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Biomedical subjects

R Nikolov

Publications and source records attributed to R Nikolov.

At least 73 records · Page 4Linked to original sources
PubMed1978

The effect of papaverine on local tissue PO2 and microflow in cat brain cortex.

The effect of intracarotid and intravenous administration of papaverine on local tissue PO2 and microflow in the cat's brain surface was studied. Local tissue PO2 was measured with a multiwire surface electrode polarographically, and microflow by local hydrogen clearance method. The intracarotid infusions were made for 1, 2 and 5 min with doses of 0.1, 0.2 and 0.5 mg/kg/min papaverine, and the intravenous ones for 5 min with doses of 0.2, 0.5 and 1 mg/kg/min. The continuous intracarotid infusions showed that papaverine in the doses used distinctly increased local tissue PO2 and microcirculation of the brain surface. With the doses applied, systemic arterial pressure (SAP) changed little. It slightly decreased only during the 5 min infusions containing 0.5 mg/kg/min. The duration of the effect increased with increases in the duration of the infusion and of the dose. The maximum duration was observed with 5 min infusions and lasted for 10--15 min after drug administration was discontinued. During the i.v. infusions, tissue PO2 and microflow rose less than with intracarotid ones. No redistribution of capillary flow was observed.

Animals↗
PubMed1978

[Analgetic and anti-inflammatory action of glaucine].

The authors examined the analgetic and antiinflammatory action of glaucine. They used the following methods for evaluation the analgetic action: chemical irritation, heating plate, heat-ray irritation, mechanical irritation of the normal and inflammatory tissues, electrical irritation and analgetic test. The following methods were used for evaluation of antiinflammatory action: effect on the edema of the rat paw and granulation phases of the inflammation in rats. Codeine and acetysal were used as control drugs. The results from the experiments showed that glaucine successfully inhibited the granulation phase of inflammation and did not affect edema of the rat paw, induce by yeast beer. The analgetic action of glaucine was weak and without practical significance.

Animals↗
PubMed1976

Effect of the drug AS2 on the central and peripheral mechanisms of vascular tone regulation.

The effect of the compound AS2 (N'-benzhydryl, N''-allylpiperazine dihydrochloride) on the central and peripheral mechanisms of vascular tone regulation is studied. Six series of experiments on cats are carried out. The effect of the compound is tested on a model of central-hypertensive reaction, on the spontaneous bioelectrical activity of the renal nerve, on the transmission of excitation to the upper cervical ganglion and the ganglia of the solar plexus. Experiments are made to study its adrenolytic a-d myotropic properties. Cinnarizine is tested as control. The results show that the compound AS2, similar to Cinnarizine, affects the central and peripheral mechanisms of vascular tone regulation. In small doses (1-5 mg/kg) AS2 manifests poor myotropic properties. Administration of the drug in doses of 10-20 mg/kg results in considerable inhibition of the vasomotor centres, brief disturbances in the excitation transmission in the sympathetic ganglia and slight inhibition of adrenergic transmission.

Animals↗
PubMedDate not supplied

Study on the cerebral effects of sabeluzole.

The cerebral effects of subeluzole have been studied using the following methods: hypobaric hypoxia in mice, complete ischemia by decapitation in mice, anoxic hypoxia in mice, hemic hypoxia in rats, incomplete ischemia by bilateral carotid ligation in rats, anoxic hypoxia in rats and asphyxic hypoxia in cats. Sabeluzole was active in all the models used: it increased the survival time in hypobaric hypoxia (maximum at 40 mg/kg--by 92.0%, p less than 0.001), survival time in anoxic hypoxia in mice (maximum at 40 mg/kg--by 27.2%, p less than 0.001), gasping in decapitation model (maximum at 20 mg/kg--by 155.4%, p less than 0.001) and survival in hemic hypoxia (maximum at 2.5 mg/kg--by 21.1%, p less than 0.05). The duration of the effect as evaluated in the decapitation model was about 6 h. In incomplete ischemia in rats, however, it showed a weak effect. In anoxic hypoxia in rats, sabeluzole (5 mg/kg i.v.) increased the time latency between onset of anoxia and negative DC-shift by 20.5% and the K+e-threshold by 25.7%. In asphyxic hypoxia in cats, sabeluzole (0.5 mg/kg i.v.) counteracted the hypoxia-induced decrease of the fast-wave amplitudes during the cortical resistance period and the hypoxia-induced decrease of the slow-wave and increase of the fast wave amplitudes during the cortical recovery period.

