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K Tabei

Publications and source records attributed to K Tabei.

At least 55 records · Page 3Linked to original sources
PubMed1992

The pharmacokinetics of fluconazole during haemodialysis in uraemic patients.

We have studied the pharmacokinetics of fluconazole in five patients on long-term haemodialysis. The single-pass extraction rate of the dialyzer was 59 (3.5)% (n = 4), and the serum concentration was reduced by haemodialysis for 3 or 4 h by 26 (3.2)% (n = 5) and 39 (2.2)% (n = 9) respectively. The estimated amount extracted by a dialysis of 4 h was 33 (3.2)% (n = 4) of the dose. During repeated administration the serum fluconazole concentration increased, reaching a plateau at about 4 times the peak concentration after the first dose. After discontinuing administration the serum fluconazole concentration fell by 25% in every 3 h dialysis session. We conclude that fluconazole should be given in the usual dose of 100 or 200 mg at the end of every haemodialysis session.

Aged↗
PubMed1992

Pharmacokinetics of carteolol in patients with impaired renal function.

In order to determine the appropriate dosage of carteolol in renal dysfunction, the pharmacokinetics of carteolol has been examined in appropriate patients. The plasma concentrations and urinary excretion of carteolol were investigated in 15 patients with varying degrees of renal impairment during the administration of 5-20 mg carteolol hydrochloride (5 mg/tablet) for 2-45 months. Plasma carteolol levels were linearly correlated with the serum creatinine concentration (r = 0.87) and reciprocally with the creatinine clearance (r = 0.82). The urinary carteolol concentration was correlated with the urinary creatinine concentration (r = 0.69) and the urinary carteolol excretion was also correlated with the creatinine clearance (r = 0.79). These relationships become even closer when the plasma carteolol concentrations and urinary excretion rate of carteolol were factored by the administered tablets. The fractional renal excretion of carteolol was virtually constant at various degrees of renal function, and it always exceeded 100%, which indicates that carteolol was actively secreted, even in patients with renal failure. The estimated tubular secretion rate of carteolol was logarithmically correlated with the fractional renal excretion of carteolol (r = 0.93). The results indicate that the dose of carteolol should be determined according to the degree of renal impairment.

Adult↗
PubMed1992

Effect of insulin on potassium secretion in rabbit cortical collecting ducts.

Insulin is known to play an important role in the regulation of extrarenal K homeostasis. Previous clearance studies have shown that insulin decreases urinary K excretion, but the responsible nephron segments have not been identified. In this microperfusion study, in vitro, the effect of insulin on K transport in the cortical collecting duct (CCD), which is thought to be an important segment for regulation of the final urinary K excretion, was investigated. Basolateral insulin (10(-6) M) significantly inhibited net K secretion by 20% (mean JK = -26.2 +/- 4.2 peq.mm-1.min-1 for controls compared with -21.1 +/- 3.4 with insulin, P less than 0.001) and depolarized the transepithelial voltage (VT, from -14.6 +/- 3.5 to -10.8 +/- 3.5 mV, P less than 0.005), recovery did not occur over 60 min. Insulin (10(-11)-10(-5) M) depressed K secretion and depolarized the VT in a concentration-dependent manner. The half-maximal concentration was 5 x 10(-10) M, which is within the physiological range of plasma insulin concentration. In tubules of deoxycorticosterone acetate-treated rabbits, insulin also produced a significant fall in K secretion (from -43.4 +/- 7.5 to -36.1 +/- 5.7 peq.mm-1.min-1, P less than 0.05). Although luminal Ba (2 mM) decreased K secretion (from -14.4 +/- 2.9 to -7.0 +/- 1.7 peq.mm-1.min-1), basolateral insulin (10(-6) M) inhibited K secretion further (to -4.7 +/- 1.3 peq.mm-1.min-1, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1991

Site and mechanism of action of epidermal growth factor in rabbit cortical collecting duct.

