell. The effect of somatostatin on insulin secretion during alpha-adrenergic blockade with phentolamine was therefore studied in three different species; the rat, the cat and the mouse. It was found that somatostatin significantly depressed insulin release during alpha-adrenoceptor blockade in all three species. In the rat, infusion of somatostatin at a dose of 0.3 microgram/kg/min decreased basal plasma insulin concentration by 92%. In the presence of phentolamine, the same dose of somatostatin lowered plasma insulin by 85%. In the cat, a similar infusion of somatostatin lowered basal plasma insulin concentration by 87%, but its depressive effect during alpha-adrenergic blockade was comparatively less pronounced (68%) than in the rat. In the mouse, a single iv injection of somatostatin induced a short-lasting depression of plasma insulin concentration during alpha-adrenergic blockade. From these results it seems unlikely that somatostatin should inhibit insulin release simply by stimulation of alpha-adrenoceptors on the B-cell. It cannot be ruled out, however, that a more complex interaction exists between somatostatin and the sympatho-adrenal system with regard to the control of insulin secretion.

Animals↗
PubMed1979

Influence of anticholinergic treatment on rat pancreatic protein and amylase concentrations.

Pancreatic protein and amylase concentrations were measured after subcutaneous administration of an anticholinergic drug (Pro-Banthine to rats in different doses. In doses comparable to those given in acute pancreatitis an increase of both pancreatic protein and amylase concentrations was found. If pancreatitis is indeed caused or maintained by proteases released from the acinar cell, anticholinergics--giving rise to an accumulation of enzymes within the pancreas--may do more harm than good in the treatment of acute pancreatitis.

Acute Disease↗
PubMed1979

Trypsin as a regulator of pancreatic secretion in the rat.

The effect of intraduodenally administered trypsin on pancreatic exocrine secretion was investigated in conscious rats surgically prepared with bile--pancreatic fistulae. Introduction of NaHCO3 into the duodenum did not influence pancreatic secretion. Reintroduction of bile--pancreatic juice into the duodenum, however, suppressed pancreatic protein output, mainly because of changes in protein concentration. Infusion of trypsin into the duodenum in the absence of intraluminal pancreatic juice significantly suppressed the secretory volume and pancreatic enzyme output; addition of trypsin inhibitor to the trypsin infusion resulted in an immediate increase of pancreatic secretion. Trypsin inhibitor per se, however, was without effect. Bile--pancreatic juice affected amylase, kipase, and trypsinogen output in a parallel fashion; after addition of trypsin inhibitor to the infusion the inhibitory effects on pancreatic enzyme output was reversed in a parallel manner. The results support the hypothesis that pancreatic exocrine secretion is regulated by a feedback mechanism exerted--at least partly--by intraluminal trypsin.

Amylases↗
PubMed1978

beta-Adrenergic insulin release and adrenergic innervation of mouse pancreatic islets.

An investigation of the stereospecificity of beta-adrenergic insulin release, its relation to alpha-adrenergic blockade and the adrenergic innervation of the pancreatic islets was performed in the mouse. It was observed that in vivo beta-adrenergic stimulation of insulin release by isopropylnoradrenaline was stereospecific for the L-stereoisomer and selectively blocked by the L-isomer of the beta-adrenergic antagonist L-propranolol. D-propranolol had no effect. Pretreatment of mice with a dose of D-isopropylnoradrenaline devoid of insulin releasing activity, slightly increased the subsequent insulin response to a half-maximal dose of L-isopropylnoradrenaline. Basal insulin secretion was blocked by L-propranolol (beta-adrenergic blockade) and increased by phentolamine (alpha-adrenergic blockade). A beta-blocked insulin response to L-isopropyl-noradrenaline could be overcome by alpha-adrenergic blockade depending on the dose of the beta-agonist, suggesting a close association between the adrenergic receptors. The adrenergic innervation of the islet cells was studied by electron microscopic autoradiography after injection of 3H-L-noradrenaline. It was observed that labelled adrenergic nerve terminals were associated with both A1- (D-), A2- and B-cells. The nerves were mainly distributed in the periphery of the islets either as single axons or as bundles. The majority of the terminals were associated with A2-cells, the most frequent cell type in the islet periphery. However, in all islets examined terminals were found close to B-cells. Adrenergic terminals often caused indentations in the contour of an islet cell and were separated from the islet cell membrane only by a narrow intercellular space, about 20 nm in width. It is concluded that the islet cells of the mouse are equipped with the morphological substrate for direct adrenergic regulation. Further it is suggested that the B-cell is supplied with L-stereospecific beta-adrenergic receptors and that the alpha- and beta-adrenergic receptors are at least partially interrelated.

Adrenergic Fibers↗
PubMed1978

Lysosomal activation in mouse skeletal muscle induced by protamine in vitro.

