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K Takeuchi

Publications and source records attributed to K Takeuchi.

1,602 records · Page 89Linked to original sources

Involvement of endothelium-derived factors in controlling the active tone of smooth muscle in aorta from hypertensive rats.

Control of the active tone by endothelium in aortae from various strains of spontaneously hypertensive rats was studied. The active tone was negligibly observed in endothelium-intact preparation. The application of N(G)-nitro-L-arginine (L-NNA, 10(-4) M) induced slowly developed active tone in the preparations from hypertensive rats but no active tone was induced in the preparation from normotensive Wistar Kyoto rats (WKY). The developed tension was stronger in preparations from rats with higher blood pressure as observed in endothelium denuded preparations. The developed active tone in the presence of L-NNA was greater than that observed in endothelium denuded preparations. The active tone was abolished by the removal of extracellular Ca2+ or by the application of Ca-antagonists. L-arginine counteracted the effects of L-NNA and depressed the developed active tone in the presence of the latter drug. The application of indomethacin (10(-5) M) depressed the active tone of the preparations from SHRSP by 25.5+/-5.2%. Increasing extracellular K+ concentration or application of tetraethylammonium (TEA) could not be used to observe the effect of endothelium-derived factors on the active tone, because of their strong contractile effect. Simultaneous application of apamin and charybdotoxin induced an elevation of tension which was often associated with spontaneous tension oscillation. It is concluded that the active tone, which is smooth muscle origin, is depressed by endothelium-derived nitric oxide (NO) strongly and potentiated by a product of arachidonic acid cascade through cyclooxygenase pathway. The involvement of endothelium-derived hyperpolarizing factor (EDHF) in the depressing effect of endothelium is thought to be small.

Animals↗

Nasal mucociliary clearance in Sjögren's syndrome. Dissociation in flow between sol and gel layers.

Nasal mucociliary clearance was measured with two methods in 8 patients with Sjögren's syndrome and in 6 normal subjects. The movement of two different tracers placed 1.5 cm posterior to the inferior turbinate tip was measured respectively. The transport rate of a 500 microns anion resin particle tagged with 99mTc was measured. The clearance of 10 microliters saline labelled with 99mTc was monitored and the clearance rate was calculated. Whereas the measurement with the particle method revealed the lowered transport rate in Sjögren's syndrome, measurement with the saline method did not reveal any difference in clearance rate between the two groups. Since the former method measures the transport of particle in the gel phase (the outer mucous layer) and the latter measures the clearance of both gel and sol (periciliary fluid) layers, it is postulated that there is a dissociation of flow between sol and gel layers in Sjögren's syndrome.

Anion Exchange Resins↗

Effect of atropine on nasal mucociliary clearance.

To investigate the effect of atropine on mucociliary function, nasal mucociliary clearance was measured with two methods in eight healthy men before and after subcutaneous injection of atropine sulphate. The movement of two different tracers placed 1.5 cm posterior to the inferior turbinate tip was measured. The transport rate of a resin particle tagged with 99mTc was measured. The clearance of 10 microliters saline labelled with 99mTc was monitored and the clearance rate calculated. Whereas atropine lowered the resin particle transport rate, the saline method did not reveal any difference in clearance rate after injection of atropine. Since the former method measures the transport of particles in the gel phase (the outer mucous layer) and the latter measures the clearance of both gel and sol (periciliary fluid) layers, it is postulated that the slowing of mucociliary transport by atropine is due to alterations in the gel layer.

Adult↗

A non-invasive CSF flowmeter.

A new non-invasive method for quantitative measurement of cerebrospinal fluid (CSF) flow in the ventriculo-peritoneal shunt tubing, used in hydrocephalus, has been developed. It is an implantable device which produces a bubble in the shunt tubing by electrolysis. This bubble is then detected in the tubing by an electrode arrangement using electric impedance or ultrasonically using a Doppler probe. The energy for electrolysis is supplied by extracorporeal high-frequency transmission. The CSF flow rate is calculated by the velocity of bubble flow in the tubing. CSF flow rates, ranging from 0.01 to 1.00 ml/min, have been measured in animal experiments with statistically good accuracy. In 11 clinical cases a flow range of between 0.01 and 1.93 ml/min have been observed.

Animals↗

[Silent lacunes in the elderly Parkinson's disease correlated with ambulatory blood pressure].