To examine the exact target cell and mechanism of action of epidermal growth factor (EGF) in the isolated cortical collecting duct from rabbit kidney, we compared electrical properties of collecting duct (CD) cells (principal cells) and intercalated (IC) cells in absence and presence of EGF at 10(-8) M. Differentiation of CD and IC cells was based on values of basolateral membrane voltage (Vb) and fractional apical membrane resistance (fRa). In CD cells, upon addition of EGF to bath, lumen-negative transepithelial voltage (VT) was decreased from -8.0 +/- 1.9 to -2.4 +/- 1.3 mV (n = 22, P less than 0.001), but Vb was little changed (from -85.1 +/- 2.8 to -83.1 +/- 2.7 mV, n = 19), indicating that EGF in bath mainly caused changes in apical membrane voltage. In addition, peritubular EGF increased transepithelial resistance (RT) from 132.9 +/- 15.8 to 153.8 +/- 18.4 omega.cm2 (n = 16, P less than 0.001) as well as fRa from 0.31 +/- 0.06 to 0.39 +/- 0.07 (n = 12, P less than 0.01). These actions of EGF were prevented by pretreatment with 50 microM luminal amiloride. Luminal EGF had no effects on VT, Vb, RT, or fRa of CD cells. In IC cells, upon addition of EGF to bath, neither Vb nor fRa was affected. From these results, we conclude that EGF acts on the CD cell at the basolateral border and inhibits mainly the amiloride-sensitive Na+ conductance in the apical membrane.

Amiloride↗
PubMed1991

Luminal vasopressin modulates transport in the rabbit cortical collecting duct.

We explored the action of luminal AVP in rabbit CCD perfused in vitro at 37 degrees C. Nanomolar concentrations of luminal AVP induced a sustained hyperpolarization of transepithelial voltage (Vt) in contrast to a transient hyperpolarization caused by basolateral AVP. 10 microM basolateral ouabain abolished the latter but not the former change in Vt. Despite a sustained hyperpolarization (from -20.7 +/- 2.9 to -34.1 +/- 4.7 mV; P less than 0.01), 10 nM luminal AVP only slightly altered net Na+ and K+ fluxes (7.6% stimulation and no significant change, respectively). Instead, luminal AVP appeared to modulate an acetazolamide-sensitive electrogenic ion transport because 200 microM basolateral acetazolamide suppressed the luminal AVP-induced hyperpolarization (percentage of Vt from -50.4 +/- 10.8 to -5.1 +/- 1.4; P less than 0.005). In terms of water transport, 10 nM luminal AVP did not change hydraulic conductivity (Lp, x 10(-7) cm/atm per s) (from 3.9 +/- 0.8 to 5.0 +/- 1.2), but suppressed the increase in Lp induced by 20 pM basolateral AVP (134.9 +/- 19.2 vs. 204.3 +/- 21.1 in control; P less than 0.05). These findings demonstrate distinct luminal action of AVP, suggesting amphilateral regulation of epithelial transport by AVP in the CCD.

Absorption↗
PubMed1991

Application of plasma perfusion in hepatic failure.

To evaluate the efficacy of plasma perfusion as a liver-assistance system, 17 patients with hepatic failure were treated with a total 37 sessions of plasma perfusion and 43 sessions of plasma exchange. For plasma perfusion, Plasma-flo AP-08-H was used as a plasma separator, and the separated plasma was passed through an adsorber, Bespore UPC-III (Jap.Med.Suppl., Hiroshima) or BR 350 (Asahi Med. Co., Tokyo). The mean treated plasma volume was 5.0 liters. The mean proportion of bilirubin removed by routine plasma exchange was 29% with a mean of plasma exchange volume of 2.1 L. In the plasma perfusion with Bespore and BR, the removal rates were 37% and 42%, respectively. The plasma ammonia level decreased by 16% (from 121 to 97 mumol/L) with plasma exchange. Likewise, plasma perfusion decreased the plasma ammonia level from 75 to 56 mumol/L with an average decrement rate of 23%. The capacity for removal of amino acids was analyzed in terms of the change in the Fisher score ([Val+Leu+Ileu]/[Tyr+Phe]). The Fisher score was improved by plasma perfusion from 1.8 to 2.4. Thus, we concluded that in terms of removal of bilirubin, ammonia and amino acids, plasma perfusion was as efficient a therapy as plasma exchange. However, further clinical evaluation will be required before this procedure can be applied for the treatment of hepatic failure.

