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At least 865 records · Page 48Linked to original sources
PubMed1997

Alteration of cytochrome P-450 isozymes by captopril and idrapril in hepatic and renal microsomes of normotensive and spontaneously hypertensive rats.

To examine the effects of angiotensin-converting enzyme (ACE)inhibitors such as captopril and idrapril on the P-450 system, these compounds were administered 100 mg/kg i.p. for 4 days to spontaneously hypertensive (SHRs) and normotensive Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats; thereafter, the principal hepatic and renal microsomal monooxygenase activities were determined. In all the rat strains used, both captopril and idrapril decreased only the P-450 2C11, (as determined by immunoblotting) and its linked activities such as 16alpha-, 2alpha- and 17-testosterone hydroxylases. These changes were accompanied by a significant decrease of blood testosterone levels both in normotensive and, more markedly, in hypertensive rats and by a reduction of systolic blood pressure, but only in SHRs. Only in SHRs as well, the renal immunodetectable P-450 4A content and the P-450 4A-dependent activities, such as the (omega)-lauric acid hydroxylase, diminished after captopril or idrapril treatment. These data suggest that the decrease of increased blood pressure in hypertensive SHRs by the ACE inhibitors may be linked to the downregulation of the circulating testosterone level, the renal P-450 4A expression, and the related formation of the potent vasoconstrictor (omega)-hydroxy arachidonic acid.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1978

Human leucocyte response to migration inhibitory activity from lymphocytes. Modification by aprotinin, Tranexamic acid and phenylmethyl sulfonylfluoride.

Human lymphokines can elicit several effects associated with inflammation, e.g. leucocyte migration inhibition and fibrinolysis. These effects can be assessed in vitro by the leucocyte migration agarose technique (LMAT) and the leucocyte migration fibrinolysis technique (LMFT). The present study shows that preincubation of normal leucocytes with aprotinin, tranexamic acid and phenyl-methyl-sulfonylfluoride (PMSF) reduces or abolishes their migration inhibition response to leucocyte migration inhibition factor. The compounds exert this effect at non-toxic concentrations, which do not otherwise interfere with migration or fibrinolysis, and are non-toxic as estimated by PHA stimulation of lymphocytes. The LMFT is more sensitive to the modifying effect than the LMAT. The effect of aprotinin and tranexamic acid is reversible, the effect of PMSF is irreversible.

Aprotinin↗
PubMed1985

Pharmacokinetics and absolute bioavailability of intramuscular tranexamic acid in man.

The bioavailability of tranexamic acid after the administration of a single intramuscular dose was estimated in three healthy male volunteers. 500 mg tranexamic acid were given intramuscularly and intravenously, as a bolus injection, to each subject on separate occasions. Following intramuscular administration, the peak plasma concentrations were attained after approximately one hour and the apparent elimination half-life was about two hours. The absolute bioavailability was 105.2 +/- 10.7% (mean +/- SD). At the dose given, the bioavailability of tranexamic acid after intramuscular administration is fast and complete.

Adult↗
PubMed1981

Effect of tranexamic acid on the growth and metastasis of V2 carcinoma in rabbits.

The antifibrinolytic action of tranexamic acid (AMCHA) on the growth and metastasis of rabbit V2 carcinoma having high fibrinolytic activity was studied. Upon oral administration of AMCHA, the growth of the tumor and metastasis to the lung tended to be inhibited, and the number of metastatic foci in the regional lymph nodes significantly decreased in the early period of tumor growth. Enhancement of fibrin deposition in the tumor and inhibition of fibrinolytic activity of the tumor were recognized in the AMCHA-treated group. The inhibitory effect of tranexamic acid on fibrin dissolution might interfere with local tumor growth and the release of tumor cells into the vessels.

Animals↗
PubMed1978

Hepatic function and fibrinolysis in patients with hereditary angioedema undergoing long-term treatment with tranexamic acid.