Lacunes on brain MRI, causal blood pressure, 24-hour ambulatory blood pressure and common carotid blood flow measured by the doppler method were studied in 31 elderly patients with Parkinson's disease (mean age 67.5 +/- 7.3 years). Nineteen patients with Parkinson's disease (61%) had at least one lacune. Patients with lacunes (P(+)) were significantly higher in age than patients without lacune (P(-)). The difference of casual blood pressure between patients in the two groups was not significant. On the other hand, the average of ambulatory blood pressure measurements during a 24-hour period was significantly higher in the P(+) group than in the P(-) group. The average of carotid blood flow was also significantly lower in the P(+) group than in the P(-) group, however, after adjustment for age, the difference between them became insignificant. In conclusion, the incidence of silent lacunes on brain MRI was fairly common in elderly patients with Parkinson's disease. A high average 24-hour ambulatory blood pressure was suggested to be one of the risk factors of lacunar stroke in elderly cases of Parkinson's disease. The concept of "combine type" in Parkinsonism was supposed to be suitable as well as in senile dementia of Alzheimer type.

Aged↗

Expression and prognostic value of the standard CD44 protein in pulmonary adenocarcinoma.

We examined immunohistochemically the expression of the standard form of CD44 (CD44S) tissue specimens from 164 patients with pulmonary adenocarcinoma. Of the 164 specimens, 79 (48%) expressed CD44S and the incidence of expression correlated with the tumor size. The prognosis for CD44S positive patients was poorer than that of CD44S negative patients. Our findings suggest that CD44S plays an important role in tumor progression and that CD44S expression is a useful prognostic marker for pulmonary adenocarcinomas.

Adenocarcinoma↗

The 5-HT2 receptor antagonist sarpogrelate reduces urinary and plasma levels of thromboxane A2 and urinary albumin excretion in non-insulin-dependent diabetes mellitus patients.

1. Therapeutic effects of a 5-HT2 receptor antagonist sarpogrelate on microalbuminuria and thromboxane (TX)A2 biosynthesis were examined in non-insulin-dependent diabetes mellitus (NIDDM) patients. 2. In protocol I, the ankle-brachial pressure index (API; an indicator of peripheral blood flow) and urinary albumin excretion (UalbV; an indicator of renal function) were determined in 42 NIDDM patients who had been treated with 300 mg/day sarpogrelate for 8 weeks. In an analysis of the results, the NIDDM patients were divided into four groups based on the severity of either vasculopathy or nephropathy as follows: group A, API < 0.9, UalbV > or = 100 mg/day; group B, API < 0.9, UalbV < 100 mg/day; group CAPI > or = 0.9, UalbV > or = 100 mg/day; and group D, API > or = 0.9, UalbV < 100 mg/day. 3. In protocol II, 10 NIDDM patients with UalbV values > 100 mg/day were divided into two groups to further confirm the effect of sarpogrelate on albuminuria: group E, the sarpogrelate treatment group (n = 5); and group F, the no treatment group (n = 5). 4. In protocol I, the incidence of a cold sensation in the lower extremities was reduced from 45.2 to 21.4% following sarpogrelate treatment. In patients with UalbV > or = 100 mg/day (groups A and C), UalbV was significantly decreased independent of API, while it did not change in patients with UalbV < 100 mg/day (groups B and D). Plasma TXB2 levels were significantly decreased following sarpogrelate treatment, whereas plasma 6-keto-prostaglandin F1 alpha levels were not. 5. In protocol II, in the sarpogrelate treatment group (group E), albuminuria was significantly improved and both plasma levels TXB2 and urinary TXB2 excretion were significantly decreased. In contrast, in the untreated group (group F), neither plasma levels TXB2 nor urinary TXB2 excretion was changed. 6. In conclusion, microalbuminuria was improved by treatment with the 5-HT2 receptor antagonist sarpogrelate independent of latent vasculopathy. Blockade of 5-HT2 receptors is suggested to be beneficial for the treatment of nephropathy in NIDDM patients. It is possible that the inhibition of TXA2 biosynthesis is involved in the therapeutic effect of 5-HT2 receptor antagonists.

Albuminuria↗

A simultaneous resection of a concomitant abdominal aortic aneurysm and hepatocellular carcinoma: two cases.