Adult↗
PubMed1989

Effect of carteolol on renal function in healthy subjects and patients with hypertension.

The effect of short- and long-term administration of carteolol on renal function has been examined in healthy subjects and in hypertensive patients with or without renal failure. In healthy subjects neither a single dose of 10 mg carteolol nor continuous administration of 20 mg/day for 7 days had any effect on creatinine clearance and renal blood flow. In all subjects the clearance rate of carteolol was about 400 ml/min and its fractional excretion of carteolol exceeded 300%, suggesting that the drug is secreted actively from renal tubules. Twenty-three hypertensive patients with or without renal dysfunction were given carteolol 10 to 20 mg/day for more than 50 weeks in addition to their standard antihypertensive regimens, which were left changed. Laboratory results were compared with the mean values of 50 weeks before and after the addition of carteolol, and none, including plasma creatinine, blood urea nitrogen and electrolytes, were significantly changed. Neither the estimated glomerular filtration rate nor the effect of the drug on blood pressure changed significantly during this prolonged treatment. It is concluded that carteolol had no effect on renal function in healthy subjects and in hypertensive patients with or without renal failure.

Adult↗
PubMed1989

Glucagon stimulates chloride transport independently of cyclic AMP in the rat medullary TAL.

The effect of glucagon on chloride transport was studied in the rat medullary thick ascending limb (MTAL) perfused in vitro. In the bath, 10(-6) M glucagon increased the efflux coefficient of Cl (KeCl) from 6.88 +/- 0.21 x 10(5) to 9.65 +/- 0.38 x 10(-5) cm.sec -1 (P less than 0.01) without changing the influx coefficient (KiCl; 2.87 +/- 0.54 x 10(-5) in control vs. 2.83 +/- 0.57 x 10(-5) cm.sec-1 with glucagon) or transepithelial potential difference (4.8 +/- 0.76 in control vs. 5.0 +/- 0.71 mV with glucagon). A physiological concentration of glucagon (10(-8), (10(-10) M) also increased chloride efflux significantly. Pretreatment of tubules with luminal furosemide (10(-5) M) and/or basolateral ouabain (10(-4) M) completely abolished the effect of glucagon. In isolated MTALs incubated in the same medium as that used in the microperfusion study, 10(-6) M glucagon stimulated cAMP production by 255.2 +/- 33.7% (P less than 0.01). However, neither dibutyryl cAMP (10(-3), 10(-4) M) nor forskolin (10(-4), 10(-6) M) increased the chloride efflux. It is concluded that: 1) Glucagon stimulates net Cl reabsorption by increasing Cl efflux in the rat MTAL; and 2) cyclic AMP is not responsible for this effect of glucagon.

Animals↗
PubMed1989

Cardiac arrhythmias in hemodialysis patients. A study of incidence and contributory factors.

Cardiac arrhythmias were evaluated in 100 patients undergoing regular maintenance hemodialysis for chronic renal failure by Holter ECG monitoring a 72-hour period beginning on the day of hemodialysis. Clinically significant ventricular arrhythmias (more than 700 beats/24 h) were found in 18 patients (the frequent group) in whom premature ventricular contractions (PVCs) were recorded frequently during and for 4 h after hemodialysis. In the frequent group, the values of the serum calcium concentration times those of phosphorus were significantly higher than those of patients without PVCs (the no arrhythmia group) or those with fewer PVCs (less than 700 beats/day; sporadic group) (54.9 +/- 3.5 vs. 43.8 +/- 3.2, 43.0 +/- 1.8, respectively; p less than 0.005). Also, in the frequent group, the percent fractional shortening of the left ventricle, as measured by two-dimensional echocardiography, was significantly lower than those in the no arrhythmia and sporadic groups (30.7 +/- 1.8% vs. 40.7 +/- 1.9%, 37.7 +/- 1.1%, respectively; p less than 0.01). On the other hand, in those with frequent premature atrial contractions, the left atrial end-diastolic dimension was significantly enlarged (42.1 +/- 1.2 mm vs. 36.5 +/- 1.1 mm, 38.1 +/- 0.9 mm, respectively; p less than 0.01). From these results, we conclude that impaired cardiac performance and a high calcium phosphate product predialysis may be correlated with an increased incidence of ventricular arrhythmias in uremic patients.

