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Biomedical subjects

K Uchino

Publications and source records attributed to K Uchino.

85 records · Page 5Linked to original sources
PubMed1984

Quantitative determination of furosemide in plasma, plasma water, urine and ascites fluid by high-performance liquid chromatography.

A high-performance liquid chromatographic method using spectrofluorometric detection is described for the determination of furosemide in plasma, plasma water, urine and ascites fluid. The extraction procedure decreases interference from endogenous substances. The detection limit of furosemide is 10 ng in 0.5 ml of biological sample. The method is sufficiently sensitive for pharmacokinetic study of furosemide with normal subjects and patients with liver cirrhosis and/or renal disease after oral administration of furosemide in a retard capsule, and for study of protein binding of furosemide in patients with various diseases.

Ascitic Fluid↗
PubMed1983

Clinical pharmacokinetics and diuretic effect of furosemide in plain tablet and retard capsule with normal subjects and cirrhotic patients.

The dissolution profiles of furosemide in various solutions were studied with plain tablet and retard capsule of furosemide. The rate constant and percent dissolution in retard capsule were lower than that in plain tablet. Clinical pharmacokinetics and diuretic effect of furosemide after oral administration of two dosage forms were also studied with 3 normal subjects and 3 cirrhotic patients. In normal subjects, the extent of furosemide absorption from retard capsule was 45% of plain tablet. The daily urine volume after oral administration of two dosage forms was comparable, however, quite different profiles were observed between these dosage forms. In patients, the extent of furosemide absorption in retard capsule was one half that of plain tablet. The dose of retard capsule was increased without adverse reactions, thus decreasing of ascites, which was not observed with plain tablet, was achieved with increasing urine volume.

Adult↗
PubMed1982

Factitious Bartter's syndrome induced by surreptitious intake of furosemide.

Studies on the electrolyte metabolism and the renin-angiotensin-aldosterone system were made in a 47-year-old female patient with factitious Bartter's syndrome induced by surreptitious use of furosemide. The diagnosis was confirmed later by detection of the diuretic in the urine. In metabolic studies patient exhibited abnormalities similar to those reported in Bartter's syndrome; viz, hypokalemic alkalosis, blunted response to exogenous angiotensin II, which reverted to normal by volume expansion with an albumin solution, and diminished fractional free water clearance per fractional distal sodium delivery. The above data, along with the known pharmacological effects of furosemide, suggest that the abnormality in Na+ or Cl- reabsorption in the ascending limb of Henle's loop is a primary cause of Bartter's syndrome.

Absorption↗
PubMed1981

Pseudo-Bartter's syndrome due to furosemide abuse: report of a case and an analytical review of Japanese literature.

Batter's syndrome characteristically exhibits the constellation of hypokalemic alkalosis, normotensive hyperreninism, hyperalodosteronism, hyporesponsiveness to pressor agent and juxtaglomerular cell hyperplasia. Recently, metabolic mimicry of Batter's syndrome by vomiting, diarrhea, laxatives and diuretics abuse has been reported. We had a 30 year-old female patient who developed so-called pseudo-Bartter's syndrome as the result of surreptitious self-administration of furosemide for about six years. In this case, calcification of bilateral renal medulla was demonstrated. Such adverse reaction has not been reported to date. Moreover, a total 14 cases of pseudo-Bartter's syndrome reported in Japanese literature is reviewed.

Adolescent↗
PubMed1979

Estimation of plasma unbound phenobarbital concentration by using mixed saliva.

Relationships among plasma total (Ct), plasma protein unbound (Cf) and mixed salivary (Cs) concentrations of phenobarbital (PB) were studied in 29 epileptic patients. A highly significant correlation was observed between Ct and Cf. Although a significant correlation was observed between Cf and Cs, Cs/Cf ratio was only 0.63. When Cs was corrected by using pKa (7.41) and pH of saliva to estimate free PB concentration (Cest f), a highly significant correlation was obtained between Cf and Cest f, and Cest f/Cr ratio was 0.96. The temporal course of Cest f obtained from Cs after an oral single dose of 50 mg PB in a healthy adult male volunteer was approximated as a triexponential equation. The peak time was 2 hr after ingestion and apparent half life was 66 hr. The prediction of minimum concentrations at steady state on the basis of these parameters corresponded well with actually obtained Cest f following repetitive administration of PB.

Adolescent↗
PubMedDate not supplied

Pharmacokinetic analysis of enterohepatic circulation of buprenorphine and its active metabolite, norbuprenorphine, in rats.

The pharmacokinetic characteristics of buprenorphine (BN) and its active metabolite, norbuprenorphine (NBN), was investigated using rats. The elimination half-life (t1/2), total body clearance (CLtot), and steady-state volume of distribution (Vdss) of BN (0.6 mg/kg iv dose) in the intact rat were 2.8 hr, 23.3 ml/min/kg, and 4.2 liters/kg, respectively, and those of NBN (0.6 mg/kg iv dose) were 0.9 hr, 35.0 ml/min/kg, and 2.0 liters/kg. Within 24 hr after administration of BN (0.6 mg/kg dose) to the bile-fistula rat, 74.1% of dose was excreted in the bile as BN glucuronide (BN-Glu) and 18.5% as NBN glucuronide (NBN-Glu), and in urine < 3.2% as BN-Glu. After administration of NBN to the bile-fistula rat, 85.1% and 9.1% of the dose were excreted as NGN-Glu in bile and urine, respectively. The existence of the enterohepatic circulation (EHC) of BN and NBN was confirmed by using paired rats: the donor and recipient rats. Within 24 hr after administration of BN (0.6 mg/kg dose) to the donor rat, 58.8% of the dose was reexcreted as NBN-Glu in bile of the recipient and 25.1% as BN-Glu. Based on the results of in vitro metabolism, it was suggested that this increase in the proportion of NBN-Glu in bile observed after one enterohepatic cycling of BN may be due to the first-pass metabolism in the liver. BN was detected in the plasma of the recipient rat after administration of BN, to the donor rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