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Biomedical subjects

K Mawatari

Publications and source records attributed to K Mawatari.

At least 37 records · Page 2Linked to original sources
PubMed1997

A comparison of open and laparoscopic cholecystectomy for patients with cirrhosis.

To evaluate the benefits of performing laparoscopic cholecystectomy (LC) in patients with cirrhosis, data on 13 patients with liver cirrhosis who underwent cholecystectomy for gallstones between 1989 and 1995 were retrospectively collected from charts filed at Fukuoka City Hospital. These 13 patients were classified into two groups; one, comprised of 7 who underwent LC, and another, comprised of 6 who underwent open cholecystectomy (OC). No statistical differences were observed in the duration of surgery or the intraoperative blood loss between the two groups; however, the C-reactive protein (CRP) level in the serum was significantly higher in the OC group than in the LC group. LC was followed by a significantly earlier resumption of a normal diet (P < 0.05) and a shorter hospital stay (P < 0.05) in comparison to OC. All of the patients who underwent OC had an uneventful clinical course; however, one of the patients who underwent LC suffered from intractable ascites postoperatively. The difference in the cost of hospitalization between the two groups was not statistically significant. These findings suggest that the therapeutic significance of performing LC in patients with cirrhosis should be assessed after carefully evaluating all factors including mortality, morbidity, and cost-effectiveness. Thus, further controlled trials are necessary.

Aged↗
PubMed1997

The effect of probucol on intimal thickening of autologous vein grafts in hyperlipidemic rabbit.

Probucol is used to treat hypercholesterolemia and also has an anti-atherogenic effect. The effects of probucol on intimal thickening of autologous vein graft in hyperlipidemic rabbits with poor distal run-off were investigated. A poor distal run-off model was prepared in the right hindlimb of 18 rabbits allocated to four groups depending on diet: normolipidemic commercial diet, (NL group, n = 5); hyperlipidemic diet (HL group, n = 5); commercial diet with 1% probucol (NP group, n = 4); and hyperlipidemic diet with 1% probucol (HP group, n = 4). After 4 weeks the femoral vein grafts were implanted into normal (n = 18) or poor (n = 18) runoff limbs. Vein grafts were harvested 4 weeks after implantation. Intimal thickening of the graft was measured and macrophages therein examined immunohistochemically. The serum cholesterol level was not reduced by probucol treatment. The mean flow rate of the graft was significantly reduced in the poor run-off limb. On histological examination intimal thickening in the poor run-off limb was significantly greater than that of controls, while intimal thickening in the HL and HP groups was enhanced compared with that in the NL and NP groups, respectively. Mean intimal thickening in each limb in HP group rabbits was significantly lower than that in HL rabbits (microm): control (HL/HP): 99.4(7.4)/58.8(0.7) (P < 0.05); poor run-off (HL/HP): 155.3(9.6)/130.3(7.3) (P < 0.O5). There was no difference between NL and NP (microm): control (NL/NP): 44.6(24.7)/31.5(12.8); poor run-off (HL/HP): 115.3(13.8)/97.5(34.0). In addition, enhanced intimal thickening due to poor distal run-off was not suppressed. Immunohistochemical staining showed intimal macrophage infiltration in the HL and HP groups; however, macrophage infiltration in grafts in the HP group was less than in the HL group. In conclusion, under hyperlipidemic conditions, probucol decreased intimal thickening enhancement of the vein graft, and suppressed intimal macrophage infiltration. These findings were similar to the anti-atherogenic effect of probucol in the native artery. Hence, probucol administration after vascular reconstruction with vein grafts in patients with hyperlipidemia may be beneficial.

Animals↗
PubMed1997

Determination of disodium cromoglycate in human urine by high-performance liquid chromatography with post-column photoirradiation-fluorescence detection.