Adult↗
PubMed1989

The role of endogenous dopamine in congestive heart failure.

Although the effects of epinephrine and norepinephrine in congestive heart failure have been extensively studied, and exogenous dopamine, another of the catecholamines, has been widely used for the treatment of congestive heart failure, little attention has been paid to the physiological significance of endogenous dopamine in this condition. The present study was therefore designed to assess the physiological significance of endogenous dopamine in congestive heart failure. Nineteen patients with congestive heart failure caused by such conditions as acute myocardial infarction, valvular disease and dilated cardiomyopathy were examined before and after treatment with diuretics, digitalis and vasodilators. Electrolyte, creatinine and catecholamine concentrations in plasma and urine were analyzed. Urinary dopamine levels were increased in 13 out of 19 cases before treatment and returned to the normal range after treatment, falling from 2448 +/- 950.7 to 528.8 +/- 56.3 micrograms/day (normal level, less than 700 micrograms/day). Urinary dopamine excretion was markedly elevated within 24 hours after the onset of symptoms of heart failure, such as chest pain, palpitations and dyspnea. The relationship between urinary dopamine excretion and time after the onset of symptoms showed a strong statistical correlation (r = 0.55, p less than 0.001). Urinary dopamine excretion was also well correlated with plasma dopamine concentration, urinary norepinephrine excretion and venous pressure. From these results, it is concluded that endogenous dopamine seems to play an important role during the acute phase of congestive heart failure.

Adult↗
PubMed1989

Dual regulatory mechanisms of proton transport in rat papillary collecting duct cells in culture.

The regulation of proton transport and cytosolic pH was studied in rat papillary collecting duct (PCD) cells in culture using a pH-sensitive fluorescence probe, 2,7-bis-carboxyethyl-5,6-carboxyfluorescein (BCECF). Data were obtained from confluent monolayers grown on glass coverslips and dipped in a HCO3- -free medium, pH 7.40. The resting intracellular pH (pHi) was 7.16 +/- 0.03 (n = 20). When PCD cells had been acidified by pretreatment with NH4Cl, pHi immediately recovered toward the resting value. Two mechanisms participated in this recovery: a Na+-dependent mechanism which could be inhibited by amiloride (indicative of Na+-H+ exchanger) and a Na+-independent process (a proton ATPase). The pHi recovery from acid loading was inhibited by amiloride to about 55% of the control recovery (half-maximal effect at 100 microM). The rate of pHi recovery after the readdition of Na+ to a sodium-free medium exhibited saturation kinetics (half maximal rate at 28 mM). Dicyclohexylcarbodiimide (DCCD), an inhibitor of a plasma membrane proton ATPase, and the depletion of cellular ATP induced by 2 mM potassium cyanide (KCN) also partially inhibited the rate of pHi recovery after cell acidification with a NH4Cl load. When PCD cells were treated with 1 mM DCCD, amiloride almost completely inhibited pHi recovery. Amiloride and the removal of external Na+ had induced a gradual fall in pHi to a new resting value and rapidly recovered when Na+ was added. We conclude that PCD cells grown in culture have at least two proton transport mechanisms: a Na+-H+ exchanger and a plasma membrane proton ATPase. The kinetics of these processes can be reliably assessed by the pH-sensitive fluorescent probe, BCECF. Both the Na+-H+ exchanger and the plasma membrane proton ATPase may contribute to urinary acidification.

Adenosine Triphosphatases↗
PubMed1989

Dosage regimen of ranitidine in patients with renal impairment.

The validity of the Giusti-Hayton method for dosage regimen adjustment in patients with renal impairment was investigated using ranitidine. Five normal healthy volunteers received a single ranitidine recommended dose of 150 mg, and 20 patients with renal disease received single administration in doses individually calculated by the Giusti-Hayton method from each patient's creatinine clearance level, and the various pharmacokinetic parameters were compared. As a result, the area under the time-concentration curve 0----infinity (AUC0----infinity) in the renal disease patients was almost comparable to that in the normal healthy volunteers. The Giusti-Hayton method was considered useful to keep both the AUC0----infinity constant and the mean blood level of the drug in a steady state, in any degree of renal impairment.

