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Biomedical subjects

K Kitani

Publications and source records attributed to K Kitani.

At least 127 records · Page 7Linked to original sources
PubMed1989

Aging impairs pancreatic response to refeeding following a protein-free diet.

Changes in content and recovery of pancreatic enzymes after a protein-free diet were examined in young (8-month) and old (26-month) Fischer-344 female rats. In control rats fed a normal diet for 15 days, no significant difference between young and old rats was observed in pancreatic weight or in pancreatic content of protein, enzymes, and DNA. A 7-day protein-free diet significantly decreased pancreatic wet weight as well as content of protein, chymotrypsin, amylase, and DNA in both age groups, whereas body weight and amount of daily food intake did not differ from respective control values (in normal diet-fed rats) in either age group. In young rats, chymotrypsin and protein contents were significantly greater than control values during the recovery period in which rats were fed a normal diet following the 7-day protein-free treatment. In contrast, these values in old rats remained lower than corresponding control values throughout the entire recovery period. These results agree with our previous study suggesting that aging probably attenuates the reserve capacity of the pancreas for enzyme secretion, but not its basal functions.

Aging↗
PubMed1989

Release of pancreatic polypeptide and its mechanism in luminal feedback regulation in the conscious rat.

Exclusion of bile and pancreatic juice (BPJ) from the proximal intestine increases the release of pancreatic polypeptide (PP) from 4.4 to 14.3 pM and its increase was diminished by the intravenous infusion of atropine (100 micrograms/kg/h) in conscious rats. Neither intravenous bolus injection nor continuous infusion of cerulein did increase plasma PP concentration. It is suggested that the increase in plasma PP concentration produced by BPJ diversion is regulated by cholinergic mechanism, but not by cholecystokinin (CCK) released despite the known fact that BPJ diversion increases plasma CCK concentration.

Animals↗
PubMed1989

Effects of porcine pancreastatin on postprandial pancreatic exocrine secretion and endocrine functions in the conscious rat.

The inhibitory effect of a newly discovered polypeptide, pancreastatin, on postprandial pancreatic exocrine secretions and endocrine functions was examined in the conscious rat with a chronic external bile, pancreatic and gastric fistula. The infusion of 100 and 200 pmol/kg/h of pancreastatin significantly inhibited meal-stimulated pancreatic secretion of fluid and protein but not bicarbonate in a dose-dependent manner. The infusion of 100 and 200 pmol/kg/h of pancreastatin increased plasma pancreastatin concentrations (mean +/- SE) up to 133.5 +/- 15.9 and 209.8 +/- 14.5 pM, respectively. However, the same doses of pancreastatin failed to inhibit postprandial insulin and gastrin releases and did not affect blood glucose levels. It is suggested that pancreastatin may be an inhibitor of postprandial pancreatic exocrine secretion. However, the doses used in the present study may not have been high enough to affect endocrine functions.

Animals↗
PubMed1989

Differences in stimulatory effects between rat pancreatic secretory trypsin inhibitor-61 and -56 on rat pancreas.

Two types of pancreatic secretory trypsin inhibitors (PSTIs) were recently purified from rat pancreatic juice. One consisted of 61 (PSTI-61) and the other of 56 (PSTI-56) amino acid residues. PSTI-61 has been reported to elicit cholecystokinin (CCK) release when injected into the duodenum. Since no information has been available about the action of PSTI-56 on CCK release, the two PSTIs were compared for their stimulatory effect on CCK release and pancreatic exocrine secretions in conscious rats after intraduodenal administration. Rats were prepared with bile and pancreatic fistulae and with two duodenal cannulae. Pancreatic juice was excluded from the duodenum for 48 h prior to the experiment because rat PSTIs were trypsin sensitive. PSTI-61 significantly stimulated pancreatic secretions and increased plasma CCK concentrations from 3.6 to 6.5 pM, whereas PSTI-56 had no effect on either CCK release or pancreatic secretions. It is suggested that the action as a regulator for CCK release and pancreatic secretions is possessed only by PSTI-61, but not by PSTI-56.

Amino Acid Sequence↗
PubMed1989

Comparative effects of mammalian pancreastatins on the pancreatic exocrine secretion.

