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Biomedical subjects

A Funakoshi

Publications and source records attributed to A Funakoshi.

At least 199 records · Page 11Linked to original sources
PubMed1989

[Pancreatic exocrine secretion and plasma gut hormones response after intraduodenal infusion of elemental diet in patients with chronic pancreatitis].

We studied the responses of pancreatic polypeptide (PP) and cholecystokinin (CCK) using specific RIAs, and simultaneously exocrine pancreatic secretion and gall bladder contraction were checked by using triple lumen tube to intraduodenal ingestion of 100 Kcal/hr semi-digested liquid meal: Clinimeal (Eisai, Tokyo) or Elemental Diet: ED (Morishita, Osaka) in 10 patients with chronic pancreatitis (CP). Intraduodenal infusion of Clinimeal did not result in a significant physiological rise of CCK and PP from the basal values. Pancreatic secretions (volume and bicarbonate output) were slightly increased paralleled to the gall bladder contraction in chronic pancreatitis. On the other hand, intraduodenal ED can significantly stimulate the release of CCK from the small intestine and PP from the pancreas with the near range of physiological concentration. This level of CCK can evoke a significant increase in pancreatic secretion and gall bladder contraction. These results suggest that in CP the physiological regulation was disturbed and pancreatic secretion was not observed after ordinary meal ingestion. Infusion of ED which contained similar components of digestive product partially improved the responses of gut hormones and pancreatic secretion. Therefore, impaired gut hormone release in CP primarily is due to the inappropriate stimuli because of pancreatic exocrine dysfunction, and not other factors(s).

Cholecystokinin↗
PubMed1989

[Basal plasma cholecystokinin levels in digestive diseases--comparison between CCK-8 like bioactivity by bioassay and CCK immunoreactivity by radioimmunoassay].

Basal plasma cholecystokinin levels were measured by a bioassay using dispersed rat pancreatic acini in various digestive diseases and compared with corresponding values by CCK-8 specific radioimmunoassay. The mean basal level in healthy volunteers was 0.40 +/- 0.06 pM. The basal level in liver cirrhosis was significantly elevated to 0.92 +/- 0.14 pM. The patients with cholestasis, that is, primary biliary cirrhosis and obstructive jaundice due to choledocholithiasis, bile duct cancer or lymph node metastasis , had markedly increased basal plasma CCK-8 like bioactivities from 1.88 pM to more than 25 pM. These CCK bioactivities were not correlative with CCK immunoreactivities. It was concluded not only that basal plasma CCK in patients with bile flow disturbance were truly increased, but also that interfering substances of the bioassay might appear in the plasma of these patients.

Adult↗
PubMed1989

[Clinical studies of serum phospholipase A2 immunoreactivity].

We tested the new radioimmunoassay method of serum phospholipase A2 (PLA2). In healthy individuals, serum PLA2 concentrations were 301 +/- 65.6 ng/dl (mean +/- SD), and in patients with acute pancreatitis, significant elevations of serum PLA2 concentrations were observed. In clinical course of acute pancreatitis, serum PLA2 was maintained high level more longer than serum amylase and elastase 1. In patients with chronic pancreatitis, serum PLA2 concentration were low at a stage of severe exocrine dysfunction, and high at a stage of acute exacerbation. In patients with pancreatic cancer, serum PLA2 concentration were changed in accord with severity of disease states. After endoscopic retrograde pancreatography, serum PLA2 levels immediately elevated significantly, and returned to basal levels 24 hours later. Serum PLA2 concentrations were within normal range in patients with other malignant tumors, diabetes mellitus, chronic liver diseases, and hypertension, whereas in patients with chronic renal failure serum PLA2 concentrations were elevated. These results suggest that measurement of serum PLA2 can be clinically useful for diagnosis of pancreatitis and monitoring of mild and severe stage of pancreatitis.

Acute Disease↗
PubMed1988

Bioactivity of synthetic human pancreastatin on exocrine pancreas.

A biological activities of synthetic human pancreastatin (1-52) and its C-terminal fragment (24-52) were evaluated for the first time in the conscious rats. Both pancreastatins inhibited CCK-stimulated pancreatic secretion in a range of 20-200 pmol/kg/h with the same potency, indicating that the C-terminal portion of this peptide has a full biological activity. The relative molar potency of this substance compared to that of porcine pancreastatin was equivalent. This study suggests that human pancreastatin has the same biological activity as that of porcine, and plays a biological action in the exocrine pancreas.

