PubMed Health⌕ Search

Biomedical subjects

G Blaskó

Publications and source records attributed to G Blaskó.

At least 19 recordsLinked to original sources
PubMed2003

The effect of drotaverine hydrochloride in acute colicky pain caused by renal and ureteric stones.

OBJECTIVE: To assess the spasmolytic effect of drotaverine hydrochloride in colicky pain caused by renal and ureteric stones. PATIENTS AND METHODS: In a placebo-controlled, multicentre, multinational, randomized, double-blind study changes in the intensity of pain were recorded using a visual analogue scale (VAS), a four-grade (five points) pain intensity (PI) scale and a pain-relief scale. The primary endpoint was the evaluation of the antispasmodic effect of drotaverine during a 3-h study period, to confirm that drotaverine abolished or significantly decreased the intensity of pain in renal colic. The painkilling effect was defined as a decrease by at least half in the PI scale, and/or a >or= 40% decrease in the VAS 40 min after either the first or the second injection of 80 mg drotaverine or placebo (if necessary the dose could be repeated once). In all, 140 patients were enrolled but 38 withdrew, leaving 102 patients for analysis (48 drotaverine, 54 placebo; mean age 42.5 years, sd 11.25, and 41.7, sd 10.79). RESULTS: Drotaverine was effective in 79% of patients and placebo in only 46% (P < 0.001). There were no serious adverse effects. There were 20 minor side-effects in the drotaverine and four in the placebo group; none of the patients required treatment. The most frequent side-effects were a transitory decrease in blood pressure, vertigo, nausea or vomiting. CONCLUSION: Intravenous drotaverine provides effective pain relief in more than two-thirds of patients with renal colic, with no serious side-effects.

Acute Disease↗
PubMed2001

Natural coagulation inhibitor proteins in young patients with cerebral ischemia.

Disturbances of coagulation and fibrinolytic pathways were studied in 53 young patients with cerebral ischemia. Upon admission 26 of 53 patients had abnormality in at least one of the antithrombin-III, protein C, protein S activities or in activated protein C (APC) ratios. Three months after the first examination the majority of the previously detected abnormalities returned to normal values and the most frequent alterations were decrease in protein S activity (3 patients) and APC resistance (3 patients). Conditions resulting in impaired fibrinolysis were frequently detected upon admission. Elevation of plasminogen activator inhibitor-1, lipoprotein (a), and alpha-2-antiplasmin was present in 23, 10, and 4 cases, respectively. It is concluded that abnormalities of coagulation as well as of the fibrinolytic systems are prevalent in the acute phase of cerebral ischemia, however, the results may be significantly influenced by the disease process or the acute phase effect.

Acute Disease↗
PubMed1999

[The rate of acetylsalicylic acid non-respondents among patients hospitalized for acute coronary disease, previously undergoing secondary salicylic acid prophylaxis].

The authors determined the rate of acetylsalicylic acid (ASA) non-responders among patients receiving secondary prevention due to cardiovascular diseases at the appearance of acute coronary events. The non-responders were defined as: patients who have been treated with ASA because of acute coronary syndrome, but the subsequently performed platelet aggregation study did not confirmed an appropriate platelet inhibition. Among the 75 patients being investigated (44 male, 31 female, average age: 61.3 ys) 21 were hospitalized due to acute myocardial infarction and 54 for unstable angina, respectively. The daily doses of ASA were 200-325 mg. The aggregation of platelets was measured within 24 h after the admission. The investigations were performed with different amounts of 4 different inducers (ADP, arachidonic acid, epinephrine and collagen) taking dose-response curves. The antiaggregatory treatment with ASA was considered to be ineffective if the typical aggregation curves were obtained above the following final concentrations of the inducers: ADP: > 5 microM, epinephrine: > 5 microM, arachidonic acid: > 250 microM, collagen: > 2 micrograms/ml. These upper-threshold concentrations of the inducers were determined with the help of the data of healthy drug free volunteers. Twenty-six of the 75 patients (34%) were found to be non-responder to ASA, whereas the antiaggregatory effect of ASA was proven in 49 cases. No differences were found in gender. The compliance was proven with the HPLC-determination of urinary metabolites of ASA performed immediately after the upon admission. Seven patients (10.9%) showed a non-compliance, not showing any traces of ASA-metabolites in their urine. The authors emphasizing the importance of the laboratory control even of the prophylactic ASA treatment in order to continue the effective antiaggregatory therapy with other effective drugs.

Acute Disease↗
PubMed1999

Differences in the platelet proaggregatory activity of immune complexes isolated from patients with myocardial infarction or pulmonary cancer.

