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Biomedical subjects

N Kolassa

Publications and source records attributed to N Kolassa.

At least 55 records · Page 3Linked to original sources
PubMed1977

Relaxation of coronary artery strips by adenosine and acidosis.

Cumulative dose-response curves of Ca2+-induced tension increments were studied in K+-depolarized helical strips of dog coronary arteries. Adenosine 10(-4) M reduced the Ca2+ sensitivity of the strips without altering the maximal tension with full Ca2+ activation. In contrast, acidosis of pH 7.05 significantly diminished the maximal tension with full Ca2+ activation. The relaxing effect of acidosis was almost completely abolished by 10(-4) M adenosine. It is concluded that adenosine inhibits Ca2+ influx, whereas acidosis depresses the contractile process of vascular smooth muscle directly.

Acidosis↗
PubMed1977

Weak electrolyte transfer in the guinea pig jejunum: secretion of trimethoxybenzoic acid.

In isolated epithelia of guinea pig jejunum the transcellular permeation of 10(-4) M (carboxyl-14C)-3,4,5-trimethoxybenzoic acid (TMBA) in the direction blood-lumen was more than 10 times greater the transcellular permeation of 10(-4) M (carboxyl-was reduced to less than 2 by anaerobiosis or by increasing TMBA concentrations of up to 10(-2) M. Under aerobic conditions the cellular uptake of TMBA (10(-4) M) from the blood side was twice as high as that from the lumen side. In anaerobiosis the percentage of TMBA taken up into the epithelium was enhanced, when TMBA was administered on the lumen side, while the percentage was unchanged after administration on the blood side; thereby the difference in cellular TMBA concentrations was abolished. Similar results were obtained under aerobic conditions, if the TMBA concentration was increased up to 10(-2) M. The results are consistent with a three-compartment model with an intermediate compartment distinguished by a high pH as compared to that of the outer compartments and by a luminal boundary highly permeable for the ionized form of the substrate in contrast to the contraluminal boundary.

Aerobiosis↗
PubMed1977

Adenosine uptake by the isolated epithelium of guine pig jejunum.

The uptake of [8-14C]adenosine by the isolated epithelium of guinea pig jejunum was faster than that of inosine, hypoxanthine, or adenine. The initial velocity of adenosine uptake from both the luminal and the antiluminal side of the epithelium exhibited saturation kinetics. The apparent Km, V, and passive permeability of luminal adenosine uptake were all lower than the corresponding values of antiluminal uptake. p-Nitrobenzyl-thioguanosine inhibited adenosine uptake from both the luminal and the antiluminal side, whilst hexobendine decreased the uptake only from the antiluminal side of the epithelium. The results suggest that adenosine enters the intestinal epithelium by a carrier-mediated process in addition to passive diffusion. The antiluminal transport system for adenosine seems similar to that of other tissues with respect to hexobendine inhibition; the luminal transport mechanism, however, exhibits different properties, being insensitive to hexobendine.

Adenine↗
PubMed1977

Salvage of adenosine, inosine, hypoxanthine, and adenisine by the isolated epithelium of guinea pig jejunum.

The metabolism of adenosine, inosine, hypoxanthine, and adenine (labelled with 14C in the carbon 8 position) at a concentration of 5 X 10(-6) M was studied in isolated epithelium of guinea pig jejunum. When adenosine or adenine was added to the antiluminal side of the epithelium, two-thirds or one-half, respectively, of cellular radioactivity was incorporated into the nucleotide fraction, mainly in the form of adenine nucleotides. Nucleotides synthesis from inosine or hypoxanthine was significantly smaller than that from adenosine. By contrast, another metabolic patern was found after luminal administration of adenosine, inosine, or hypoxanthine: the incorporation rate into the nucleotide fraction was equally high and the label was recovered in IMP and adenine nucleotides to about the same extent with all three substrates. Purine riboside (10(-4) M) significantly depressed nucleotide formation from adenosine, with respect to IMP formation in particular, while no change was observed in inosine or hypoxanthine salvage. The results suggest compartmentation of the enzymes of purine metabolism within the intestinal mucosa. The significance of this conclusion with regard to the salvage pathway is discussed.

Adenine↗
PubMed1976

Limitations of the direct linear plot in evaluation of drug-protein binding parameters.

The applicability of the direct linear plot is compared with that of the Scatchard plot for the estimation of protein binding parameters. Only, if one class of binding sites exists in the system tested, binding parameters may be estimated by use of the direct linear plot. On the other hand the Scatchard plot also provides estimates in systems with more that one class of binding sites.

Binding Sites↗
PubMed1976

Myocardial glucose uptake and breakdown during adenosine-induced vasodilation.

In isolated K+ (16.2 mM)-arrested cat hearts perfused at constant pressure adenosine infusions (0.8 mumoles - min-1 - 100 g-1 for 10 min) caused an increase in myocardial 14C-glucose uptake and release of 14CO2 + H14CO3- AND 14C-lactate simultaneously with a rise in coronary flow. The ratio of the release of 14CO2 + H14CO3- to that of 14C-lactate and the specific activity of lactate in the effuate were not altered. In K+ -arrested hearts perfused with constant volume neither glucose uptake nor glucose breakdown were influenced by 0.8 or 100 mumoles - min-1 - 100 g-1 adenosine with 0.1 - 5 mM glucose in the perfusion medium. It is concluded that adenosine does not affect directly the myocardial glucose carrier system, aerobic or anaerobic glucose breakdown or glycogenolysis, but enhances glucose uptake secondarily by increasing coronary flow. This interpretation is substantiated by the finding that mechanically produced increases in perfusion volume caused similar increases in myocardial glucose uptake as were observed with comparable adenosine-induced coronary flow increments.