Animals↗
PubMed1988

Antagonistic effect of dibutyryl cyclic GMP on caerulein induced insulin secretion in isolated perifused rat islets.

The effects of caerulein and dibutyryl cyclic GMP on isolated rat islets were studied using the perifusion system. One, 20, 50 and 100 nM caerulein stimulated insulin secretion in the perifused rat islets, in a dose dependent manner. Insulin secretion reached a maximal level in the presence of 50 nM caerulein. Caerulein-induced insulin secretion showed a predominant first and minimal second phase. After cessation of stimulation with 50 nM caerulein, the insulin secretion level did not return to the basal value, but enhanced hormone secretion was sustained to a significant extent (p less than 0.01). The simultaneous administration of 10(-3) M dibutyryl cyclic GMP, a specific membrane antagonist against cholecystokinin (CCK), inhibited the first and second phases of caerulein-induced insulin secretion. Moreover, with this nucleotide, "persistent" insulin secretion induced by 50 nM caerulein was inhibited. These data indicate that caerulein directly stimulates pancreatic B cells and that this peptide causes "persistent" insulin secretion. Dibutyryl cyclic GMP counteracts the effects of caerulein. Thus, both pancreatic B cells and pancreatic acinar cells possibly possess a CCK receptor.

Animals↗
PubMed1988

Effects of cisapride on the pancreatic exocrine secretion in rats.

Exocrine pancreatic secretion to intravenous injections of a new stimulant of gastrointestinal motility, R51,619 (cisapride) was studied in conscious rats, and in the isolated pancreatic acini in vitro. The injection of cisapride (2 mg/kg) significantly increased fluid, bicarbonate and protein output in vivo. Atropine completely abolished the pancreatic responses to cisapride, and CR 1409, a new glutaramic acid derivative and a competitive cholecystokinin (CCK) inhibitor, tended to decrease the cisapride-induced pancreatic exocrine secretion. However, amylase release and Ca2+ efflux from the isolated pancreatic acini were not stimulated. These results suggest that cisapride indirectly affects the pancreatic exocrine secretion primarily by releasing acethycholine from the intrapancreatic nerve endings and in part by releasing CCK from the duodenum, but has no direct action on the pancreas.

Acetylcholine↗
PubMed1988

Effect of somatostatin on pancreatic enzyme secretion.

The effect of somatostatin (SS) on the pancreatic enzyme secretion was studied in a perfusion system using dispersed pancreatic rat acini in vitro. In addition the effect of SS on pancreatic secretion in vivo was also studied in conscious rats for comparison. In an in vitro study, 6 x 10(-7) M SS-14 caused no significant change in amylase release when added 20 min before stimulation by 10(-5) M carbamylcholine (Cch), 10(-6) M A23187, 5 x 10(-7) M secretin and 2 mM dibutyryl cyclic AMP. The addition of 6 x 10(-7) M SS-28 also caused no significant change in amylase release stimulated by 10(-5) M Cch. High performance liquid chromatographic examination indicated that no degradation of either SS-14 or SS-28 occurred after reaction with dispersed acini. In an in vivo study SS-14 caused marked inhibition of basal pancreatic secretion and stimulated pancreatic secretion by bile-pancreatic juice diversion. These results indicate that SS has no direct inhibitory action on rat pancreatic secretion, and that SS may inhibit the pancreatic secretion by indirect mechanisms.

Amylases↗
PubMed1988

Effects of somatostatin and pancreatic polypeptide on exocrine and endocrine pancreas in the rats.

The effects of somatostatin-14 (SS) and rat pancreatic polypeptide (rPP) on endocrine and exocrine functions of the pancreas, stimulated by 40 ng/kg cholecystokinin octapeptide during continuous infusion of 1 U/kg/h secretin, were investigated in the rat, in vivo. Protein output in the pancreatic juice and integrated insulin (IRI) secretion were inhibited, in a dose related fashion, by continuous infusion of SS, in doses of 0.5, 5 and 50 micrograms/100g/h. On the other hand, bicarbonate and volume output were not inhibited by SS. The rPP significantly inhibited not only the protein output but also the bicarbonate and volume output of the pancreatic juice in doses of 0.1 and 1 microgram/100g/h. Integrated IRI secretion was inhibited significantly by rPP, but the inhibition of IRI secretion was much greater in the portal than in the jugular vein. Plasma SS and rPP concentrations showed physiological ranges during infusion of doses of 0.5 and 0.1 microgram/100g/h of SS and rPP, respectively. Therefore, there was a marked difference between the inhibition by rPP and that by SS on the exocrine and endocrine pancreas. These observations suggest that SS and PP may play a physiological role in the pancreas and that their effects on the pancreas relate to different mechanisms.