Immune complexes were isolated immediately after the onset of the symptoms of myocardial infarction on an anti-Clq affinity column. The platelet proaggregatory effects of these immune complexes were compared with those isolated from patients suffering from pulmonary cancer. A markedly increased proaggregatory effect of immune complexes derived from patients with myocardial infarction and changes in the sensitivity of platelets from healthy volunteers to PGI(2) (prostacyclin) and PGD(2) were found. In contrast, immune complexes from patients with pulmonary cancer did not show any significant effect. The antigenic part of immune complexes is probably relevant in the induction of platelet aggregation.

Journal Article↗
PubMed1998

[Hemostatic abnormalities in ischemic stroke].

The authors studied whether haemostatic abnormalities connected with the development of cerebral circulatory disturbances can be demonstrated in young stroke patients in whom Doppler and angiographic examination failed to reveal deviations indicative of stroke. They determined the in vivo activation of the coagulation system (TAT, F 1 + 2), the degree of secondary fibrinolysis (D-dimer), the plasma levels of the markers of fibrinolysis, with special regard to inhibitors: plasminogen activator inhibitor (PAI-1), alpha 2 antiplasmin (alpha 2 AP), alpha 2 macroglobulin (alpha 2 M), the frequency of pathologic serum lipoprotein (a)-Lp(a)-values and the association of PAI-1 and Lp(a) with the fibrinolytic system. They conclude that in the acute phase of the disease, the TAT and F 1 + 2 values were significantly elevated compared to the control, without change in the D-dimer value. The results suggest that in the tested period increased thrombin generation dominated and it significantly surpassed plasmin activity since the D-dimer values of that period did not indicate substantial increase in secondary fibrinolysis. The results of the study were separately analyzed in acute, chronic TIA and stroke groups. In the TIA and acute group the F 1 + 2 values, while in stroke the TAT values were more elevated. The in vitro fibrinolytic capacity of the patients significantly decreased compared to controls, showing significant correlation with the Lp(a) level, but not with the PAI value. Examination of the marker molecules renders possible to assess the degree of hypercoaguability and of endogenous lysis. Their knowledge is held important for judging the progression of the disease and the therapeutic consequences.

Adult↗
PubMed1997

Inhibition of gamma-aminobutyric acid uptake by bicuculline analogues.

Enantiomers of norbicuculline, (+)[1S,9R] and (-)[1R,9S]erythro-1-[1'-(4',5'-methylenedioxyphthalidyl)]-6,7-meth ylenedioxy-1,2,3,4-tetrahydroisoquinoline and of the N-methyl derivatives {(+)[1S,9R] and (-)[1R,9S]bicuculline} were found to inhibit the progress of the gamma-aminobutyric acid transporter-mediated uptake of 40 microM [14C]gamma-aminobutyric acid into native plasma membrane vesicles from the rat cerebral cortex at 30 degrees C. The values for the dissociation constants of the reversible inhibition, relative to (+)[1S,9R]bicuculline, in order of increasing inhibition, were: (-)[1R,9S]bicuculline, 3.3; (+)[1S,9R]-bicuculline, 1.0; (-)[1R,9S]norbicuculline, 0.4 approximately (+)[1S,9R]norbicuculline; guvacine, 0.02. The norbicucullines have higher potencies than (+)[1S,9R]bicuculline for the gamma-aminobutyric acid transporter, in contrast to the relative potencies of these inhibitors for the inhibition of function and gamma-aminobutyric acid binding of the gamma-aminobutyric acid type A receptor.

Animals↗
PubMed1996

[The Hungarian nifedipines].

The short history of the nifedipine drug substance containing Cordaflex product family--produced by EGIS Pharmaceuticals Ltd.--is presented.

Calcium Channel Blockers↗
PubMed1993

Investigations of indomethacin-induced gastric ulcer in rats.

The pathogenesis of non-steroidal anti-inflammatory drugs (NSAIDs)-induced ulceration is still not completely understood, but it is possible that these effects are associated with a cytoprotective prostaglandin deficiency. Visible marks of gastric mucosa erosions induced by 25 mg/kg indomethacin in rats were determined parallel with the changes of PGE2, PGI2, TxA2 and leukotrienes content in gastric mucosa at various intervals. Beside the decreased level of the so-called cytoprotective prostaglandins caused by the inhibition of cyclooxygenase enzyme an overproduction of 5-lipoxygenase products (leukotrienes) was also found. To investigate the hypothesis that the gastric damage caused by NSAIDs is due not only to the decreased level of cyclooxygenase products but to the increased level of lipoxygenase products as well, different lipoxygenase inhibitors and leukotriene antagonists were tested. A lipoxygenase inhibitor and the structurally similar phenidone inhibited the ulcerogenic effect of indomethacin at the same high dose range. The selective lipoxygenase inhibitor nordihydroquaiaretic acid and dual inhibitors can reduce the severity of ulcer formation in lower concentrations as well. The first specific antagonist of SRS-A and a potent and selective antagonist of LTD4 produced a significant gastroprotective effect at i.p. treatment only at high doses. All of these results suggest that an overproduction of leukotrienes and other lipoxygenase products, following cyclooxygenase blockade induced by NSAIDs, may play a role in the development of gastric mucosal damage.