We report two cases of simultaneous surgical treatment in patients with a concomitant abdominal aortic aneurysm (AAA) and hepatocellular carcinoma (HCC). The first patient underwent abdominal echography and was observed to have an abnormal hepatic mass. A consecutive computed tomographic (CT) scan showed an AAA, measuring 8 cm in size. The hepatic mass, which reached 5 cm in size, existed in the S5 and was strongly suspected to be HCC. The second patient was observed to have AAA by CT scan three years ago and also shown to have a hepatic mass, which reached 3 cm in size, in the S8. Both patients underwent a simultaneous resection. At first, a resection and reconstruction of the aneurysm was performed, followed by an extended right lobectomy and anterior segmentectomy of the liver. The postoperative course was uneventful and they were discharged on the 29th and 22nd postoperative day. To our knowledge, this is the first report of patients who underwent a successful simultaneous resection of an AAA and HCC.

Aged↗

Stimulation by nitric oxide of HCO3- secretion in bullfrog duodenum in vitro--roles of cyclooxygenase-1 and prostaglandins.

The effect of nitric oxide (NO) on HCO3- secretion was examined in vitro using the isolated preparation of bullfrog duodenum, in relation to cyclooxygenase (COX) isozymes and endogenous prostaglandins (PGs). The tissue was bathed in unbuffered Ringer solution gassed with 100% O2 on the mucosal side and HCO3- Ringer's solution gassed with 95% O2-5% CO2 on the serosal side. The HCO3- secretion was measured by a pH-stat method using 10 mM HCl as the titrant to keep the mucosal pH at 7.4. NOR-3 [(+/-)-(E)-Ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamine] was used as a NO donor and added to the serosal solution. To analyze the NOR-3 action, the effects of dibutyryl guanosine-3', 5'-cyclic monophosphate (dbcGMP), methylene blue, indomethacin (nonselective COX-inhibitor) and NS-398 (selective COX-2 inhibitor) on the HCO3- response were also examined. NOR-3 (1 x 10(-4) and 3 x 10(-4) M) caused an increase of HCO3- secretion in a dose-dependent manner, reaching the level of 2.5 times greater than basal values at 2 hr later. Likewise, dbcGMP (1 x 10(-3) M) also caused a significant increase of the duodenal HCO3- secretion. The HCO3- stimulatory action of NOR-3 was significantly attenuated by methylene blue (5 x 10(-5) M) and indomethacin (1 x 10(-5) M) but not by NS-398 (1 x 10(-5) M), and indomethacin also suppressed the HCO3- response to dbcGMP. The serosal release of PGE2 was significantly increased by both NOR-3 and dbcGMP, and these responses were inhibited by indomethacin but not NS-398. These results suggest that NO increases HCO3- secretion in Bullfrog duodenum in vitro, and this action is dependent on cGMP-related COX-1 activation and mediated by PGs.

16,16-Dimethylprostaglandin E2↗

Permissive role of neutrophils in pathogenesis of indomethacin-induced gastric lesions in rats.

INTRODUCTION: We examined the possible role of neutrophils in the pathogenesis of indomethacin-induced gastric lesions, in comparison with prostaglandin (PG) deficiency. MATERIAL AND METHODS: Rats were given indomethacin (35 mg/kg, s.c.) and killed 4 hr later. Gastric motility, mucosal PGE2 levels, and myeloperoxidase (MPO) activity were measured following indomethacin. Atropine was given s.c. 30 min before administration of indomethacin, while 16, 16-dimethyl PGE2 (dmPGE2) or anti-rat neutrophil antiserum (ANS) was given i.v. 10 min or 1 hr, respectively, before indomethacin treatment. RESULTS: Indomethacin reduced PGE2 contents in the stomach and produced hemorrhagic lesions in the stomach, with an increase of gastric motility and MPO activity. Indomethacin-induced gastric lesions were significantly prevented by dmPGE2 as well as atropine, at any time points during a 4 hr-test period. By contrast, the pretreatment of ANS did not prevent the development of gastric lesions when examined at either 1, 2 or 3 hr following indomethacin, but significantly reduced the severity of these lesions at 4 hr after indomethacin treatment. Both dmPGE2 and atropine inhibited the increase of gastric motility and MPO activity in response to indomethacin, whereas ANS prevented the increase of MPO activity, without any effect on the gastric hypermotility. CONCLUSION: These results confirmed that indomethacin-induced gastric lesions occurred in association with gastric hypermotility, in both atropine and PG-sensitive manners, and further suggest that the neutrophil activation/migration is not sufficient by itself to induce damage in the stomach and may be implicated in the process of later extension of damage.

16,16-Dimethylprostaglandin E2↗

Effect of polaprezinc on impaired healing of chronic gastric ulcers in adjuvant-induced arthritic rats--role of insulin-like growth factors (IGF)-1.

