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Biomedical subjects

Y Takamitsu

Publications and source records attributed to Y Takamitsu.

At least 19 recordsLinked to original sources
PubMed1995

Na+/myo-inositol cotransport is regulated by tonicity in cultured rat mesangial cells.

Mesangial cells are considered to be faced with osmotic stress under physiological (such as extraglomerular mesangial cells) and pathophysiological (for example, diabetes mellitus) conditions. To see if mesangial cells have an osmoregulatory mechanism, like renal medullary cells, we measured the intracellular contents of organic osmolytes in isotonic and hypertonic conditions. Cultured rat mesangial cells are well tolerant of acute increase in osmolality up to 500 mOsm/kg. The myo-inositol content increased in hypertonic cells more than six-fold the value in isotonic cells. The contents of glycerophosphorylcholine and sorbitol also increased but were less than that of myo-inositol. The Na(+)-dependent myo-inositol uptake in hypertonic cells was a 12-fold uptake in isotonic cells, reaching a maximum 24 hours after the switch to a hypertonic medium. The uptake rate increased as medium osmolality increased from 300 to 500 mOsm/kg. Raffinose is the most effective solute to increase the myo-inositol uptake. NaCl, glucose and mannitol also increased the uptake rate (NaCl > glucose > mannitol). The increased uptake by hypertonicity was the result of an increase in Vmax without change in Km and was dependent on RNA and protein synthesis. These results indicate that mesangial cells respond to extracellular hypertonicity by increasing myo-inositol transport activity and accumulating myo-inositol into the cells, suggesting that myo-inositol functions as an organic osmolyte in mesangial cells.

Animals↗
PubMed1995

Elevated serum pepsinogens in chronic renal failure patients.

Human pepsinogens, the precursors of pepsin, originating from the stomach mucosa, are classified into two biochemically distinct groups, namely pepsinogen I (PG I) and pepsinogen II (PG II). We studied the serum levels of PG I and II in 51 normal volunteers, 23 chronic glomerulonephritis patients, 21 continuous ambulatory peritoneal dialysis (CAPD) patients and 40 hemodialysis patients. Serum pepsinogen levels were measured with a competitive binding double antibody radioimmunoassay. In the group of chronic glomerulonephritis patients, a positive correlation between the serum creatinine and the pepsinogen levels were found. The serum pepsinogen levels were remarkably elevated in CAPD and hemodialysis patients. The median levels of post-hemodialysis PG I (265.4 +/- 165.2 ng/ml) and PG II (41.7 +/- 38.0 ng/ml) were significantly higher than prehemodialysis values (PG I 207.4 +/- 127.5 ng/ml, PG II 29.0 +/- 16.6 ng/ml). Pepsinogen release by isolated gastric glands of guinea pigs was suppressed by guanidinosuccinic acid and was facilitated by calcium. The data suggest that both removal of guanidinosuccinic acid and infusion of calcium during hemodialysis contribute to the raised serum levels of these pepsinogens after hemodialysis.

Adult↗
PubMed1995

[Chylomicron and VLDL metabolism in daunomycin-induced nephrotic rats].

Lipid metabolism in chylomicron and VLDL were examined in daunomycin-induced nephrotic rats. 1) There was no difference in intestinal cholesterogenesis between the control rats and daunomycin-induced nephrotic rats. 2) The apoprotein content of chylomicron and VLDL increased in daunomycin-induced nephrotic rats. 3) Daunomycin-induced nephrotic rats showed increases in the content of apo B-48 and C-III, and a decrease in that of apo E in chylomicron. The apoprotein composition of VLDL in daunomycin-induced nephrotic rats showed increased apo B and decreased apo E. These results suggest that increased chylomicron-cholesterol is not due to increased intestinal cholesterogenesis, but to decreased chylomicron catabolism in daunomycin-induced nephrotic rats. Increased apoprotein in VLDL may contribute to the decreased catabolism by reducing LPL activity in the plasma and increased secretion from the liver of daunomycin induced nephrotic rats.

Animals↗
PubMed1995

[Perioperative management of dialysed patients for orthopedic surgery].