Animals↗
PubMedDate not supplied

Cerebroprotective effect of flunarizine.

The cerebroprotective effect of flunarizine was studied using the following methods: hypobaric hypoxia in mice, complete ischemia by decapitation in mice, anoxic hypoxia in mice, hemic hypoxia in rats, incomplete ischemia by bilateral carotid ligation in rats and asphyxic hypoxia in cats. Piracetam, meclofenoxate, nicergoline, naftidrofuryl, cinnarizine and nifedipine were studied as reference drugs. Flunarizine increased the survival time in all survival models. Its effect was most pronounced in complete ischemia model, and considerably higher than that of reference drugs. In asphyxic hypoxia flunarizine increased cortical resistance and shortened cortical recovery. The EEG frequency-amplitude analysis during asphyxic hypoxia showed a significant decrease of the slow-waves amplitudes of delta and theta range, and an increase of the fast-waves amplitudes of beta-2 range, changes indicating protective action.

Animals↗
PubMedDate not supplied

Effect of prostacyclin (PGI2) on the mechanical activity of isolated longitudinal and circular muscle strips of guinea-pig stomach.

Muscle strips isolated in longitudinal and circular directions from the fundus, corpus and antrum, and from the pyloric sphincter of the guinea-pig stomach were placed in organ baths for recording their spontaneous contractility. Concentrations of the order of 10(-9) to 10(-6) M of prostacyclin (PGI2) were tested and compared with the effect of PGE1, PGE2, PGF2 alpha and acetylcholine. Furthermore, a modification of PGI2 effect was studied in the presence of adrenergic and cholinergic blocking agents, tetrodotoxin, indomethacin and the PG antagonist SC-19220. Like PGE1, PGE2, PGF2 alpha and acetylcholine, PGI2 increased the tone of the longitudinal strips from fundus, corpus and antrum, its effect being less potent than the effects of PGE1 and PGE2 and more potent than the effects of PGF2 alpha and acetylcholine. All the PGs inhibited the phasic contractions of the circular muscle of antrum and pyloric sphincter in a dose-dependent manner. These effects were not significantly changed in the presence of adrenergic and cholinergic blocking agents, nor in the presence of tetrodotoxin, and could therefore be interpreted as being myogenic in nature. Indomethacin exerted effects opposite to those of PGI2. It shifted the log concentration-effect curve for PGI2 to the right suppressing the maximum response of PGI2 by about 50%. SC-19220 reversibly inhibited the spontaneous tone and the excitatory responses of the gastric muscle to PGI2. The concentration-effect curves for PGI2 were shifted to the right in the presence of SC-19220. Analysis of the data gave the pA2 value for PGI2 5.3, the slope of Schild plot being 1.23, which suggests that SC-19220 is a competitive antagonist.

Animals↗
PubMedDate not supplied

Study on the prostaglandin antagonistic activity of aligeron and piracetam.

The interaction of aligeron and piracetam with the effects of prostaglandin F2 alpha (PGF2 alpha) E2 (PGE2) was studied using in vitro and in vivo tests for evaluation of PG antagonistic activity. Aligeron was found to be a non-selective PG antagonist in isolated guinea-pig stomach smooth muscle preparations. It antagonized the PGF2 alpha and PGE2-induced fall in blood pressure in cats prevented diarrhoea induced by PGF2 alpha in mice, inhibited rat paw oedema induced by PGE2 in rats, but did not modify the PGF2 alpha induced bronchoconstriction in guinea-pigs. Piracetam did not antagonize the smooth muscle contractile effects of PGF2 alpha and PGE2 and in the in vivo tests it inhibited only the rat paw oedema induced by PGE2. It is concluded that aligeron is active in vitro and in vivo as an antagonist of some of the actions of PGs studied. Its effect in vitro lacks selectivity and is probably due to interference with the action of Ca2+. The probable clinical implication of these results will be discussed. Piracetam can not be considered a PG antagonist.

Animals↗
PubMedDate not supplied

Protective effect of piracetam against PGF2 alpha-impaired cerebral resistance to hypoxia.