Polaprezinc, N-(3-aminopropionyl)-L-histidinatozinc, has been shown to stimulate the production of insulin-like growth factor-1 (IGF-1) in mesenchymal cells, the polypeptide playing a role in the gastric epithelial wound repair. The present study was performed to examine the effect of polaprezinc on the impaired healing of chronic gastric ulcers in adjuvant-induced arthritic rats, in relation to IGF-1. Arthritis was induced in male Dark Agouti (DA) rats by a single injection of Freund's complete adjuvant (FCA), and the gastric ulcers were induced by thermal cauterization (70 degrees C for 30 sec) 7 days after FCA injection. Omeprazole (30 mg/kg) was administered p.o. once daily, while recombinant human IGF-1 (rhIGF-1) (30 micrograms/kg, s.c.) or polaprezinc (3-10 mg/kg, p.o.) was administered twice daily, starting from 3 days after ulceration for 14 days. The healing of gastric ulcers was significantly delayed in arthritic rats as compared to normal rats on day 10 and 17 following ulceration. The expression of IGF-1 mRNA was markedly increased in the ulcerated mucosa, but this response was apparently attenuated in arthritic rats. Repeated administration of polaprezinc accelerated the healing of gastric ulcers in both normal and arthritic rats, in a dose-dependent manner, and this effect was more pronounced in arthritic rats. Likewise, treatment with omeprazole also significantly promoted the healing of gastric ulcers in both normal and arthritic rats. On the other hand, rhIGF-1 significantly promoted the gastric ulcer healing in arthritic rats without any effect on that in normal rats. These results suggest that the impaired healing of chronic gastric ulcers in arthritic rats is, at least partly, accounted for by less expression of IGF-1, and the polaprezinc improves the delayed healing of gastric ulcers in arthritic rats, probably through an increase in IGF-1 production.

Animals↗

Intestinal protection by lafutidine, a histamine H(2)-receptor antagonist, against indomethacin-induced damage in rats--role of endogenous nitric oxide.

BACKGROUND: We previously reported that lafutidine ((I)-2-(furfurylsulfinyl)-N-[4-[4-(piperidinomethyl)-2-pyridyl]oxy-(Z)-2-butenyl] acetamide), a novel histamine H(2)-receptor antagonist, protects the small intestine against indomethacin-induced damage, mediated by capsaicin-sensitive afferent neurons (CSN). MATERIAL AND METHODS: In the present study, we investigated whether or not the protective action of lafutidine against indomethacin-induced intestinal damage is mediated by endogenous nitric oxide (NO). Male SD rats were given indomethacin (10 mg/kg, s.c), killed 24 hr later, and the small intestinal mucosa was examined. Lafutidine (10 mg/kg) and capsaicin (10 mg/kg) was given p.o. twice 0.5 hr before and 9 hr after indomethacin. The NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME: 10 mg/kg) or the selective iNOS inhibitor aminoguanidine (10 mg/kg) was given s.c. 1 hr before lafutidine, while L-arginine (200 mg/kg) was given i.p. 10 min before L-NAME. RESULTS: Indomethacin produced severe lesions in the small intestine, accompanied by increases in enterobacterial translocation in the mucosa. Both lafutidine and capsaicin significantly reduced the severity of these lesions, together with suppression of bacterial translocation. The protective action of lafutidine as well as capsaicin was almost totally abolished by L-NAME but not aminoguanidine, in a L-arginine-sensitive manner. Both lafutidine and capsaicin significantly increased intestinal mucus secretion, and these effects were also attenuated by prior administration of L-NAME. The exogenous NO donor NOR-3 prevented indomethacin-induced intestinal lesions at the dose that stimulated the mucus secretion and inhibited the bacterial translocation. CONCLUSIONS: These results suggest that lafutidine protects the small intestine against indomethacin-induced damage, the action being dependent on CSN and mediated by endogenous NO produced by cNOS. The protective action of lafutidine may be attributable to suppression of the bacterial translocation following indomethacin, probably due to stimulation of intestinal mucus secretion.

Acetamides↗

Effect of YM-14673, an analogue of thyrotropin-releasing hormone, on duodenal bicarbonate secretion in the rat.

