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K Hátle

Publications and source records attributed to K Hátle.

17 recordsLinked to original sources
PubMed1995

The effect of calcium channel blockers on cyclosporine A (Cs A) induced nephrotoxicity in rats.

The limiting factor in the therapeutical use of cyclosporine A (Cs A) is its nephrotoxicity, which may lead to renal failure. Cs A nephrotoxicity may present itself as an acute decrease in GFR, or as a chronic renal injury. Nephrotoxicity is caused by the indirect vasoconstriction effect mainly on proximal tubule and afferent arteriols. In our study we have concentrated on the effect of Ca-channel blockers on Cs A nephrotoxicity. As parameters of toxic kidney damage we have used the urine levels of the following enzymes: N-acetyl-beta-D-glucosaminidase (NAG), gama-glutamyltransferase (GMT) and alkaline phosphatase (ALP). Daily intragastric application of verapamil (V) (dose 1.0 mg/kg BW) or nifedipine (N) (dose 0.1 mg/kg BW) was started in a group of male Wistar rats. Cs A (Sandimun Sandoz, Switzerland) was applied daily intraperitoneally 30 minutes after the application of V or N. The dose of Cs A ranged from 5 mg/kg BW to 25 mg/kg BW in individual groups. The animals were observed for 10 days after the drugs application. Urine samples were collected and examined at the end of the whole experiment. The individual parameters were evaluated in the groups receiving the 3 different doses of Cs A (5-25 mg/kg BW). The serum creatinine rose moderately during the experiment. When the Ca-channel blockers were administered, the rise was not as steep, but when the highest dose of Cs A was administered, the Ca-channel blockers did not influence the elevation of the serum creatinine. Using the standard dose of Cs A (5 mg/kg BW) the protective effect of Ca-channel blockers can be found. In higher doses of Cs A this protective effect was not expressed.

Animals↗
PubMed1990

[Manifestations of dysfunction of the proximal tubules after intravenous urography].

The aim of the work was to investigate functional changes of tubular cells after i.v. urography. As evidence the authors used assessment of urinary levels of membrane-bound enzymes--alkaline phosphatase (AP), gamma-glutamyl-transpeptidase, lysosomally bound enzymes N-acetyl-beta-D-glucosaminidase and its isoenzyme B and the low molecular protein, beta-2-microglobulin. The above substance were assessed in 15 patients with different nephropathies where i.v. urography was indicated. The examinations were made in 24-hour urine samples before i.v. urography and in two 24-hour samples after administration of the contrast substance. In all patients a significant rise of tubular enzyme excretion was observated as well as of beta-2-microglobulin. The greatest rise was recorded in alkaline phosphatase in the second sample after administration of the contrast substance (432% of the initial value). Beta-2-microglobulin and N-acetyl-D-glucoseaminidase rose already during the first collection period (B2M to 357% and NAG to 181% of the initial values). The authors conclude that i.v. urography made by hyperosmolar iodinated preparations (Verografin, Iodamide) significantly affects the function and integrity of the proximal tubule. The applied spectrum of examinations is suitable also for further investigations of the effect of contrast substances on cells of the proximal renal tubule.

Adult↗
PubMed1990

[The effect of streptozotocin-induced diabetes treated with insulin on the metabolism of calcium, magnesium and phosphorus].

In a group of rats with streptozotocin induced diabetes the excretion of calcium, magnesium, phosphorus and creatinine in urine was investigated and the calcium, magnesium and phosphorus content of bone in relation to the duration of the disease. The authors observed that in diabetic rats the urinary losses of calcium, magnesium and phosphorus increase significantly. The creatinine excretion is also significant but lower in relation to calciuria and therefore the value of Nordin's index in diabetic rats rises markedly. Bone of diabetic rats in the early stage of diabetes (32 days) loses magnesium, while the calcium and phosphorus content does not change significantly. During longer persistence of severe diabetes (70 days) a significant drop of all three minerals in bone was observed. The bones of diabetic animals on the 70th experimental day were macroscopically smaller and were very fragile. The authors' findings suggest a marked influence of streptozotocin diabetes on calcium phosphate metabolism and bone metabolism, in particular on account of STZ diabetes, on an early drop of magnesium in bone. The possible impact of this finding for clinical practice will have to be tested further.

Animals↗
PubMed1989

[Excretion of phenoltetrachlorophthalein in the bile in rats].

Phenoltetrachlorphthalein secretion into bile was followed in Wistar strain rats intoxicated per os by tetrachlormethane (0.25, 0.50, 2.00, and 3.00 ml/kg) after 1, 2, 4 and 8 days after intoxication. Biotransformation processes resulting in the formation of phenoltetrachlorphthalein metabolites are altered during the intoxication unequally. So far mutual relation of secreted metabolites has not been proved to serve generally as a simple criterion for absolute activity assessment of hepatic glucuroniltransferase or other hepatic enzymes.

Animals↗
PubMed1981

Effect of phenobarbital pretreatment on benzene biotransformation in the rat. II. 9,000 g supernatant and isolated perfused liver versus living rat.

Factors responsible for different quantitative effect of phenobarbital (PB) pretreatment (sodium phenobarbital, 50 mg kg-1 day-1 for 3 days) on benzene metabolism to phenol in vivo and in vitro were studied in male Wistar rats. A more than 4-fold increase of benzene metabolism was observed wih 9,000 g supernatant of liver homogenate, 2.8- to 4-fold increase with isolated perfused liver; phenol formation in vivo after oral benzene was increased by PB 2-fold, but only shortly following benzene administration and the enhancement rapidly diminished to 1.15-fold increase in the total excreted phenol. Benzene concentrations i 9,000 g supernatant incubations were 2 mM, those with isolated perfused livers were up to 4 mM, but those in blood in vivo were below 0.3 mM; the effect of PB induction in vivo disappeared along with decreasing benzene and increasing phenol blood concentrations which surpassed benzene 2-3 h after oral benzene administration. The effect of benzene concentration on the manifestation of PB induction is also supported by almost a 2-fold increased phenol formation in PB rats over controls in vivo after repeated administration of benzene. The elimination of radioactive metabolites of orally administered benzene-14C, 3 mmoles kg-1, in urine was markedly inhibited by intraperitoneal administration of phenol (1.2 mmol kg-1), but not by pyrocatechol, resorcinol or hydroquinol (0.6 mmole kg-1, respectively) suggesting that phenol might inhibit benzene metabolism in vivo especially when its concentration exceeds that of benzene.

Animals↗