[Effect of exogenous donors of nitric oxide and inhibitors of its enzymatic synthesis on experimental ischemic thrombosis in conjunctive veins of the rabbit eyes].
The beneficial action of dinitrosyl iron complex with glutathione on conjunctive veins of eyes in rabbits with experimental thrombosis of conjunctive veins has been demonstrated. Aqueous solutions of dinitrosyl iron complexes were added subconjunctively at doses of 5.4-8.1 micromole per eye. The average duration of thrombosis by the action of dinitrosyl iron complex decreased from 6.4 days in control animals to 2 days. The addition of dinitrosyl iron complex resulted in blood flow recovery in occlusive vessels and prevented ischemia and necrosis of tissues. The enhancement of hemorrhagic activity induced by dinitrosyl iron complexes was abrogated with combined addition of the nonselective NO synthase inhibitor N-nitro-L-arginine. In contrast, S-nitrosoglutathione affected adversely the veins: the duration of thrombosis in experimental thrombosis of conjunctive veins increased to 7 days. Intensive hemorhage developed in the conjunctive. The formation of protein-bound dinitrosyl iron complexes was observed by the EPR method in eye tissues after the subconjunctive or parabulbar addition of dinitrosyl iron complex with glutathione. This was not the case when the complex was injected intravenously. It was shown that dinitrosyl iron complex with glutathione induces the blockade of pellet aggregation or strengthens the fibrinolytic activity of plasma of patients with eye vessel pathology. The beneficial action of dinitrosyl iron complexes on conjunctive veins was proposed to be due to the capacity of dinitrosyl iron complexes to donate NO primarily to its biological targets. The release of free NO molecules in large amounts is not characteristic for dinitrosyl iron complexes. This process is characteristic of S-nitrosoglutathione, which sharply increases the probability of the accumulation of peroxynitrite, which produces a toxic effect on cells and tissues.
M A
MA
Arkhipova
V D
VD
Mikoian
A F
AF
Vanin
D000818:Animals; D003228:Conjunctiva / Q000098:blood supply*; D003545:Cysteine / Q000031:analogs & derivatives / Q000627:therapeutic use; D004578:Electron Spin Resonance Spectroscopy; D005130:Eye Hemorrhage / Q000188:drug therapy; D005296:Ferrous Compounds / Q000627:therapeutic use; D005342:Fibrinolysis; D005978:Glutathione / Q000031:analogs & derivatives / Q000627:therapeutic use; D006801:Humans; D006973:Hypertension / Q000150:complications; D066298:In Vitro Techniques; D007511:Ischemia / Q000150:complications*; D020030:Nitric Oxide Donors / Q000627:therapeutic use*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D010974:Platelet Aggregation / Q000187:drug effects; D011817:Rabbits; D012164:Retinal Diseases / Q000097:blood / Q000209:etiology; D026422:S-Nitrosoglutathione / Q000627:therapeutic use; D020246:Venous Thrombosis / Q000188:drug therapy* / Q000209:etiology
D005296:Ferrous Compounds; D020030:Nitric Oxide Donors; C072081:dinitrosyl-iron(II)-cysteine; C404202:dinitrosylbis(glutathione)iron(II); D026422:S-Nitrosoglutathione; D019001:Nitric Oxide Synthase; D005978:Glutathione; D003545:Cysteine