The effects of YM-14673, an analogue of thyrotropin-releasing hormone, on duodenal HCO3- secretion were characterized in comparison with those of prostaglandin E2 and carbachol in anesthetized rats. The proximal duodenum was perfused with saline (pH 4.5), the pH of the perfusate and of the transmucosal potential difference were continuously monitored, and HCO3- output was determined by back-titration of the perfusate and by pH change. YM-14673 (0.1, 0.3 and 1 mg/kg) increased these parameters in a dose-related manner; the total HCO3- output at 1 mg/kg (5.8 +/- 0.7 mumol) was about 50% of that induced by prostaglandin E2 (1 mg/kg, i.v.) and 2 times greater than that induced by carbachol (4 micrograms/kg, i.v.). These responses, induced by YM-14673, were almost completely blocked by bilateral vagotomy and significantly inhibited by atropine (0.3 mg/kg, i.v.) or cyclooxygenase inhibitors, such as indomethacin (5 mg/kg, s.c.) and acetylsalicylic acid (40 mg/kg, s.c.), but not affected by pirenzepine (1 mg/kg, i.v.), a selective M1 antagonist. None of the latter agents had any effect on the HCO3(-)-stimulating action of prostaglandin E2, while the carbachol-induced HCO3- output was significantly reduced by atropine. These results suggest that YM-14673 induces the vagal-dependent HCO3- secretion in the rat duodenum and that this mechanism is mediated by muscarinic cholinoceptors, excluding the M1-subtype, and may involve endogenous prostaglandins.

Animals↗

Ultrasonically guided 19-gauge Surecut needle biopsy of apical and superior mediastinal tumors.

Four patients with apical tumors of the lung and two with superior mediastinal tumors underwent ultrasonically guided percutaneous needle biopsy through a supraclavicular approach in which a 19-gauge Surecut needle was used. Tissue cores were successfully obtained and could be used for diagnosis in all six patients: histological diagnoses of neurinoma were made in two cases and malignant tumors were diagnosed in four. No major complications such as pneumothorax, bleeding, or neurological injuries were seen. This procedure proved to be a safe and useful approach for the histological diagnosis of apical and superior mediastinal tumors.

Adult↗

Weight of resected liver is positively correlated with serum hHGF level.

BACKGROUND/AIMS: Human hepatocyte growth factor (hHGF) is involved in the control of liver regeneration. MATERIAL AND METHODS: We measured serum hHGF levels before and after partial hepatectomy in 43 patients and recorded the weight of the resected liver. RESULTS: Serum hHGF levels increased soon after operation and decreased thereafter. In the noncirrhotic group, the maximum hHGF concentration and the area under the curve of hHGF seven days postoperatively correlated with the weight of the resected liver. CONCLUSION: The amount of injured liver tissue can be approximated by the serum hHGF levels. This calculation can be useful in evaluating cases of hepatectomy, general hepatic injury, liver transplantation, and other types of hepatic damage.

Adult↗

An experimental study of hepatic resection using an in situ hypothermic perfusion technique.

BACKGROUND/AIMS: Recently, along with the progression of hepatic surgery, the in situ hypothermic perfusion technique has been used for major hepatic resection. The aim of this study was to elucidate the utility of the hypothermic perfusion technique in hepatic resection. METHODOLOGY: Two experimental models: a Total Vascular Occlusion group (TVO) and a Total Vascular Occlusion under Hypothermic Perfusion group (HP) were utilized using adult mongrel dogs. An approximately 40-45% hepatic resection was performed under total vascular occlusion with a systemic and portal shunt. In the HP group, the liver was perfused through the portal vein with lactated ringer's solution at 4 degrees C. In the TVO group, hepatic resection was done without perfusion. RESULTS: Serum AST and ALT levels after reperfusion were significantly increased in the TVO group. From the change of serum hyaluronic acid and xanthine oxidase activity, sinusoidal endothelial cell function was maintained in HP more than in TVO. The mean arterial pressure, portal venous pressure and portal venous blood flow were maintained in HP after reperfusion. Examination of vascular permeability using monastral blue showed that vascular permeability of the small intestine, lung and liver was clearly increased in TVO. Chemiluminescense intensity of the hepatic venous blood after reperfusion gradually increased only in TVO. In addition, the chemiluminescense intensity of the hepatic venous blood congested in the liver increased markedly as vascular occlusion continued in TVO. The hepatic venous blood serum congested in the liver induced morphological changes in the human umbilical vein endothelial cells and increased their permeability. The SDS-PAGE of the hepatic venous blood serum congested in the liver revealed several proteins between 37 and 42 KD. CONCLUSION: The hypothermic perfusion technique in hepatic resection may be very useful in preserving the hepatocytes and sinusoidal endothelial cells and in maintaining stability of the systemic or hepatic circulation after reperfusion because of the cooling of the liver and the washing out of congested blood in the liver.

Animals↗