Recently, renal osteodystrophy is a remarkable problem in patients on long-term hemodialysis (HD). In this retrospective study, we evaluated the perioperative management of 21 patients receiving orthopedic surgery between January 1990 and December 1992. These patients had been maintained on HD for an average of 8.6 years (range, 18 months-20 years). The primary causes of orthopedic surgery were amyloidosis, diabetic gangrene, rheumatoid arthritis and fractures. Laminectomy, replacement of arthropathy, osteosynthesis and amputation of the lower extremity were undertaken. General anesthesia was performed on six patients. Vecuronium was given to all of these patients. Isoflurane was used in 5 patients and sevoflurane in 1 patient. Regional anesthesia was used in 15 patients. During anesthesia, the average infusion rate of intravenous fluids was 2.7 ml.kg-1.h-1, and the intraoperative complications included hypertension in 16, hypotension in 12, arrhythmia in 4 and prolonged sedation in 2 patients. Postoperative complications included hyperkalemia in 2, pneumonia in 2, psychological disorder in 3, clotting fistula in 1 and delayed wound healing in 7 patients. One early death in a diabetic patient following amputation occurred on the 13th postoperative day. Preoperative HD was performed within 24 hours and postoperative HD within 72 hours of the operation. Nafamostat mesilate was used as an anticoagulant. Excessive removal of potassium must be avoided during preoperative HD to prevent arrhythmia. The well-managed elective patients gave a good result. However, extreme care in nutrition and infection control should be taken, especially in diabetic patients.

Anesthesia↗
PubMed1994

Adsorption of human recombinant erythropoietin on dialysis membranes in vitro.

The adsorptive characteristics of 5 dialysis membranes for recombinant human erythropoietin (EPO) were studied in vitro in a closed circuit system. For 120 min, EPO added with bovine serum was significantly adsorbed by polymethylmethacrylate (PMMA) and polyacrylonitrile (PAN) membranes but not by Cuprophan, ethylene vinyl alcohol (EVAL), or polysulfone (PS) membranes. In addition the EPO adsorptive rate, as well as that of beta 2-microglobulin (beta 2-MG), was greater with a PMMA membrane than with a PAN membrane. EPO was not detected in the ultrafiltrate at 15 min with 5 membranes. These results indicate that EPO was eliminated by membrane adsorption only with some dialysis membranes.

Acrylic Resins↗
PubMed1994

Impairment of renal medullary osmolyte accumulation in potassium-depleted rats.

To determine the relationship between accumulation of osmolytes and maximal urinary concentration in potassium depletion, we tested the effects of experimental water diuresis or potassium depletion on osmolytes in the renal medulla of rats. Hyperosmotic stress was imposed by 4 days of water deprivation for the purpose of establishing the maximal concentrating ability or by the infusion of sodium for the purpose of loading the equal amounts of sodium to the renal medulla. In the diuresis group, water deprivation failed to increase betaine, sorbitol, and taurine contents to the same level as the untreated group, although sodium infusion increased betaine and sorbitol. In the potassium depletion group followed by water deprivation, urine osmolality (2,490 +/- 241 vs. 3,425 +/- 268 mosmol/kgH2O) and all osmolytes were significantly lower than in the untreated group. In response to hyperosmolality with sodium infusion, myo-inositol and glycerophosphorylcholine contents rose to the level of the untreated group. Medullary betaine (67.6 +/- 6.8 vs. 99.5 +/- 8.9), taurine (44.7 +/- 2.4 vs. 61.4 +/- 6.2) and sorbitol (35.6 +/- 4.4 vs. 57.0 +/- 8.4 mmol/kg protein) contents were reduced in potassium-depleted rats when the renal medulla was as hypertonic as in the untreated group. In conclusion, the processing of betaine, taurine, and sorbitol accumulation appeared to be impaired in potassium depletion.

Animals↗
PubMed1994

Organic osmolytes in rat renal inner medulla are modulated by vasopressin V1 and/or V2 antagonists.