The protective effect of piracetam against PGF2 alpha-impaired cerebral resistance to hypoxia was investigated by EEG study in relaxed and artificially ventilated cats. Asphyxic anoxia was performed after 5 min of intracarotid (i.c.) or i.v. infusion of 10 micrograms/kg/min PGF2 alpha before and 30 min after piracetam (100 mg/kg i.v.). The following parameters were determined: cortical resistance (CRs)--as time between stopping the ventilation and the extinction of EEG; cortical recovery (CRc) - as time between restitution of ventilation and reappearance of brain activity; anoxia resistance index (ARI) - as the ratio between these two parameters (CRs/Crc). Both the i.c. and i.v. infusion of PGF2 alpha led to a significant decrease in CRs and lengthening of CRc which resulted in a decrease in ARI. Piracetam reverses the PGF2 alpha-induced changes in asphyxic anoxia. The possible mechanism of piracetam's effect and the probable therapeutic value of the latter are considered.

Animals↗
PubMedDate not supplied

Effect of aligeron on the cerebral venous outflow and cerebrospinal fluid pressure in dogs.

The effect of Aligeron (1-benzhydril-4-allyl-piperazine dihydrochloride) on the cranial circulation was studied in dogs under chloralose-urethan anaesthesia. The parameters followed were: venous outflow from the confluence of the cerebral sinusses (CVO), cerebrospinal fluid pressure in cysterna magna (CSFP), systemic arterial blood pressure (BP) and pulse rate (PR). CVP was measured using the technique of Rapela and Green (1964). Aligeron was applied at doses of 5 and 10 mg/kg i.v. Papaverine hydrochloride was used as a reference compound. aligeron administration at a dose of 5 mg/kg led to quick increase of the CVO with a duration of the effect approximately 30 min. CSFP also increased in a similar way. BP and PR showed insignificant changes. The administration of 10 mg/kg did not lead to an increase of its effect on CVO. Papaverine (1 mg/kg i.v.) had a weaker effect than that of Aligeron. According to the classical concepts the changes observed in our experiments were due to the cerebral vasodilator effect of Aligeron which caused a fall in cerebrovascular resistance and an increase of the intracranial blood volume. Our experiments suggest that Aligeron influenced the resistance vessels more than the capacitance ones.

Animals↗
PubMedDate not supplied

L-NAME augments the antinociceptive effects of intracerebroventricularly applied ET-1 and ET-3.

The interaction between endothelin-1 (ET-1) (5 pmol/mouse, i.c.v.) and endothelin-3 (ET-3) (5 pmol/mouse, i.c.v.) with NG-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg i.p., 30 min pretreatment) was investigated in mice by the use of two experimental procedures: hot plate and tail flick tests in mice. L-NAME showed slight insignificant antinociceptive action, but augmented significantly the antinociceptive effects of i.c.v. administered ET-1 and ET-3 in both experimental tests.

Analgesia↗
PubMedDate not supplied

Studies on the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) in brain hypoxia and on the participation of brain prostanoids in their actions.

The effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) in brain hypoxia have been studied in mice using the following experimental models: hypobaric hypoxia induced by low atmospheric pressure, histotoxic hypoxia induced by 12.5 mg/kg KCN i.p., and complete ischemia induced by decapitation. ET-1 and ET-3 were injected intracerebroventricularly (i.c.v.) 15 min before the tests. Forebrain tissue concentrations of 6-keto-PGF1 alpha and thromboxane B2 (TxB2) were measured 15 min following i.c.v. administration of ET-1 (5 pmol/mouse) and ET-3 (10 pmol/mouse). ET-1 (1-5 pmol/mouse) and ET-3 (5-25 pmol/mouse) showed a dose-dependent increase in the survival/gasping time in all models of hypoxia. The effect reached its maximum between 15 and 30 min after ET administration and lasted for about 120 min. ET-1 and ET-3 did not significantly change the brain levels of 6-keto-PGF1 alpha and TxB2. The protective effect of ET-1 and ET-3 was unexpected, because endothelins (ETs) are the most potent vasoconstrictors known, and in doses close to those used in this study they cause vasoconstriction and decrease in cerebral blood flow. The protection was not likely to be due either to stimulation of the endogenous release of prostacyclin (PGI2) or to a decrease in the deleterious prostanoid thromboxane A2 (TxA2). Additional experiments are necessary to explain the cerebroprotective effects of ET-1 and ET-3.

Animals↗