We have reported that porcine pancreastatin inhibits cholecystokinin (CCK)-stimulated pancreatic exocrine secretion in conscious rats. In the present study, the effects of mammalian pancreastatins on exocrine pancreatic functions in rats were compared using synthetic pancreastatins (porcine, bovine, human, and rat). Rats were prepared with cannulae draining pure pancreatic juice and bile separately and a duodenal cannula to return bile-pancreatic juice to the intestine and with a jugular vein cannula. After 90-min basal collection of pancreatic juice, CCK-8 (100 pmol/(kg.h] was infused for 3 h with or without pancreastatins (100 pmol/(kg.h]. All pancreastatins significantly inhibited protein output at an equivalent molar potency. These results suggest that mammalian pancreastatins have the same biological activity of a comparable magnitude and exert a similar biological action on the exocrine pancreas.

Amino Acid Sequence↗
PubMed1989

The nature of choleresis induced by deoxycholate and its conjugates in the rabbit.

A hypothesis for the mechanism of bile salt-induced choleresis with increased bile bicarbonate concentration (cholehepatic recycling; CHR), requires a relatively high pK'a value of a bile salt to be easily protonated in bile canaliculi. If the choleresis induced by taurodeoxycholate and glycodeoxycholate (which increase bile bicarbonate concentration in rabbits) is to be explained by this thesis, these bile salts must be extensively deconjugated in the liver, enabling a bile salt having a higher pK'a value, free deoxycholate, to undergo CHR. With a stepwise increase in the infusion rate, the increments of bicarbonate concentration, as well as the bile flow rate induced by taurodeoxycholate and glycodeoxycholate, were as efficient as those caused by an equimolar infusion of deoxycholate. With infusion of conjugated deoxycholates, the major bile salts excreted in the bile were those which had been infused. In studies with conjugated deoxycholates, unconjugated deoxycholate was not detectable in the bile. Furthermore, deoxycholate concentration in the liver significantly increased after a 2-h infusion of deoxycholate but did not increase after infusion of either glycodeoxycholate or taurodeoxycholate. The present results suggest that the choleresis induced by conjugated deoxycholates in rabbits requires an explanation other than CHR of deoxycholate.

Animals↗
PubMed1989

Interactions between bile and pancreatic juice diversions on cholecystokinin release and pancreas in conscious rats.

Pancreatic exocrine secretion in the conscious rat is regulated by proteases secreted by the pancreas, and cholecystokinin (CCK) is known to be involved in its mechanism. It has also been reported that the absence of either pancreatic juice or bile in the duodenum could stimulate pancreatic secretion. Therefore, differences in CCK release responding to the exclusion of bile, pancreatic juice (PJ), or both bile and pancreatic juice (BPJ) from the intestine were examined by using a bioassay for cholecystokinin. Plasma CCK levels were increased by all three treatments compared with the basal value, the order of their effects being BPJ greater than PJ greater than bile diversion, and CCK concentrations produced by BPJ diversion were much greater than can be explained as simply summed effect of exclusions of bile and PJ. Pancreatic exocrine secretions were significantly increased by PJ and BPJ diversions, but the effect of bile diversion on the pancreas was not statistically significant. An additional infusion of CR-1409 (0.1 mg/rat), one of CCK receptor antagonists, inhibited exocrine function stimulated by BPJ diversion. We conclude (i) BPJ diversion is the strongest endogenous stimulant on CCK release; (ii) the potentiation between bile and PJ diversions is induced on CCK release; (iii) pancreatic protein secretion during BPJ diversion is mainly modulated by CCK.

Animals↗
PubMed1989

[Effect of pancreastatin on pancreatic exocrine secretion in vivo and in vitro].

The effects of pancreastatin on pancreatic exocrine secretion were examined both in vivo and in vitro in rats. Pancreastatin inhibited pancreatic fluid and protein outputs stimulated by the exclusion of pancreatic juice from the intestine with the intraduodenal infusion of Trasylol but did not inhibit bicarbonate output stimulated by HCl in vivo in conscious rats. However, pancreastatin did not affect amylase release from dispersed acini or Ca concentration in acinar cells. Therefore, it is concluded that pancreastatin inhibits pancreatic exocrine secretion but the effect is indirect.