Animals↗
PubMed1988

Pancreatic polypeptide secretion from the isolated perfused ventral and dorsal areas of the rat pancreas.

The secretion of pancreatic polypeptide (PP) by neuropeptides [vasoactive intestinal polypeptide, gastrin-releasing peptide (GRP), neuromedin B, and neuromedin C] and carbachol was investigated using the isolated perfused ventral part of the rat pancreas, with or without atropine, and a specific radioimmunoassay for rat PP. The release of PP from the dorsal part of the rat pancreas by GRP and carbachol was also studied. Carbachol and GRP stimulated, in a dose-dependent manner ranging from 10(-6) to 10(-9) M, PP secretion from the ventral part of the pancreas. Maximum responses were observed with 10(-7) to 10(-8) M carbachol and 10(-7) M GRP. The response with 10(-7) M carbachol was biphasic and was abolished by 10(-5) M atropine. The response with 10(-7) M GRP, however, was transient, monophasic, and not inhibited by atropine. Vasoactive intestinal polypeptide (10(-7) M) stimulated a weak PP secretion that was not inhibited by atropine. The potency of GRP and vasoactive intestinal polypeptide relative to carbachol at 10(-7) M was 24% and 7%, respectively. Neuromedin C had almost the same bioactivity as GRP with respect to the release of PP, whereas neuromedin B was one-third less potent than GRP and neuromedin C. The relative secretion of PP from the dorsal compared with the ventral part of the pancreas after stimulation by 10(-7) M carbachol and GRP was 19% and 22%, respectively. These data show that peptidergic nerves may play some role in PP secretion. In addition, the main source of PP to the systemic circulation may be the ventral part of the pancreas.

Animals↗
PubMed1988

Gastrin-releasing peptide stimulates cholecystokinin secretion in perfused rat duodenum.

We examined the effect of porcine gastrin-releasing peptide (GRP-27) and other analogous neuropeptides on cholecystokinin (CCK) secretion from the isolated perfused rat duodenum. GRP-27 stimulated CCK secretion in a monophasic pattern and in a dose-dependent manner ranging from 10(-9) M to 10(-6) M, and 10(-7) M of GRP-27 led to an increment of 442 +/- 120.8 fmol/3 min. The stimulatory effect of GRP-27 on CCK was not inhibited by 10(-5) M of atropine. 10(-7) M of neuromedin C and B, analogs of GRP, stimulated CCK secretion to increments of 382 +/- 64.1 and 289 +/- 47.2 fmol/3 min, respectively. Carbachol (10(-9) to 10(-6) M), VIP (10(-9)M), secretin (10(-9)M) and glucose (11 mM) did not stimulate CCK secretion, and the addition of atropine (10(-5)M) to them led to no significant changes. These results suggest that GRP may directly stimulate CCK secretion from the duodenum and work as a non-cholinergic, peptidergic neurotransmitter.

Animals↗
PubMed1988

Distribution of pancreatic polypeptide-like immunoreactivity in rat tissues.

The distribution of pancreatic polypeptide (PP)-like immunoreactivity (LI) in rat tissue was determined by a specific radioimmunoassay (RIA) after extraction with boiling 1 N acetic acid. The concentration of PP-LI in the ventral area of the pancreas (0.917 +/- 0.106 micrograms/g tissue) was about 10 times greater than that in the dorsal area of the pancreas (0.085 +/- 0.006 micrograms/g tissue). Extrapancreatic PP-LI was present in the colon (0.034 +/- 0.010 micrograms/g tissue) and rectum (0.019 +/- 0.001 micrograms/g tissue). The remainder of the gastrointestinal tract, the lung, kidney, liver, spleen, heart, adrenal gland, and central nervous system contained no measurable PP-LI. Reverse-phase high performance liquid chromatography analysis of the PP-LI materials from the pancreas, colon, and rectum revealed one peak which corresponds to the rat PP standard, under conditions of elution which clearly separated PP, NPY, PYY. These results show that distribution of PP-LI in the rat is different from other known distributions in the PP family of peptides.

Animals↗
PubMed1988

A prospective WISC-R study in children with epilepsy.

