RESUMO
We studied the effect of radioprotector indralin (B-190) alone or in combination with monizol on BP and HR in rabbits, reduction of blood supply and spleen weight in rats and (CBA×C57Bl/6)F1 hybrids mice, and on blood loss from a wound on tip of the tail in mice. Being an α1-adrenomimetic, indralin caused hypertensive reaction with the development of bradycardia, reduced blood supply and spleen weight, and sharply reduced blood loss from the wound. Monizol as nitrate reduced BP without affecting HR and reduced blood loss from the wound. Monizol administered prior to indralin eliminated radioprotector-induced hypertensive reaction, reduced bradycardia by more than 2 times, and attenuated the effect of indralin on spleen weight and blood loss from the wound by 1.6-1.8 times. Monizol administered after indralin had no effect on shifts in peripheral blood supply caused by the radioprotector.
Assuntos
Anti-Hipertensivos/farmacologia , Hemorragia/prevenção & controle , Nitratos/farmacologia , Fenóis/farmacologia , Protetores contra Radiação/farmacologia , Baço/efeitos dos fármacos , Ferida Cirúrgica/tratamento farmacológico , Animais , Pressão Sanguínea/efeitos dos fármacos , Cruzamentos Genéticos , Esquema de Medicação , Combinação de Medicamentos , Sinergismo Farmacológico , Feminino , Frequência Cardíaca/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos CBA , Tamanho do Órgão/efeitos dos fármacos , Coelhos , Ratos , Baço/irrigação sanguíneaRESUMO
It was investigated the effect of two adamantane derivatives, memantine and 5-hydroxyadamantan-2-one (5-HA), in patients with cerebrovascular disorders. In vitro studies showed that 5-HA, unlike memantine, exhibited antiplatelet activity. Experiments showed that memantine reduced cerebral blood flow in the brain cortex of intact rats and those under conditions of transient global ischemia, whereas 5-HA only selectively improved blood flow in ischemic brain and was superior to the reference drug nimodipine. The obtained data indicate the leading role of the GABA-ergic (rather than glutamatergic mechanisms) in implementation of the anti-ischemic cerebrovascular activity.
Assuntos
Adamantano/farmacologia , Antagonistas de Aminoácidos Excitatórios/farmacologia , Hipóxia-Isquemia Encefálica/tratamento farmacológico , Ataque Isquêmico Transitório/tratamento farmacológico , Memantina/farmacologia , Adamantano/análogos & derivados , Difosfato de Adenosina/farmacologia , Idoso , Animais , Animais não Endogâmicos , Plaquetas/efeitos dos fármacos , Células Cultivadas , Córtex Cerebral/irrigação sanguínea , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/patologia , Circulação Cerebrovascular/efeitos dos fármacos , Epinefrina/farmacologia , Feminino , Humanos , Hipóxia-Isquemia Encefálica/patologia , Ataque Isquêmico Transitório/patologia , Fluxometria por Laser-Doppler , Masculino , Pessoa de Meia-Idade , Nimodipina/farmacologia , Agregação Plaquetária/efeitos dos fármacos , Ratos , Vasodilatadores/farmacologiaRESUMO
The effect of the new antimigraine drug tropoxin - the serotonin receptor (5-HT2) antagonist - on the human platelet aggregation in vitro induced by ADP (1 x 10(-5) M) and epinephrine (2.5 x 10(-6) M) was studied. Tropoxin reliably inhibited the ADP-induced platelet aggregation in a concentration range of 0.01 - 7 mg/ml. A significant inhibition effect with respect to the epinephrine-induced platelet aggregation was observed in a drug concentration range of 2 - 7 mg/ml, although a reliable antiaggregant activity was also observed below 2 mg/ml. A bolus administration of tropoxin (10 mg/kg) in rabbits decreased the ADP-induced platelet aggregation ex vivo by a factor of 1.2 - 1.4. The effect appeared 45 min after treatment and was observed during subsequent 30 min.