For the purpose of clarifying the role of vasopressin V1 and V2 receptors in osmolyte accumulation, we determined the effects on the inner medullary osmolyte content of the administration of orally active vasopressin V1 and/or V2 receptor antagonists OPC-21268 (i.e., 1-(1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl)- 3,4-dihydro-2(1H)-quinolinone) and OPC-31260 (i.e., 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tet rah ydro-1H- benzazepine] under a condition of maximal urine concentration achieved by water deprivation for 4 days. Taurine content increased significantly with the use of the V2 antagonist, irrespective of the use of the V1 antagonist. Inner medullary betaine content decreased with the administration of the V1 antagonist, irrespective of the administration of V2 antagonist. The administration of either the V1 or V2 antagonist alone did not affect sorbitol content, aldose reductase activity, or aldose reductase mRNA abundance in renal inner medulla. However, the combined administration of the V1 and V2 antagonists decreased all of these significantly. Myo-inositol content was not affected by the administration of the V1 or V2 antagonists. Glycerophosphorylcholine content was decreased with the use of the V2 antagonist, irrespective of the use of the V1 antagonist, and this effect paralleled urine osmolality. In conclusion, the individual organic osmolytes responded differently to the antagonists of vasopressin V1 and/or V2 receptors. The mechanisms linked to vasopressin V1 and/or V2 receptors appeared to modulate the accumulation of some organic osmolytes in the inner medulla. Aldose reductase mRNA abundance and sorbitol accumulation in the inner medulla appeared to be mediated through either V1 or V2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehyde Reductase↗
PubMed1994

In vivo osmoregulation of Na/myo-inositol cotransporter mRNA in rat kidney medulla.

myo-Inositol, a major compatible osmolyte in renal medulla, is accumulated in kidney-derived epithelial cells cultured in hypertonic media via Na/myoinositol cotransporter (SMIT). The altered medium osmolality of Madin-Darby canine kidney cells leads to changes in the transcription of the SMIT gene and mRNA abundance. To investigate whether SMIT is regulated by tonicity in vivo, renal medullary myoinositol and SMIT mRNA was measured in rats in hydrated and dehydrated states. Rats were divided into two groups: (1) hydrated rats, free access to 3% sucrose water; (2) dehydrated rats, 3 days of water deprivation. Urine sodium, potassium, urea, and osmolality in dehydrated rats were significantly higher than in hydrated rats. Renal medullary sodium, urea, and myo-inositol in dehydrated rats were significantly higher than in hydrated rats. Northern analysis revealed that there was a message hybridized to SMIT cDNA in the cortex and outer and inner medulla of the kidney. Compared with hydrated rats, SMIT mRNA in dehydrated rats was 2.6-fold higher in the outer medulla and 2.5-fold higher in the inner medulla. These results indicate that there is osmoregulatory SMIT in the outer and inner medulla of the kidney and that myo-inositol accumulation in this region is probably due to the increased expression of the SMIT gene.

Animals↗
PubMed1992

Adsorption of nafamostat mesilate by hemodialysis membranes.

The adsorption of the anticoagulant nafamostat mesilate (FUT-175) by five different hemodialysis membranes was studied in vivo and in vitro. In vivo, FUT-175 was adsorbed strongly by a polyacrylonitrile (AN69) membrane and slightly by another polyacrylonitrile (J-PAN) membrane but not by Cuprophan (CU), hemophan (HE), or polymethylmethacrylate (PMMA) membranes during hemodialysis performed in 4 patients in whom FUT-175 was used as an anticoagulant. Only during hemodialysis using the AN69 membrane did FUT-175 not induce a significant prolongation of celite-activated coagulation time. In vitro studies showed that FUT-175 was adsorbed by the AN69, J-PAN, and PMMA membranes but not by the CU and HE membranes. Methylene blue, a dye that possesses a cationic portion in its chemical structure, stained AN69, J-PAN, and PMMA membranes. Since FUT-175 also possesses a cationic portion, we conclude that FUT-175 is adsorbed by negatively charged membranes via an ionic bond and is unsuited for use as an anticoagulant in hemodialysis using an AN69 membrane because of that membrane's marked capacity to adsorb FUT-175.

Adsorption↗
PubMed1992

Dopaminergic modulation of the pressure-natriuresis response in rats.