Animals↗
PubMed1993

[The benzodiazepine story].

Benzopyrylium salt (3) was converted by means of excess of hydrazine hydrate into a substance of a composition C22H26N2O4. The structure of this compound was elucidated by means of detailed NMR and mass-spectroscopic studies and the structure of 1-(3,4- dimethoxyphenyl)-5-ethyl-7,8-dimethoxy-4-methyl-5H-2,3-benzodiazepine (4) has been proved. Conformation analysis was performed as well and it has been established that two conformers (A and B) exist in reversible equilibrium. The molecule contains a chiral centre and the enantiomers were separated via optical resolution. Two different 14C-labelled 4 were prepared for pharmacological studies. The compound is known as GrandaxinR in the medicinal practice (INN = tofisopam).

Anti-Anxiety Agents↗
PubMed1992

Comparative studies of drotaverine--acephyllinate (Depogen) and pentoxifylline (Trental).

Pentoxifylline is an orally active agent for the treatment of peripherial and cerebral vascular diseases. Pentoxifylline increases the deformability of red blood cells in vitro, reduces blood viscosity and decreases platelet aggregation and thrombus formation. Depogen has shown antiaggregatory effect both in vitro and in ex vivo. The inhibitory effect of Pentoxifylline was about 3-5 times weaker than that of Depogen. IC50 = 900/micrograms/ml for Depogén and 3600/micrograms/ml for Pentoxifylline on human platelet rich plasma. Depogen has shown ex vivo antiaggregatory effect on anesthetised rabbits, ID50 = 7 mg/kg in case of iv. administration, and ID50 = 300 mg/kg in case of orally administration. Both compound inhibit the release of platelet precoagulation factor, but the effect of Pentoxifylline was slighter.

Animals↗
PubMed1990

Spectral assignment and cytotoxicity of 22-hydroxytingenone from Glyptopetalum sclerocarpum.

22-Hydroxytingenone was reisolated from a new source, Glyptopetalum sclerocarpum M. Laws and, for the first time, its unambiguous 13C-NMR assignments were accomplished through the use of APT, HETCOR, and selective INEPT spectroscopy. Intense, but nonspecific cytotoxic activity was observed when this substance was evaluated with a battery of cell lines comprised of the P-388 lymphocytic leukemia, KB carcinoma of the nasopharynx, and a number of human cancer cell types, i.e. HT-1080 fibrosarcoma, LU-1 lung cancer, COL-2 colon cancer, MEL-2 melanoma, and BC-1 breast cancer.

Animals↗
PubMed1989

[Distribution of the causes of congenital thrombophilia].

In recent years there have been discovered more and more such connatal mostly hereditary coagulopathies, which can explain the thrombosis susceptibility of the given individual or/and the family. The International Thrombosis and Haemostasis Society made a survey to estimate the frequency of those defects causing thrombophilias. In this survey the authors analysed the cases of their patients according to the given points of view. In their work they discuss some theoretical and practical problems of the theme, which can have an importance in respect to the everyday medical practice.

Adult↗
PubMed1989

Synthesis of prostacyclin and thromboxane A2 by rat gastric mucosa. Comparison of 1,6-dimethyl-4-oxo-1,6,7,8,9,9a-hexahydro-4H-pyrido (1,1-a)-pyrimidine-3-carboxamide and cimetidine.

The production of prostacyclin (PGI2) and thromboxane A2 (TXA2) was studied in an indometacin-induced ulcer model in rats. The specific activities of prostacyclin synthetase and thromboxane synthetase as well as the tissue content of these prostaglandins were determined. The anti-ulcer effect of cimetidine and a novel agent, i.e. 1,6-dimethyl-4-oxo-1,6,7,8,9,9a-hexahydro-4H-pyrido(1,1-a)-pyrimidine-3- carboxamide (Chinoin-127) was compared in this respect. The indometacin treatment shifted the balance of TXA2/PGI2 to the formation of TXA2, and the anti-ulcer agents repaired it. The role of this balance in cytoprotection is discussed.

Animals↗