[Prostaglandin-like inhibitors of prostaglandin-H-synthase]. / Prostaglandinopodobnye ingibitory prostaglandin-H-sintazy.

The effect of none prostaglandin-like cyclopentanone derivatives on the prostaglandin H synthase activity was studied. Seven substances proved to be inhibitors of the enzyme, some of the being similar to the well-known nonsteroid antiinflammatory drugs with respect to their inhibitory activity.

[2-component inhibition of prostaglandin H synthetase by nonsteroidal anti-inflammatory preparations]. / Dvukhkomponentnoe ingibirovanie prostaglandin-H-sintetazy nesteroidnymi protivovospalitel'nymi preparatami.

A combined effect on the irreversible inhibitor aspirin and fast reversible inhibitors ibuprofen, naproxen and sodium salicylate on prostaglandin-H-synthetase was studied on microsomal fractions from ram vesicular glands. The fast reversible inhibitors were shown to bind to prostaglandin-H-synthetase at the same site as aspirin and thereby to protect the enzyme against irreversible inactivation by aspirin.

[Nature of the interaction of voltaren and other pyrazolone and aniline derivatives with prostaglandin endoperoxide synthetase]. / O kharaktere vzaimodeistviia vol'tarena i nekotorykh proizvodnykh pirazolona i anilina s éndoperoksiprostaglandinsintetazoi.

A study was made of the nature and mechanism of interaction of voltaren, butadion, analgin, phenacetin and paracetamol with endoperoxide prostaglandin synthetase (PGH-synthetase) of sheep vesicular glands. Activity of the enzyme was measured by polarography with the aid of a Clark's electrode. Butadion and analgin reversibly inhibited PGH-synthetase at concentrations of the order of 10(-4) M, whereas voltaren at those of the order of 10(-6) M. As regards the mechanism of action, butadion and analgin are competitive inhibitors of PGH-synthetase in respect to arachidonic acid and uncompetitive inhibitors in respect to the electron donor adrenaline. Phenacetin administered at concentrations up to 4 X 10(-2) M did not inhibit PGH-synthetase, whereas paracetamol (10(-3)-10(-2) M) increased its catalytic activity, apparently due to the electron donor properties.

[Mechanism of ibuprofen and naproxen interaction with endoperoxide prostaglandin synthetase]. / O mekhanizme vzaimodeistviia ibuprofena i naproksena s éndoperoksidprostaglandinsintetazoi.

The authors studied the pattern and mechanism of ibuprophen and naproxen interaction with endoperoxideprostaglandin synthetase (PGH synthetase) of sheep vesicular glands. The enzymatic activity of PGH synthetase was determined polarographically with the aid of a Clark electrode. Ibuprophen and naproxen were found to inhibit completely PGH synthetase at concentrations of the order of 1 X 10(-5) M. As regards the mechanism of action both the drugs are competitive inhibitors of this enzyme with reference to arachidonic acid and incompetitive inhibitors with reference to adrenaline, an electron donor.

[Mechanisms of interaction of acetylsalicylic acid and indomethacin with endoperoxide prostaglandin synthetase]. / O mekhanizmakh vzaimodeistviia atsetilsalitsilovoi kisloty i indometatsina s éndoperoksidprostaglandinsintetazoi.

A study was made of the character and kinetics of interaction of acetylsalicylic acid and indomethacin with endoperoxide prostaglandin synthetase (PGH-synthetase) of sheep vesicular glands and human platelets. Enzymatic activity of PGH-synthetase was determined polarographically with the aid of Clark's electrodes. Acetylsalicylic acid was found to inhibit PGH-synthetase of sheep vesicular glands and human platelets at concentrations of the order of 1 x 10(-6) and 1 x 10(-4) M, whereas indomethacin at concentrations of 1 x 10(-6) and 1 x 10(-7) M, respectively. Acetylsalicylic acid inhibited PGH-synthetase from sheep vesicular glands and that from human platelets at an equal rate. Indomethacin inhibited the enzyme from sheep vesicular glands to a higher degree. Indomethacin reversibly interacted with PGH-synthetase. Meanwhile acetylsalicylic acid inhibited this enzyme irreversibly.

On some properties of a new steroid curare-like compound pipecurium bromide.

In experiments on cats it has been shown that 2 beta, 16 beta-bis (4'-dimethyl-1'-piperazino)-3 alpha, 17 beta-diacetoxy-5 alpha-androstane dibromide (pipecurium bromide, RGH-1106, Arduan), is a non-depolarizing muscular blocker. The order of myorelaxation evoked by this agent is characteristic: first the chewing and limb muscles, then abdominal muscles and diaphragm and at the end intercostal muscles are relaxed. Pipercurium bromide has no cardiotropic, atropine-like, or ganglion-blocking activity. It fails to influence the coronary blood-supply or myocardial oxygen consumption. No acetylcholinesterase inhibiting action of the compound was seen. It does not affect the central nervous system.

[Effect of prostaglandins E, A1 and F2 alpha on local brain blood circulation in non-narcotized animals]. / Vliianie prostaglandinov E, A1 i F2 al'fa na lokal'noe mozgovoe krovoobrashchenie u nenarkotizirovannykh zhivotnykh.

The effect of prostaglandins (PG) E1, A1, and F2 alpha on the systemic arterial blood pressure, local brain circulation, vascular resistance and oxygen tension in the motor region of the cortex, reticular formation and ventromedial nucleus of the hypothalamus was studied in experiments on non-narcotizied rabbits. Intravenous administration of PGE1 (10 microgram/kg/min); PGA1 (50 microgram/kg/min) and PGF2 alpha (50 microgram/kg/min) produced systemic hypotension accompanied by reduction of the local brain blood flow, vascular resistance and oxygen tension in the cortex and subcortical structures. The most pronounced changes in the systemic arterial blood pressure and local brain blood flow were recorded after PGE1 administration, these changes being less marked after PGA1 and PGF2 alpha injections.

[Evaluation of the pharmacological properties of a new steroid curarelike agent, RGH 1106]. / Otsenka nekotorykh farmakologicheskikh svoistv novogo steroidnogo kurarepodobnogo sredstva RGH 1106.

Tests on cats showed the compound RGH 1106 to possess an antidepolarizing mechanism of action. The sequence of myorelaxation, arising under the effect of this agent, is characterized by relaxation in the first place of the musculus masseter, muscles of limbs, then of abdominal muscles and those of the diaphragm and, finally, of the intercostal muscles. RGH 1106 doses not possess cardiotropic m-cholinolytic action, does not exert a ganglion blocking effect, nor affects the central nervous system. It neither changes the blood supply of the myocardium and the uptake of oxygen by the latter, nor inhibits the acetylcholinesterase.