Amylases↗
PubMed1989

[Acute myelogenous leukemia with recurrence of the meningeal, spinal cord and the optic nerve infiltration with remission induction by Co therapy and maintained by intrathecal chemotherapy with Ommaya reservoir].

A 42-year-old woman was diagnosed as having acute myelogenous leukemia (M 2 of FAB classification) in May, 1985. Complete remission was achieved with the BHAC-DP therapy (BHAC, daunomycin and prednisolone). Whole skull irradiation and intra thecal chemotherapy were performed by way of prevention. In 1986, she developed her visual disturbance and paraplegia. Myelography and metrizamide CT indicate intraspinal and meningeal infiltration of leukemic cells in the upper thoracic spine. Leukemic cells were found in the cerebrospinal fluid but not in the bone marrow. Complete remission was obtained by irradiation and intrathecal chemotherapy. In Dec. 1986, Ommaya tubing was repeated. Hematological and neurological examinations showed no evidence of malignancy for 3 years. In Oct. 1988, she admitted to our hospital for the maintenance of the remission state, and died of sepsis. The result of autopsy revealed no leukemic cells in her CNS. It is said the intraspinal infiltration of leukemic cells is rather rare. As it is said the intrathecal injection of anti-leukemic agents is not effective for the intraspinal infiltration, irradiation should be needed. Therefore it is very important to critically differentiated intraspinal from meningeal infiltration. Furthermore, Ommaya tubing is effective in order to maintain remission in a patient with CNS leukemia.

Adult↗
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

Biliary albumin excretion induced by bile salts in rats is a pathological phenomenon.

The bile to plasma 125I-albumin concentration ratio (B/P ratio) was examined before and during various bile salt infusions in male Wistar rats that had previously received iv injection of 125I-albumin. Endogenous rat albumin and IgG concentrations in the bile were also determined by a single radial immunodiffusion method. Taurocholate (TC) infusion (1.0 mumol/min/100 g body wt) significantly increased the bile flow rate in the first hr but the flow began to decline in the second hr. The B/P ratio as well as rat albumin (and IgG) excretion into the bile significantly increased as early as 15 min after the start of TC infusion, and the increase became more pronounced in the second hr, when the bile flow began to decrease. Infusion of taurochenodeoxycholate (TCDC, 0.4 mumol/min/100 g) caused a reduction in bile flow 15 min after the start of infusion but the B/P ratio increased 40 times at its peak compared with the basal value before the bile salt infusion. Simultaneous infusion of tauroursodeoxycholate (TUDC, 0.6 mumol/min/100 g) and TCDC not only abolished the cholestasis induced by TCDC but maintained stable choleresis as long as for 2 hr. During this choleretic period, the B/P ration never exceeded the basal value. The choleresis induced by either taurodehydrocholate (TDHC) or bucolome was not accompanied by enhanced albumin excretion. In rats given TDHC infusion, albumin excretion started to increase only after the bile flow began to decline following the initial choleretic period. The enhanced excretion of albumin induced by TC and TCDC is therefore suggested to be caused not by the choleresis per se but by a possible concomitant increase in the communication between sinusoids and bile canaliculi, which eventually leads to cholestasis. Our results suggest that the biliary excretion of albumin enhanced by bile salt infusion in rats is primarily the result of hepatocyte damage closely related to cholestasis rather than to choleresis, and that the rate of such excretion can be used as a convenient and reliable marker for hepatocyte damage.

Albumins↗
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

Characterization of the autofluorescence of rat liver plasma membranes.

The autofluorescence of isolated rat liver cell plasma membranes was characterized in vitro in relation to the autofluorescence used previously for fluorescence recovery after photobleaching (FRAP) studies. The fluorescence of membrane preparations displayed an emission pattern with a maximum at around 525 nm when excited with a 468 nm blue light. The excitation spectrum monitored at 525 nm closely resembled that of flavin compounds (riboflavin, FAD, FMN). The chloroform extract of the membrane fraction showed practically no fluorescence, whereas, both the water-soluble and water-insoluble protein fractions remaining after chloroform extraction were strongly fluorescent. The fluorescence disappeared almost completely under the effect of sodium hydrosulfite, and recovered after oxidation either by shaking in air or by adding buffered hydrogen peroxide solution. The fluorescence of the acid extract of the plasma membranes photolyzed in an alkaline medium was quite similar to that of lumiflavin obtained from the photolysis of riboflavin in an alkaline medium. The plasma membranes prepared from isolated hepatocytes (which were completely devoid of endothelial cell contamination) exhibited the same autofluorescence in the liver cell plasma membranes. The results suggest that the autofluorescence of the liver cell plasma membranes is most likely of a character similar to that of flavin, bound to hepatocyte plasma membrane proteins. This fluorescence is suitable for measuring the average lateral diffusion constant of proteins by means of FRAP methods.