For the determination of disodium cromoglycate in urine, a fluorimetric method using HPLC post-column photoirradiation has been developed. The mobile phase consisted of a 35 mmol l-1 phosphate buffer (pH 8)-methanol (7 + 3, %v/v) containing 75 mmol l-1 hydrogen peroxide and 20 mmol l-1 18-crown-6. The 18-crown-6 was used for separation adjustment of the disodium cromoglycate in the urine sample. Photoirradiation was carried out in tubing wound around a germicidal light in a reactor equipped with an air-cooling fan. The fluorescence was monitored with excitation at 325 nm and emission at 448 nm. The calibration graph for disodium cromoglycate was linear over the range 38-2340 ng ml-1 using an injection volume of 100 microliters. The pretreatment of the urine samples consisted of diluting and filtering steps. The mean recovery of disodium cromoglycate from urine was 99.1 +/- 2.4% (n = 6).

Administration, Inhalation↗
PubMed1997

The inhibition of canine vein graft intimal thickening using a newly developed antiplatelet agent.

OBJECTIVE: The purpose of this study was to evaluate the efficacy of a newly developed antiplatelet agent, 4-cyano-5, 5-bis[methoxyphenyl]-4-pentenoic acid (E5510) on intimal hyperplasia of experimental autologous vein grafts in a distal poor runoff canine model. METHOD: The femoral vein was implanted into the femoral artery preparing a distal poor runoff model. These animals were divided into three groups consisting of the E5510 group, the Aspirin group, and the Control group. The vein grafts were harvested at either 1 or 4 weeks after implantation. RESULTS: At 4 weeks, the degree of intimal hyperplasia of the graft of E5510 group was significantly less than that of the Aspirin group and the Control group (p < 0.05). No significant difference was observed between the Aspirin group and the Control group. At 1 week, the degree of intimal cell proliferation was determined by bromodeoxyuridine (BrdU) incorporation and was expressed as the BrdU labeling index. The BrdU labeling index of the E5510 group was also significantly lower than that of the Control group (p < 0.05). CONCLUSIONS: These data demonstrate the efficacy of E5510 in reducing intimal hyperplasia of vein grafts under distal poor runoff conditions by reducing the degree of smooth muscle cell proliferation.

Animals↗
PubMed1997

Effects of serotonin and endothelin on the smooth muscle cells of autogenous vein grafts.

BACKGROUND: The purpose of this study was to compare the effects of vasoconstrictor substances such as 5-hydroxytryptamine (5-HT) and endothelin on the smooth muscle of canine femoral veins and vein grafts. METHODS: The right canine femoral vein was grafted into the right femoral artery. The left femoral vein was used as a control. In other experiments to examine the effects of surgical procedures such as dissection of the adventitia and the effects of grafting (vein-to-vein bypass), the right femoral vein was dissected out but not removed for grafting and an autogenous vein bypass of the right femoral vein was made using the left femoral vein. In all experiments, the veins were removed 4 weeks after operation and suspended in organ chambers for isometric tension recording. RESULTS: Maximum contractions to endothelin were comparable in control vein and vein grafts. In control vein, the maximum contraction to 5-HT was small, and was inhibited by both methiothepin, a 5-HT, and 5-HT2 antagonist, and sarpogrelate hydrochloride, a 5-HT2 antagonist. In vein grafts 5-HT produced significantly larger contractions than in control veins, which were inhibited by methiothepin but not by the 5-HT2 antagonist. In veins with adventitial dissection alone and vein-to-vein grafts, 5-HT produced small contractions which were comparable to those in control vein. CONCLUSION: The larger contraction response to 5-HT in canine vein grafts may be due to an increased responsiveness of the 5-HT1 receptor caused by grafting into the arterial circulation.

Animals↗
PubMed1996

Fluorimetric determination of nicorandil in human plasma by a high-performance liquid chromatographic-postcolumn ultraviolet irradiation [corrected] system equipped with on-line back-pressure tubing.

For the determination of nicorandil in plasma, a fluorometric technique using HPLC-postcolumn UV radiation [corrected] has been developed. The chromatographic system consisted of a single pump, photoreactor and on-line back-pressure tubing. The system was suitable for the separation of nicorandil under the present reaction conditions. The calibration graph was linear over the range 6.5-1170 ng ml-1 using an injected volume of 100 microliters. The pretreatment of the plasma samples consisted only of deproteinizing steps by adding perchloric acid. The mean recovery from plasma was 90.2%.