A prospective intraindividual study of WISC-R testing in the 45 children with epilepsy revealed that: 1) antiepileptic drugs, phenobarbital in particular, resulted in a detrimental effect on the WISC-R scores, 2) of the WISC-R subtests, vocabulary tasks of the verbal test were the most susceptible indicators in children whose FSIQ scores either improved or deteriorated, and 3) in children whose antiepileptic drug dosage remained unchanged while the seizure frequency remained unchanged, both the VIQ and PIQ scores decreased. It was evident that either recurrent seizures or inappropriate medication may exert a detrimental effect on intelligence as expressed by the WISC-R testing. In addition, the possibility that the underlying cerebral pathology associated with the etiology of epilepsy may play a role in a progressive intellectual deterioration was suggested.

Brain Damage, Chronic↗
PubMed1988

Effects of human pancreatic polypeptide on exocrine pancreatic function in conscious rats.

The effect of newly synthesized human pancreatic polypeptide (hPP) on pancreatic secretion stimulated by a diversion of bile-pancreatic juice (BPJ) from the intestine, and plasma hPP concentration were examined in conscious rats. Exogenous hPP infusion (1, 10 micrograms/kg/hr) inhibited pancreatic protein, bicarbonate and fluid outputs during BPJ diversion in a dose-dependent manner. During 1 and 10 micrograms/kg/hr hPP infusion plasma hPP immunoreactivity increased to 369 +/- 22.9 and 1,125 +/- 90.2 pg/ml, respectively. These results suggest that newly synthesized hPP has an inhibitory activity on exocrine function of the pancreas.

Animals↗
PubMed1988

Inhibitory effect of CR-1409, a competitive inhibitor of cholecystokinin, on pancreatic exocrine secretion in the conscious rat.

The inhibitory effect of CR-1409, a new glutaramic acid derivative and a competitive inhibitor for cholecystokinin (CCK), on the basal and CCK-stimulated pancreatic secretion was examined in the conscious rat in vivo. Rats were prepared with cannulae draining pure bile and pancreatic juice separately and with a duodenal cannula and right and left jugular vein cannulae. Plasma CCK level increased to 3.65 +/- 0.79 and 19.9 +/- 4.47 pM (mean +/- S.E.) by a 2-hr infusion of 100 and 300 pmole/kg/hr of CCK-octapeptide (CCK-8), respectively. Simultaneous infusion of 170 nmole/kg/hr of CR-1409 completely abolished pancreatic responses to 100 pmole/kg/hr of CCK-8. Infusion of CR-1409 at rate of 57 nmole/kg/hr slightly but significantly inhibited CCK-8 (100 pmole/kg/hr)-stimulated secretion. Pancreatic responses to 300 pmole/kg/hr of CCK-8 were partially inhibited but not completely abolished by the 170 nmole/kg/hr of CR-1409. Neither the basal pancreatic secretion nor the bile secretion was affected by CR-1409. We conclude that CR-1409 inhibited CCK-stimulated pancreatic secretion in vivo.

Animals↗
PubMed1988

Plasma basal concentration of pancreatic polypeptide (PP) does not increase with ageing in the female Fischer (F-344) conscious rat.

Plasma concentrations of pancreatic polypeptide (PP) were compared for young (6 to 12 month-old) and old (24 to 25 month-old) conscious female Fischer rats by means of a radioimmunoassay. Basal plasma PP concentration was not different between young and old rats, nor was PP release stimulated by cerulein in either age group. The mechanism of PP release in rats is quite different from that in other species such as dogs and humans.

Aging↗
PubMed1988

Evidence for the direct action of gastrin-releasing peptide (GRP) on amylase secretion from rat pancreatic acini: an assessment using a perifusion system.

We examined the effects of porcine gastrin-releasing peptide (GRP) on exocrine secretion from dispersed rat pancreatic acini using a perifusion system. GRP stimulated amylase secretion, in a dose-dependent manner in the range of 10(-10)-10(-5) M. The submaximum response was observed at 10(-8) M. Stimulation with 10(-8) M GRP caused a biphasic release of amylase. Amylase secretion by GRP stimulation was not affected by the addition of carbachol, dibutyryl cyclic GMP, or atropine. W-7, a calmodulin antagonist, inhibited the amylase secretion induced by GRP. The addition of isobutylmethylxanthine or secretin increased amylase secretion caused by GRP stimulation. These observations suggest that GRP facilitates enzyme secretion by a direct action on pancreatic acini and not through muscarinic and cholecystokinin receptors. The interaction by the Ca2+-calmodulin complex was suggested.

Amylases↗