OBJECTIVE: The present study was carried out to examine the involvement of dopamine in the pressure-natriuresis phenomenon which has been postulated as a major regulator of extracellular fluid volume and thereby arterial pressure. DESIGN: Dopaminergic modulation of the pressure-natriuresis response was studied in the innervated and denervated rat kidney, to allow a distinction between the effects of neural and extraneural dopamine. METHODS: The pressure-natriuresis response was studied in anesthetized Sprague-Dawley rats, in which neural and hormonal influences on the kidney were fixed by denervating the kidney and by intravenous infusion of aldosterone, hydrocortisone, vasopressin and norepinephrine. The innervation to the kidney remained intact in some experiments with the selective dopamine-1 antagonist SCH 23390. Urinary excretion of dopamine during the pressure-natriuresis response was also examined in the innervated and denervated rat kidney. RESULTS: Although infusion of dopamine at a dose of 2 micrograms/kg per min had no effect on the pressure-natriuresis response in rats in which neural and hormonal influences on the kidney were fixed, the slopes of the relations between urine flow, sodium excretion and mean arterial pressure in rats given 10 micrograms/kg per min dopamine were significantly greater than those found in the control rats. Renal plasma flow increased significantly in the dopamine-treated rats whilst glomerular filtration rate did not differ between the control and dopamine-treated rats. The dopamine-induced increase in the slope of pressure-natriuresis relationship and renal plasma flow were completely blocked by 0.5 micrograms/kg per min SCH 23390. However, infusion of SCH 23390 alone at 0.5 micrograms/kg per min did not significantly alter the pressure-natriuresis response in rats with either denervated or innervated kidney. In addition, urinary excretion of dopamine derived from neither neural nor extraneural origins was altered in parallel with variations in mean arterial pressure. CONCLUSION: These results suggest that exogenous administration of dopamine may affect the pressure-natriuresis response by altering the magnitude of arterial pressure-induced changes in tubular sodium reabsorption, via an action of dopamine-1 receptors. However, endogenous dopamine does not appear to be capable of modulating the pressure-natriuresis response.

Animals↗
PubMed1992

[Doppler ultrasound measurement of phasic renal arterial blood flow velocity in patients with chronic glomerulonephritis].

The phasic renal arterial blood flow velocity was measured using a Doppler-Based Toshiba SSH-160A scanner in 25 healthy subjects and 78 patients with chronic glomerulonephritis. Renal arterial blood flow at the renal hilum was visualized with color Doppler ultrasound, and the velocity waveform was obtained by pulsed Doppler ultrasound. The velocity waveform was then analyzed to give the peak systolic velocity (S), end-diastolic velocity (D), resistive index (RI), and pulsatility index (PI). Creatinine clearance correlated with S (r = 0.76), D (r = 0.80), RI (r = -0.74), and PI (r = -0.85). The split renal glomerular filtration rate, calculated by a method which makes use of the early renal uptake of Tc-99m DTPA, also correlated well with these parameters. These findings suggest that renal arterial blood flow as detected by Doppler ultrasound may be useful for the noninvasive, direct, rapid, and simple evaluation of renal hemodynamics and renal function, although various modifying factors also need to be considered.

Adolescent↗
PubMed1991

Noninvasive detection and monitoring of renal arteriovenous fistula by color Doppler.

The diagnosis of a renal arteriovenous fistula is usually confirmed by angiography. Described is the utilization of color Doppler ultrasound to monitor a renal arteriovenous fistula before and after treatment by transcatheter steel coil embolization in a 63-year-old woman. Using color Doppler, the arteriovenous fistula with an aneurysmal lesion was clearly visualized. A pulsed-wave Doppler analysis showed increased flow velocity and decreased pulsatility in the supplying artery. After successful transcatheter occlusion of the fistula, these findings disappeared. The Doppler ultrasound technique is likely to be useful to detect and monitor a renal arteriovenous fistula noninvasively, simply, and quickly.

Arteriovenous Fistula↗
PubMed1991

Total and split renal function assessed by ultrasound Doppler techniques.