Administration, Oral↗
PubMed1996

Alanine protects liver from injury caused by F-galactosamine and CCl4.

The liver is the main organ involved in amino acid metabolism, and it utilizes glucogenic amino acids as substrates for glucose or adenosine triphosphate (ATP), but this process is impaired in clinical and experimental liver diseases. In this study, we administered high doses of amino acids in rats or cultured hepatocytes with experimental models of liver injury to examine whether such supplementation could attenuate liver damage. We found that the addition of alanine reduced enzyme leakage from primary cultured rat hepatocytes treated with D-galactosamine (D-gal), while other amino acids did not. A significant decrease of lactate dehydrogenase (LDH) leakage was observed when cells were cultured with >6 from mmol/L alanine. Alanine also reduced enzyme leakage from normal hepatocytes that were not treated with D-gal. In D-gal-treated rats, constant infusion of a high dose of alanine significantly reduced the plasma transaminase and total bilirubin levels when compared with infusion of an amino acid mixture. Bolus administration of alanine significantly prevented the elevation of plasma transaminase levels and histological liver damage in CCl4-treated rats, while fructose-1,6 bisphosphate (FDP) had little effect. Alanine might promote the restoration of damaged liver in hepatotoxicant-treated rats, because significant effect was found after the elevation in plasma transaminase levels. Alanine also prevented the decrease of cellular ATP caused by D-gal and appeared to promote ATP production in primary cultured rat hepatocytes. These results indicate that alanine reduces experimental liver damage by a direct effect on hepatocytes.

Adenosine Triphosphate↗
PubMed1996

Reactive oxygen species involved in the glutamate toxicity of C6 glioma cells via xc antiporter system.

We recently demonstrated that continuous L-glutamate exposure led to cell death in C6 glioma cells over a period of 24-36 h, due to inhibition of cystine uptake through the cystine/glutamate (XC) antiporter. The antioxidant vitamin E provided protection against this effect, supporting the hypothesis that depletion of glutathione might be responsible, resulting from insufficient cystine uptake. To clarify the content of oxidative stress after glutathione depletion, the present study was done to investigate accumulation and target molecules of reactive oxygen species induced by glutamate treatment. The accumulation of reactive oxygen species was increased three-fold as compared to a control culture. Membrane oxidation, as judged by lipid peroxidation, was increased two-fold after glutamate treatment. Cellular ATP content was significantly reduced by glutamate exposure. For the two cytosolic enzymes examined, activity of glyceraldehyde 3-phosphate dehydrogenase was slightly enhanced by glutamate treatment, while activity of glutamine synthetase was not changed. Impairment of nuclear DNA after glutamate exposure was also revealed by nuclear chromatin condensation with DNA fragmentation. Thus, the multiple targets (membrane, cytoplasm and nuclei) of oxygen radicals in glutamate toxicity through the xc antiporter system were evaluated for the first time. Furthermore, prevention from cell death and from cellular toxicity induced by oxygen radicals could be seen using three specific oxygen radical scavengers, catalase, 3,3,5,5-tetramethyl-pyrroline N-oxide and alpha-phenyl-N-t-butylnitrone, without restoring the glutathione deficit. This indicates that radical scavengers did not interact with the xc antiporter system, but directly scavenged the oxygen radicals. Taken together, the data strongly suggest that O2-, H2O2 and OH accumulate in response to oxidative stress after glutathione depletion, resulting in glutamate cell death of C6 glioma cells.

Adenosine Triphosphate↗
PubMed1996

Effect of alanine on D-galactosamine-induced acute liver failure in rats.