Incubation of mouse skeletal muscle in a physiological Ringer solution containing protamine (60 microgram/ml) at +37 degrees C for 1 h induced ultrastructural changes including proliferation of tubular profiles and vesicles at the I-band level close to the A-I junction, formation of numerous acid phosphatase positive lysosomes in the longitudinal sarcoplasmic reticulum and autophagic vacuolation starting at the level of the A-I junction. Biochemical determination of acid phosphatase in the incubated muscles showed that protamine caused an increase in acid phosphatase activity of about 25% compared to enzyme activities obtained from muscles incubated without protamine at +37 degrees C or with protamine at +4 degrees C. The morphological findings suggest that the vesicles arising adjacent to the A-I junction originate from transverse tubules. Such vesicles, designated as endocytic, may acquire acid phosphatase activity in the longitudinal SR ano be active in an autophagic process resulting in large vacuoles. A causal relationship between endocytosis and lysosomal activation is suggested.

Acid Phosphatase↗
PubMed1978

Zinc and copper concentrations in serum, blood and liver in moderate experimental pancreatic insufficiency.

Serum and liver concentrations of zinc and copper were studied in the rat after ligation of the pancreatic duct. Ligation of the bile duct was done close to the duodenum and high up in the hilum of the liver. The bile flow was by-passed into the intestine via a plastic catheter. The surgical method used was found suitable for a study of moderate exocrine pancreatic insufficiency since significant--although markedly reduced--concentrations of amylase and trypsin were estimated in intestinal contents at sacrifice 19 weeks after the operation. The serum zinc level was unaffected by duct ligation except for a slight decrease after 2 weeks. Similarly zinc in whole blood was unaffected. The copper concentration in serum was, however, significantly enhanced during in first 10 weeks. The copper zinc ration was markedly increased in duct ligated rats during the whole period. Zinc and copper concentrations in liver tissue were significantly decreased after 19 weeks. The findings suggest that a decrease function of exocrine pancreas might induce a disturbed balance of zinc and copper in the rat.

Amylases↗
PubMed1978

Glucose-stimulated 45Calcium efflux from isolated rat pancreatic islets.

Kinetics of (45)Ca efflux and insulin release were studied in collagenase-isolated rat islets during 2-h perifusions with calcium-depleted (0.05 mM) bicarbonate-phosphate buffer containing 2.2 mM glucose. Addition of glucose (16.7 mM) suppressed (45)Ca efflux by 30%. Removal of glucose caused an "off response" of insulin release. The perifusion of a normal concentration of Ca (2.3 mM) greatly stimulated (45)Ca efflux, indicating Ca <--> (45)Ca exchange. When Ca and glucose were superimposed, the effects on (45)Ca efflux and insulin release depended upon the order of presentation of the stimuli: when Ca was added to an ongoing 16.7-mM glucose perifusion, biphasic patterns of (45)Ca and insulin release were seen; when glucose was superimposed on a Ca perifusion, an inhibition of the Ca-stimulated (45)Ca efflux occurred, and a reduced but clearly biphasic insulin response was seen. The subsequent insulin off response after with-drawal of the glucose was also reduced. Mathematical "peeling" of (45)Ca efflux curves from unstimulated islets suggests that there are at least two, and probably three, different intracellular Ca compartments (not including the extracellular sucrose space). At the beginning of perifusion, these three compartments (I, II, III) contain 25, 56, and 19% of the intracellular (45)Ca, and their rates of efflux are 6.7, 1.2, and 0.1%/min, respectively. Glucose appears to suppress efflux from the largest compartment (II); Ca appears to exchange with (45)Ca from a more inert compartment (III). The relationship between insulin and (45)Ca release is not stoichiometric.

Animals↗
PubMed1978

Localization of insulinomas and islet cell hyperplasias by pancreatic vein catheterization and insulin assay.

Percutaneous transhepatic portal vein catheterization and transfemoral portal and caval catheterizations were performed under local anesthesia in five patients with symptoms of organic hypoglycemia. During the investigation, results of pancreatic phlebography revealed the pancreatic venous anatomy. Blood obtained from the celiac artery, caval branches and pancreatic veins was assayed for insulin by two different radioimmunoassay methods. Pathologically high, pancreatic arteriovenous insulin differences in two patients with insulinomas and in two patients with islet cell hyperplasia. In one of the patients with an insulinoma, one of the assays failed to detect the tumor insulin. This inconsistency still remains unexplained. Angiography revealed a pancreatic abnormality in only two patients. During operation, two of the tumors were found upon palpation and inspection. Pancreatic resections were performed according to the findings of pathologic hormone differences in all five patients. Immunocytochemistry revealed that three of the patients had insulin-producing tumors and two had local islet cell hyperplasia. Catheterizations performed two months postoperatively confirmed the radicality of the operation in all patients, with the possible exception of one patient. In one patient, a recurrance was detected by catheterization ten months postoperatively.

Adenoma, Islet Cell↗
PubMed1977

Effect of alloxan on rat pancreatic polypeptide (PP) cells.

Injection of alloxan caused an almost total disappearance of insulin cells in the rat pancreas. Planimetric analysis revealed a 50 per cent reduction of the mean islet volume. The number of immunoreactive pancreatic polypeptide (PP) cells per sectioned islet was significantly increased, and the PP cell volume per islet doubled. Assuming an unchanged number of islets, the results indicate an increase in total PP cell mass following alloxan administration.

Animals↗