Administration, Oral↗
PubMed1987

K transport in upper portion of descending limbs of long-loop nephron from hamster.

By use of the in vitro microperfusion technique, we investigated potassium transport in the upper portion of the descending limb of the long-loop nephron isolated from hamster kidney. The net potassium flux determined by ultramicro-flame photometry was -0.63 +/- 1.84 pmol X mm-1 X min-1, a value that was not significantly different from zero. The salt permeability for KCl was calculated from the amount of potassium entering the tubular lumen when the concentration of potassium in the bath was increased by approximately 5 mM. The value was 38.9 +/- 1.9 X 10(-5) cm X s-1. The bidirectional fluxes of 86Rb were measured as indices of potassium fluxes. Flux coefficients from lumen-to-bath and bath-to-lumen were 51.2 +/- 9.2 and 48.8 +/- 13.5 X 10(-5) cm X s-1, respectively. These values were not significantly different, confirming that there was no net flux for 86Rb. In another series of five experiments, the lumen-to-bath 86Rb flux coefficients were 69.4 +/- 13.2 X 10(-5) cm X s-1 in the absence of unlabeled Rb, and 70.2 +/- 13.9 X 10(-5) cm X s-1 in the presence of 5 mM unlabeled Rb. The lumen-to-bath 42K flux coefficient measured in the same series of animals was 85.3 +/- 10.5 X 10(-5) cm X s-1 (n = 10), a value that is slightly higher than, but not significantly different from, that of 86Rb. These data show that active potassium transport may exist in this segment and that the passive permeability for potassium is very high.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Profiles of water and solute transport along long-loop descending limb: analysis by mathematical model.

We simulated profiles of water and solute transport along the descending limb of the long-loop nephron by a mathematical model based on mass balance equations for water, sodium, potassium, and urea, using phenomenological coefficients reported for hamsters. We assumed that interstitial concentration of sodium, potassium, and urea increased linearly along the descending limb from 150 to 350, from 5 to 50, and from 5 to 300 mM, respectively. Under this condition an increase in osmolality at the end-descending limb was mainly accounted for by the absorption of water. Considerable amounts of potassium and urea were secreted along the descending limb. Sodium was reabsorbed rather than secreted along the descending limb by both diffusion and solvent drag. The secreted amounts of urea and potassium were comparable to those observed by micropuncture studies. The sodium concentration in the lumen was higher than in the interstitium, with the transmural sodium gradient being 15 meq/liter at the hairpin turn. The potassium mass flow rate at the end-descending limb increased by 2.4 times. Large variations in potassium concentration of the delivered fluid scarcely changed the potassium mass flow rate at the end-descending limb. The secretion of urea and potassium and the reabsorption of sodium were increased as a function of delivered flow rate. An increase in corticomedullary urea gradient decreased the net potassium secretion along the descending limb. When the transport parameters for rabbits were used, both reabsorption of sodium and addition of urea were decreased, but a similar amount of potassium was secreted. These analyses indicate that the mathematical model that takes the species difference and internephron heterogeneity into consideration is useful in illustrating the transport processes along the descending limb of Henle's loop under various physiological and pathophysiological conditions.

Biological Transport, Active↗
PubMed1987

A case of rhabdomyolysis in chronic renal failure.

Rhabdomyolysis can be induced by a variety of physical and chemical insults to skeletal muscle. Though there are only a few reports of myositis associated with viral diseases, and no reported cases of virus-induced rhabdomyolysis in uremic patients. Chronic uremic states have been known to potentiate a variety of metabolic and immunological abnormalities. Present case had an acute, progressive and fatal rhabdomyolysis which was thought to be induced by virus infection. A 43-year-old man had received hemodialysis therapy for 8 years. He suffered from an upper respiratory tract infection 11 days before admission. On admission, he was diagnosed as rhabdomyolysis with severe lactic acidosis and marked hyperkalemia. Although intensive care had been performed, he died of uncontrollable hyperkalemia (10.0 mEq/L) 2 days after admission. Maximum CPK and GOT levels were 105,200 and 56,800 mU/ml, respectively. Most probable cause of rhabdomyolysis was thought to be Parainfluenza type-3 infection, though histological examination failed to prove virus infection.

Adult↗