The effect of high-dose alanine on survival and liver function in rats with acute liver failure caused by a lethal dose of D-galactosamine (D-gal) was studied. Greater than 90% of control animals died within 5 days after D-gal injection, but alanine significantly decreased mortality, even when treatment was started at 12 hours after D-gal injection. Alanyl-glutamine had a slight effect, but glucose produced no improvement. There was marked elevation of the plasma aspartate transaminase (AST) level, prolongation of the prothrombin time, and a decrease of the arterial ketone body ratio (AKBR) and hepatic adenosine triphosphate (ATP) content within 12 hours after D-gal injection. The AKBR decreased in parallel with the decrease of the hepatic ATP content. These parameters were significantly improved in alanine-treated rats at 48 hours after the induction of liver damage, which was just before control rats began to die. The hepatic ATP content was significantly greater in alanine-treated rats than in the other rats (including normal controls), but glucose pretreatment had no effect. It was also found that the liver labeling index of partially hepatectomized rats was significantly elevated by alanine administration at 3 hours before measurement. In conclusion, alanine is effective for the treatment of experimental acute liver failure, probably caused by promotion of ATP synthesis. Ala may be a good candidate for clinical application because of its preventive effect on hepatocyte necrosis and its promotive effect on liver regeneration.

Adenosine Triphosphate↗
PubMed1995

Studies of the oxidation states of hemoglobin M Boston and hemoglobin M Saskatoon in blood by EPR spectroscopy.

The extent of the oxidation of Hemoglobin (Hb) M Saskatoon (beta 63His-->Tyr) and Hb M Boston (alpha 58His-->Tyr) in the patient's blood was determined by measurement of the intensity of EPR signals at g perpendicular = 6.0 for the normal subunits, g1 = 6.7 for the mutant subunits of Hb M Saskatoon and g1 = 6.3 for those of Hb M Boston, respectively. The amounts of reduced mutant subunits were estimated from the EPR signal intensities and the amounts of Hb present as mutant Hb in the blood. About 50% and 76% of mutant subunits in Hb M Boston and Hb M Saskatoon remained reduced in the fresh blood. Gentle shaking of the blood at 37 degrees C for 15 hours in air brought about autoxidation of the normal subunits as well as the mutant subunits of the two Hbs M, indicating that the presence of the mutant subunits facilitated autoxidation of the normal subunits. Possible involvement of NADH-metHb reductase in erythrocytes in maintenance of the reduced mutant subunits of Hb M Saskatoon was discussed.

Electron Spin Resonance Spectroscopy↗
PubMed1995

Endothelium-dependent relaxation in response to adenosine diphosphate is impaired under poor runoff conditions in the canine femoral artery.

To examine whether poor distal runoff conditions of the canine femoral artery modulates endothelium-dependent relaxations, we developed a poor distal runoff limb in the canine right femoral artery (poor runoff group). The left femoral artery was used as a control. Endothelium-dependent responses were examined in vitro. The rings of femoral artery were obtained from dogs pretreated with 6 weeks of poor distal runoff. In the control, flow rate and tau-variation were 79.1 ml/min and 214.2 dynes/cm2, respectively. In the poor runoff group, the flow rate and tau-variation were 27.4 ml/min and 52.7 dynes/cm2. There were significant differences between the two groups. In the rings taken from the control group contracted with norepinephrine, adenosine diphosphate (ADP) and A23187 caused endothelium-dependent relaxations. In the poor runoff group, the endothelium-dependent relaxations in response to ADP were impaired, while A23187 caused comparable endothelium-dependent relaxations. Direct relaxations in response to sodium nitroprusside were comparable between the two groups. These experiments indicate that under poor runoff conditions, the endothelium-dependent relaxations to ADP are impaired without changing the properties of the smooth muscle cells. This dysfunction of the endothelium under conditions of abnormal flow may accelerate a loss of late patency of the reconstructed arteries.

Adenosine Diphosphate↗
PubMed1995

Eicosapentanoic acid reduces the intimal thickening of autogenous vein grafts and enhances endothelium-derived relaxing factor.