Prophylactic treatment with antifibrinolytic agents, epsilon-aminocaproic and tranexamic acid, reduces the incidence and severity of attacks in patients with hereditary angioedema. Long-term effectiveness or risk of antifibrinolytic agents has not been established. Sixteen patients needing continuous prophylaxis because of frequency and severity of attacks were treated with tranexamic acid. In four patients this treatment was ineffective and the drug was withdrawn after 2 months. A remission or reduction in the frequency or severity of attacks was observed in 12 patients treated for a period ranging from 8 to 34 months. Hepatic tests and blood fibrinolytic activity were not influenced by long-term oral treatment with tranexamic acid.

Adolescent↗
PubMed1984

Gamma-aminobutyric acid turnover in rat striatum: effects of glutamate and kainic acid.

The turnover rate of gamma-aminobutyric acid (GABA) in the rat striatum was estimated by measuring its accumulation after inhibition of GABA-transaminase (GABA-T) with gabaculine. Intrastriatal injections of 100 micrograms gabaculine induced a rapid and complete inhibition of GABA-T. GABA accumulation was linear with time for at least 60 min (estimated turnover rate = 25 nmol/mg protein/h). The accumulation of GABA after gabaculine administration in animals that had been treated with kainic acid (5 nmol intrastriatally, 7 days) was only 40% of the control value, indicating that a major fraction of the net increase in GABA content induced by gabaculine originates in kainic acid-sensitive neurons. Intrastriatal injection of a mixture of kainic acid (5 nmol) and gabaculine caused a net increase in striatal GABA content significantly greater than that observed in controls, suggesting that neuronal death induced by kainic acid is preceded by a period of increased neuronal activity. Glutamic acid, the putative neurotransmitter for the excitatory corticostriatal pathway, also produced a significant increase in striatal GABA accumulation when injected together with gabaculine. This effect was blocked by the administration of the glutamate receptor antagonist glutamic acid diethyl ester. The interactions between GABAergic neurons and other neurotransmitters present in the striatum were also analyzed.

Animals↗
PubMed1979

Tranexamic acid and corneal deturgescence.

Recent work has demonstrated decreased corneal thickness in patients with Fuch's dystrophy and in patients following cataract extraction who were given systemic acid. Although tranexamic acid is a known antifibrinolytic drug its mechanism in reducing corneal thickness is not known. This experiment demonstrated no increase in the rate of corneal deturgescence of swollen rabbit corneas in the specular microscope when they were perfused for three h with 1 mM or 10 mM tranexamic acid. Pre-treatment of rabbits with intravenous tranexamic acid for three days and subsequent perfusion of corneas with tranexamic acid 10 mM also did not increase the rate of corneal deturgescence when compared with controls.

Animals↗
PubMed1985

[Pharmacokinetic and pharmacological studies on cetraxate, an anti-ulcer agent].

Cetraxate hydrochloride was administered either orally or intravenously to rabbits, and its concentration in body fluids was determined by using the HPLC method. Cetraxate was easily hydrolyzed in the gastrointestinal tract and blood, and it was metabolized to p-hydroxyphenylpropionic acid (PHPA) and a new metabolite, p-hydroxybenzoic acid (PHBA). After oral administration of cetraxate hydrochloride, a large amount of unchanged drug was distributed to the gastric wall. PHPA was distributed in all the organs examined, excluding the brain. To determine whether or not the anti-ulcer action of cetraxate hydrochloride was due to the unchanged drug, PHPA, or tranexamic acid, studies with aspirin and water-immersion -induced gastric ulcers in rats were performed. As a result, it was found that tranexamic acid had an anti-ulcer action similar to that of cetraxate hydrochloride.

Animals↗
PubMed1986

Reversal of coagulopathy in Kasabach-Merritt syndrome with tranexamic acid.

An infant with a giant cavernous haemangioma developed a severe consumption coagulopathy and systemic bleeding. Replacement therapy with cryoprecipitate produced only a transient improvement in the abnormal clotting, but the addition of tranexamic acid resulted in sustained correction, permitting corrective surgery to be performed.

Afibrinogenemia↗
PubMed1977

[Result of an antifibrinolytic treatment using tranexamic acid for the reduction of blood-loss during and after tonsillectomy].