We evaluated total and split renal functions from the pattern for renal arterial blood flow detected by ultrasound Doppler in healthy subjects and patients with varying degrees of renal function and disorders other than renovascular hypertension or severe aortic valvular disease. A renal-time pulsed ultrasonic echo-Doppler device at 2.5 MHz was used with a translumbar approach. The ratio of peak diastolic (D) to systolic (S) velocity correlated well with both p-aminohippurate clearance and creatinine clearance. Acceleration time was correlated with the clearance of neither compound. To evaluate the clinical usefulness of ultrasound Doppler in the assessment of split renal function, we compared the D/S ratio with the renal function obtained by radionuclide methods for individuals. The split renal glomerular filtration rate, calculated by a method which makes use of the early renal uptake of 99mTc-diethylenetriam-inepentaacetic acid, correlated well with the D/S ratio. These results indicate that the ultrasonic measurement of renal arterial blood flow by the pulsed Doppler method should be useful for assessment of total and split renal functions.

Adolescent↗
PubMed1991

[Effect of azosemide and furosemide on body fluid distribution and vasoactive hormones].

We examined the diuretic action of orally administered azosemide (AZ: 60 mg) and furosemide (FM: 40 mg) and their effects on body fluid distribution and circulatory vasoactive hormones in normal male volunteers. Urine volume and urinary sodium excretion were increased, peaking during 0 to 2 hours in FM and 2 to 4 hours in AZ in response to administration of both diuretics. The cumulative urine volume and urinary sodium excretion for 8 hours showed no significant difference between AZ and FM. Total body water (TBW) was measured by the dynamic distribution of deuterium oxide and a percentage change in circulating plasma volume (ICG ratio) was determined by using indocyanine green. The decrease in TBW and ICG ratio was detected in proportion to the increase in urine volume after administration of AZ and FM. Plasma renin activity (PRA) and plasma concentration of aldosterone (PAC), angiotensin II (ANG II) and arginine vasopressin (AVP) were elevated in response to the reduction in ICG ratio by both diuretics. The responses of PRA, PAC and ANG II to AZ were delayed about 2 hours as compared with those of FM. The increase in AVP with FM was significantly greater than that with AZ detected 2 hours after administration. The elevation of AVP in AZ was delayed and blunted compared with FM. These data indicate that the difference in diuretic property of AZ and FM may induce different stimulation to the secretion of vasoactive hormones through the changes in body fluid distribution and these hormones might modify the anti-edematic effect of AZ and FM.

Administration, Oral↗
PubMed1990

[Evaluation of the changes in intracranial water, sodium, phosphorus metabolites and intracellular cerebral pH in rats with acute dilutional hyponatremia].

Although most prominent among the clinical manifestations associated with hyponatremia are central nervous system (CNS) symptoms, the alterations in brain function remain poorly understood. In the present study, the alterations in intracellular cerebral pH and intracranial water, sodium and phosphorus metabolites content in rats with acute dilutional hyponatremia were examined by using an in vivo nuclear magnetic resonance (NMR) technique which noninvasively provides continuous informations on intracellular phenomena. Acute dilutional hyponatremia was induced on anesthetized male Sprague-Dawley rats by intraperitoneal injection of distilled water with an initial dose of 10 ml/100 g bw, followed by an additional dose of 5 ml/100 g bw 40 min later. Arterial blood sampling and NMR measurements were made before and every 60 min after the initial injection of distilled water. The treatment with distilled water resulted in dramatic falls in serum Na, Cl and osmolality at 60 min after water loading (Na; from 143.4 +/- 2.6 to 112.3 +/- 1.3 mmol/l, Cl; from 101.02 +/- 2.2 to 78.4 +/- 5.4 mmol/l, Osm; from 306.3 +/- 5.8 to 247.3 +/- 7.3 mOsm/kg H20). 1H-NMR imaging showed the accumulation of brain water as dilutional hyponatremia developed. Intracranial Na content measured by 23Na-NMR spectroscopy decreased significantly at 60 min after of water loading to about 70% of that observed under control condition. Since it has been demonstrated that solute extrusion from the brain with resultant reduction of brain swelling occurs within 60 min after the dilution, this result may be, at least in part, explained by this protective mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1990

[Hyponatremia in isolated deficiency of adrenocorticotropic hormone: role of a decrease in aldosterone secretion independent of antidiuretic hormone excess].

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.

Adrenocorticotropic Hormone↗