The present study examined the effect of purified eicosapentanoic acid (EPA) on intimal thickening of an autogenous vein graft. In addition, experiments were performed to determine whether EPA supplementation would alter the endothelium-dependent responses of the reversed vein graft. Segments of femoral veins were grafted into the femoral arteries of dogs. Six dogs received regular chow (control group) and six other dogs regular chow with 1500 mg/day 90.0% pure EPA (EPA group). At 6 weeks after surgery, the vein grafts were removed from the dogs, cut into rings, and suspended in organ chambers for isometric tension recording. In some rings, the endothelial cells were removed. When the rings taken from the control group were contracted with norepinephrine, adenosine diphosphate (ADP) and A23187 caused endothelium-dependent relaxations. In the EPA group, the endothelium-dependent responses to ADP were significantly augmented, while A23187 caused comparable endothelium-dependent relaxations. Direct relaxation in response to sodium nitroprusside was comparable between the two groups. Intimal thickening of the grafts in the control group (29.0 +/- 1.8 microns) was significantly (P < 0.05) greater than in the EPA group (12.5 +/- 1.8 microns). These results suggest that EPA enhances the release of endothelium-derived relaxing factor in autogenous vein grafts. This may be one of the effects of EPA in reducing the intimal thickening of autogenous vein grafts.

Animals↗
PubMed1994

Impaired vasodilation of peripheral arteries in response to acetylcholine in human beings with abdominal aortic aneurysm.

PURPOSE: Most aneurysms are generally presumed to be atherosclerotic in origin. Endothelium-dependent dilations were impaired in the cases of atherosclerosis. It is not clear whether the endothelial function of the peripheral arteries in humans with abdominal aortic aneurysm is impaired. The purpose of this study is to characterize endothelium-dependent relaxations in patients with abdominal aortic aneurysm. METHODS: Responses of external iliac artery blood flow to acetylcholine (30 micrograms/min: an endothelium-dependent vasodilator) and sodium nitroprusside (10 micrograms/min: a direct dilator of smooth muscle) were examined by electromagnetic blood flow meter in a group of 13 patients consisting of six patients with abdominal aortic aneurysm, six patients with colorectal cancer, and one patient with abdominal aortic aneurysm and rectal cancer. RESULTS: The mean blood flow before administration of drugs was comparable between the two groups. In the patients with abdominal aortic aneurysm, infusion of acetylcholine did not significantly increase the mean blood flow, whereas in the patients with colorectal cancer, acetylcholine increased the blood flow significantly. The increases of blood flow by an infusion of sodium nitroprusside were comparable between the two groups. In one patient with abdominal aortic aneurysm and rectal cancer, acetylcholine did not alter the blood flow, and sodium nitroprusside increased the blood flow, which was similar to what the patient with abdominal aortic aneurysm experienced. CONCLUSIONS: These results suggest that in patients with abdominal aortic aneurysm, the endothelium-dependent vasodilations of the peripheral artery were impaired without changing the smooth muscle property.

Acetylcholine↗
PubMed1994

Effect of combined alanine and glutamine administration on the inhibition of liver regeneration caused by long-term administration of alcohol.

We studied the effect of administration of a mixture of alanine and glutamine on the inhibition of liver regeneration caused by alcohol in rats undergoing partial hepatectomy 6 weeks after the start of alcohol administration. DNA synthesis was inhibited 24 hr after partial hepatectomy in rats given alcohol, but treatment with alanine and glutamine partially prevented this inhibition. To identify the mechanism of this effect, polyamine metabolism was studied. Administration of alcohol or alanine plus glutamine had no effect on the activity of ornithine decarboxylase, a rate-limiting enzyme of polyamine metabolism. In the liver, of the three polyamines, only the spermine concentration changed significantly. It decreased during long-term administration of alcohol, and this decrease was prevented by treatment with alanine and glutamine. The level of N(1)-acetylspermidine, the acetylated product of spermidine, was increased by alcohol, and its elevation was significantly less when alanine and glutamine were given. Hepatic spermidine/spermine N(1)-acetyltransferase, the key enzyme of polyamine acetylation, was induced by long-term administration of alcohol, and this induction was suppressed by alanine plus glutamine. The results suggest that treatment with alanine and glutamine can help to prevent the inhibition of liver regeneration caused by alcohol by maintaining the spermine level and suppressing the acetylation of spermidine.

Alanine↗
PubMed1993

Cystine/glutamate antiporter expression in retinal Müller glial cells: implications for DL-alpha-aminoadipate toxicity.