Animals↗
PubMed1988

Effect of perfringolysin O on the lateral diffusion constant of membrane proteins of hepatocytes as revealed by fluorescence recovery after photobleaching.

Perfringolysin O is a thiol-activated cytolytic exotoxin the primary receptor of which is the membrane cholesterol on the cell surface. The effect of perfringolysin O was tested in various hepatocyte preparations. (i) Smears of fresh liver exposed to a mild H2O2 (1.0 mM) injury for 10 min at 37 degrees C, develop a 'peroxide-induced autofluorescence' (PIAF) on the membrane proteins. PIAF is suitable for measuring the average lateral diffusion constant (D) of the membrane proteins by means of fluorescence recovery after photobleaching technique (FRAP). Incubation for 5 min with 600 or 2000 units/ml of the perfringolysin O resulted in a significant increase (32 and 46%, respectively) of D as compared to the controls of the same age group (13-14 months). Various tests like heat denaturation of cholesterol saturation of perfringolysin O before its application as well as thiol-activation of the smears with dithiothreitol revealed that the increase of D is a specific toxin effect due mot probably to the reaction of perfringolysin O with cholesterol. (ii) Isolated hepatocytes were exposed to perfringolysin O and their viability as well as the release of two cytosolic enzymes (lactate dehydrogenase and glutamic-pyruvic transaminase) were measured; 40-60 units/ml of perfringolysin O in 30 min reduced the viability of the hepatocytes to zero and caused a release of about 70% of both cytosolic enzymes. The significance of the results is discussed from the points of view of both the toxin-effect and the FRAP method.

Animals↗
PubMed1988

Age-dependent decrease in the hepatic uptake and biliary excretion of ouabain in rats.

The biliary excretion of i.v. injected ouabain was examined in male and female Wistar-derived rats in relation to age. The hepatic uptake velocity for ouabain was also determined in isolated hepatocyte preparations obtained from male rats of various ages. Biliary recovery values of ouabain (percent of the dose) were fairly comparable for young male and female rats (3-4 month old). Recovery progressively decreased with age, the first 10-min recoveries at 24 months being about one-third those of respective young values in both sexes. A significant linear relation was demonstrated between the first 10-min recovery (Y, percent of the dose) and rat age (X, month), yielding the relations of Y = 17.75-0.43X for males and Y = 18.99-0.43X for females respectively. Similarly, the initial uptake velocity (Y, nmol/mg/min) for ouabain decreased in a linear fashion with age (X, month), yielding a significant negative correlation (Y = 0.704-0.0021X, r = -0.839, P less than 0.005, N = 21) at an ouabain concentration of 8 microM. Kinetic studies using non-linear regression analysis revealed a significantly lower Vmax value (0.533 +/- 0.041 nmol/mg/min) in old (24-29 months) rats compared to the young (4-4.5 months) value (1.193 +/- 0.105 nmol per mg/min, P less than 0.05), while the affinity constant (Km, microM) did not differ significantly between young and old animals (203.12 +/- 25.42 microM in young rats vs 283.68 +/- 28.90 microM in old rats, mean +/- SE, 0.05 less than P less than 0.1). The results of the present study suggest that the age-dependent decrease in the biliary recovery of i.v. injected ouabain in rats can be largely explained by the decrease with age in the hepatic uptake of ouabain. Furthermore, the results provide further support for our previous thesis that the decrease in the lateral mobility of hepatocyte plasma membrane proteins, as revealed by the fluorescence recovery after photobleaching technique, may play a significant role in the age-dependent decrease in the physiological function(s) of the hepatocyte plasma membrane, such as the hepatobiliary transport of ouabain.

Aging↗
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↗