Adenosine↗
PubMed1975

Blood histamine levels and arteriovenous concentration differences after the intravenous administration of the basic compounds l-3 and 48/80 in the anaesthetized dog.

The effects of the i.v. administration of inulin trinicotinate-monomethochloride (L-3) on haemodynamics, airway pressure and blood histamine levels were studied in chloralose-anaesthetized dogs and compared with the effects of compound 48/80. The control arterial histamine level was 0.041 plus or minus 0.002 mug/ml (mean plus or minus SEM) as determined by a fluorometric assay. L-3 (0.15 mg/kg) released high amounts of histamine, as indicated by a peak level in arterial histamine of 0.212 plus or minus 0.027 mug/ml within 3 min, which was not futher enhanced on increasing the dosage of L-3 to 1 mg/kg. After the i.v. injection of 0.15 mg/kg of 48/80 the peak level in arterial histamine was 0.146 plus or minus 0.008 mug/ml, and the level was further markedly elevated to 0.918 plus or minus 0.068 mug/ml after the administration of 1 mg/kg of 48/80. The concomitant fall in systemic blood pressure and the rise in airway pressure can be satisfactorily explained on the basis of histamine liberation. Whereas these parameters as well as the blood histamine concentration gradually returned to control values, the heart rate remained elevated during the observation period of 2 h. The arteriovenous differences in blood histamine across various tissues and organs following L-3 and 48/80 administration indicated histamine release mainly from skin and muscle and histamine uptake by the kidney, the digestive tract and to a lesser extent the lungs. The portal-hepatic vein differences revealed no consistent changes in liver histamine balance. As regards the lungs and liver, the present results suggest a dynamic equilibrium between histamine release and uptake in these organs in the intact animal. Both, L-3 and 48/80 elicited a similar pattern of histamine release and uptake. The extreme histamine releasing capacity of 1 mg/kg of 48/80 may be explained by an additional non-selective mechanism of histamine liberation.

Airway Resistance↗
PubMed1975

[Pharmacokinetics and action of digitoxin and ouabain in the isolated hearts of guinea pigs and rats].

Isolated guinea pig and rat hearts were perfused with 3H-digitoxin and 3H-ouabain. After varying perfusion periods (3-90 min) the glycoside content in the tissue was determined. With digitoxin the tissue/medium-ratio at equilibrium was found to be 14 in guinea pigs and 8 in rats, with ouabain the corresponding values were 2 and 1. In further experiments the efflux of radioactivity from isolated perfused hearts preloaded with 3H-glycosides was measured in 3 min intervals. A compartmental analysis was carried out. The efflux could be described by the sum of two exponentials indicating the existence of two compartments. The half lives of compartment 1 (2.1-4.0 min) and those of compartment 2 (16.8-20.6 min) were similar with both glycosides and both species. The development and decline of the positive inotropic effect in guinea pig hearts exhibited a time course similar to that of the glycoside content in compartment 1: the time for reaching the half maximum effect was 3-4 min with ouabain and 5-6 min with digitoxin. It is suggested that compartment 1 represents the site of the positive inotropic action of cardiac glycosides.

Animals↗
PubMed1975

[Studies on the pharmacokinetics of hexobendine in rats. I. Distribution following i.v. administration (author's transl)].

The distribution of 14C-labelled N,N'-dimethyl-N,N'-bis-[3-(3',4',5'-trimethoxy-benzoxy)-propyl]-ethylenediamine-hydrochloride (hexobendine, Ustimon, Reoxyl) in the organs of rats was studied after i.v. injections of 0.5 mg/kg. Up to the 81st min 70-90 percent of the 14C-activity in the lung, heart, skeletal muscle, spleen and brain were formed by unchanged hexobendine, identified by thin-layer chromatography in tissue extracts. In the kidneys and erythrocytes less than 70 percent, in serum and liver less than 50 percent of the measured radioactivity consisted of hexobendine. The serum concentration of hexobendine was 0.1 mug/ml 3 min after administration. This concentration declined with a half-life of 7 min distribution and a half-life of 45 min for elimination. In certain organs the hexobendine concentration rose above the serum level: After 3 min the tissue/serum ratio in the lung was 69, in the kidneys 20, in the heart 7, in the spleen 5, in the liver and skeletal muscle 4, in the erythrocytes 1.2 and in the brain 0.7. The time-dependent decrease in hexobendine concentrations in the various organs was only slightly slower than that in the serum. Only 1 percent of the infected 14C could be detected in the analysed material 12 h after hexobendine administration.

Animals↗
PubMed1975

[Studies on the pharmacokinetics of hexobendine in rats / 2nd communication: Elimination following i.v. administration (author's transl)].

The elimination of 14C and of 3H was studied in rats after i.v. administration of 0.22--0.33 mg/kg of 14C- or 0.67 mg/kg of 3H-labelled N,N'-dimethyl-N,N'-bis-[3-(3',4',5'-trimethoxy-benzoxy)-propyl]-ethylenediamine-dihydrochloride (hexobendine, Ustimon, Reoxyl), respectively. Regarding the obtained results shortcomings in methods are discussed which may falsify the elimination pattern of radioactively labelled substances. Under certain experimental conditions (closed metabolism chamber with absorption of CO2 or H2O, respectively) 99-100% of the administered radioactivity were detected in the excretion products. The appearance of 14CO2 in the expired air was prevented when the bile duct was cannulated and the bile was drained to the outside before reaching the gut with its probably decarboxylating bacteria.

Animals↗