A cytotoxicity of glutamate or related amino acids (10 mM) mediated by a cystine/glutamate antiporter (system Xc) has recently been demonstrated in N18 neuroblastoma-rat retina hybrid (N18RE105) cells and C6 glioma cells. The antiporter usually transports glutamate outside and cystine inside, thereby maintaining cellular concentrations of glutathione. High concentrations of glutamate inhibit cystine uptake and lead to depletion of cellular levels of glutathione. Among related amino acids, DL-alpha-aminoadipic acid (DL-alpha-AAA), which is well known as a selective gliotoxin in the retina, is also toxic to these cells. However, this does not explain why DL-alpha-AAA acts gliospecifically on the retina. To answer this question we first examined the effects of DL-alpha-AAA on the [35S]cystine uptake with parental N18 neuroblastoma cells and rat retina of the hybrid cells. DL-alpha-AAA showed a competitive inhibition of [35S]cystine uptake in the rat retina but not in the N18 cells. Such a competitive inhibition of cystine uptake by DL-alpha-AAA could also be seen in the carp retina. The cystine uptake with carp retina was mainly Na(+)-independent and Cl(-)-dependent as already described as a characteristic ion dependency of the Xc antiporter. We next examined the effects of exogenous cystine on the glutamate release from the retina. Cystine (1 mM) actually induced a glutamate release approximately twice that of the control. Furthermore, the glutamate release induced by cystine was also Na(+)-independent and Cl(-)-dependent, and was blocked by DL-alpha-AAA. An autoradiogram of [35S]cystine uptake in the carp retina showed typical radial glial Müller cells. A large incorporation of [35S]cystine into retinal glutathione fraction was detected by a high pressure liquid chromatography method during a 1-4-h incubation. A significant or large decrease of retinal levels of glutathione was observed one day ater an intravitreal injection of 8 mumol DL-alpha-AAA or L-alpha-AAA, respectively. Buthionine sulfoximine (2.5 mumol), a specific inhibitor of glutathione synthesis, induced a large decrease of retinal levels of glutathione and a loss of electroretinographic b-wave 20-30 h after treatment. Taken together, our present data with rat and carp retinas strongly indicate that the expression of cystine/glutamate antiporter is enriched in the retina, particularly in the glial Müller cells which have a rapid turnover pool for glutathione. The gliotoxin DL-alpha-AAA inhibits cystine uptake through this antiporter on the glial cells and elicits reduction of cellular levels of glutathione.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Aminoadipic Acid↗
PubMed1993

Isovolumetric relaxation flow in patients with ischemic heart disease.

OBJECTIVES: The purpose of this study was to clarify the characteristics of flow during the isovolumetric relaxation period and to analyze the relation between these flow patterns and standard hemodynamic indexes. BACKGROUND: Outward motion of the left ventricle during the isovolumetric relaxation period has been observed by cineangiography. However, there is little information about blood flow during this period. METHODS: Seventy-nine patients with ischemic heart disease were examined by pulsed Doppler echocardiography and cardiac catheterization. All patients were classified into three groups according to the observed patterns of isovolumetric relaxation flow: group I (n = 41), flow directed toward the apex; group II (n = 21), flow directed toward the base, and group III (n = 17), low velocity flow (< 12 cm/s) without a dominant direction. Patients in group I were further classified into group Ia (n = 19) with normal ventriculograms and group Ib (n = 22) with asynergy. RESULTS: Left ventricular ejection fraction and negative first derivative of left ventricular pressure were significantly lower in group II (49 +/- 9% and 1,274 +/- 212 mm Hg/s, respectively) and group III (38 +/- 8% and 1,147 +/- 280 mm Hg/s, respectively) than in group Ia (68 +/- 7% and 1,727 +/- 358 mm Hg/s), each p < 0.01. Time constant was significantly prolonged in group II (49 +/- 6 ms) and group III (48 +/- 6 ms) compared with that in group Ia (41 +/- 6 ms), p < 0.05. On left ventriculography, patterns of outward wall motion during the isovolumetric relaxation period were associated with the patterns of isovolumetric relaxation flow. CONCLUSIONS: Changes in left ventricular relaxation are accompanied by alterations in isovolumetric relaxation flow. It is therefore useful to evaluate isovolumetric relaxation flow when investigating early diastolic ventricular function.

Adult↗