Blood loss during and after tonsillectomy was assessed in 80 patients, 40 of whom were treated with tranexamic acid. A statistically significant reduction of blood loss (28%) was observed in this group during operation. Later bleedings occurred only in 27.5% (control: 67.5%) and stopped after 2 h (mean of control: 5.6h). Bleedings in the tranexamic acid group were mild and scarcely required other hemostyptic treatment, while in the control group some patients had to be treated with etamsylate or fibrogen for a longer period to stop bleeding. Tranexamic acid appears to be an effective and well-tolerated agent for reduction of blood loss caused by local hyperfibrinolysis.

Adolescent↗
PubMed1998

Negative modultors of excitatory amino acids in episodic and chronic migraine: preventing and reverting chronic migraine. Special lecture 7th INWIN Congress.

The mechanism capable of transforming episodic migraine into chronic migraine is attributed by the authors to hyperalgesia and related neuroplastic changes, chiefly long-term potentiation, due to the action of excitatory amino acids, chiefly the ones acting at N-methyl D-aspartate (NMDA) receptor. A preeminent role has been attributed to 'third hyperalgesia', a newly observed type of hyperalgesia which is inheritable and can act as a ground for the above-mentioned mechanism of 'chronicization' of migraine. The role of primary and secondary hyperalgesia in giving redundance to neuraxial abnormalities is also discussed. The fact that NMDA noncompetitive antagonist ketamine and gabapentin, inhibitor of the neuronal synthesis of L-glutamate, can cure chronic migraine, so far considered refractory to prophylactic therapies, gives indirect but evident support to the mechanism suggested above. The antinociceptive role of the above-mentioned negative modulators of excitatory amino acids and the possible interplay between ionotropic and metabotropic receptors are also taken into consideration.

Acetates↗
PubMed2006

Phosphodiesterase inhibitors in airways disease.

Phosphodiesterases hydrolyse intracellular cyclic nucleotides, cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) into inactive 5' monophosphates, and exist as 11 families. They are found in a variety of inflammatory and structural cells. Inhibitors of PDEs allow the elevation of cAMP and cGMP which lead to a variety of cellular effects including airway smooth muscle relaxation and inhibition of cellular inflammation or of immune responses. PDE4 inhibitors specifically prevent the hydrolysis of cAMP, and PDE4 isozymes are present in inflammatory cells. Selective PDE4 inhibitors have broad spectrum anti-inflammatory effects such as inhibition of cell trafficking, cytokine and chemokine release from inflammatory cells, such as neutrophils, eosinophils, macrophages and T cells. The second generation PDE4 inhibitors, cilomilast and roflumilast, have reached clinical trial stage and have some demonstrable beneficial effects in asthma and chronic obstructive pulmonary disease (COPD). The effectiveness of these PDE4 inhibitors may be limited by their clinical potency using doses that have minimal effects on nausea and vomiting. Topical administration of PDE4 inhibitors may provide a wider effective to side-effect profile. Development of inhibitors of other PDE classes, combined with PDE4 inhibition, may be another way forward. PDE5 is an inactivator of cGMP and may have beneficial effects on hypoxic pulmonary hypertension and vascular remodelling. PDE3 and PDE7 are other cAMP specific inactivators of cAMP. PDE7 is involved in T cell activation and a dual PDE4-PDE7 inhibitor may be more effective in asthma and COPD. A dual PDE3-PDE4 compound may provide more bronchodilator and bronchoprotective effect in addition to the beneficial PDE4 effects.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1981

Pharmacokinetics and bioavailability of tranexamic acid.

Tranexamic acid 1 g was given intravenously to three healthy volunteers. Plasma concentrations decayed in three monoexponential phases. Most elimination took place during the first eight hours, giving an apparent elimination half-life of approximately two hours. Plasma clearance ranged between 110-116 ml/min. The urinary recovery of tranexamic acid exceeded 95% of the dose. Ten healthy volunteers were given tranexamic acid 2 g orally on an empty stomach, and together with a meal. Food had no influence on the absorption of tranexamic acid, as judged by comparison of the peak plasma concentration, the time required to reach the peak, the AUC from zero to six hours, and the urinary excretion data. The oral bioavailability of tranexamic acid, calculated from 24 h urinary excretion after oral and intravenous administration, was 34% of the dose.

Administration, Oral↗