ABSTRACT
The influence of a hydrogen sulfide donor NaHS (2×10-5-10-3 M) on the rat erythrocyte deformability was analyzed by laser diffractometry. NaHS (6×10-5 M) increased, while NaHS (10-3 M) reduced erythrocyte deformability. The effect of NaHS (6×10-5 M) was similar to that of NO donor sodium nitroprusside (SNP, 10-7 M). However, simultaneous use of NaHS (6×10-5 M) and SNP induced less pronounced changes in erythrocyte deformability than their individual application. It is likely H2S, similar to NO, is involved in the regulation of erythrocyte deformability in the microvascular bed.
Subject(s)
Erythrocyte Deformability/drug effects , Erythrocytes/drug effects , Hydrogen Sulfide/pharmacology , Sulfides/pharmacology , Animals , Erythrocytes/chemistry , Erythrocytes/cytology , Hydrogen Sulfide/chemistry , Light , Male , Nitric Oxide/pharmacology , Nitroprusside/chemistry , Nitroprusside/pharmacology , Primary Cell Culture , Rats , Scattering, Radiation , Sulfides/chemistrySubject(s)
Adrenocorticotropic Hormone/analogs & derivatives , Brain Ischemia/pathology , Erythrocytes/cytology , Peptide Fragments/pharmacology , Adrenocorticotropic Hormone/pharmacology , Animals , Brain/pathology , Erythrocyte Deformability , Erythrocytes/pathology , Male , Microcirculation , Neuroprotective Agents/pharmacology , Rats , Rats, Wistar , Rheology/methods , Shear Strength , Time Factors , ViscosityABSTRACT
Contractile responses of the basilar artery to serotonin were examined in vitro on two models of circulation disturbances in the vertebrobasilar region of the brain. Two days after 30-min reversible occlusion of vertebral arteries, the sensitivity of the basilar artery to serotonin decreased, while chronic vertebrobasilar insufficiency had no effect on serotonin-induced contraction.
Subject(s)
Basilar Artery/physiopathology , Brain Ischemia/physiopathology , Rhombencephalon/physiopathology , Serotonin/pharmacology , Vertebrobasilar Insufficiency/physiopathology , Animals , RatsABSTRACT
The C-terminal fragment Pro-Gly-Pro of semax does not modulate the development of symptoms of neurological deficiency and mortality in rats with incomplete global cerebral ischemia. Hence, previously revealed neuroprotective effects of semax are mainly determined by corticotropin ACTH4-7 fragment.
Subject(s)
Brain Ischemia/prevention & control , Neuroprotective Agents/pharmacology , Oligopeptides/pharmacology , Proline/analogs & derivatives , Animals , Proline/pharmacology , RatsABSTRACT
Erythrocyte deformability was studied by laser interferometry in rats with cerebral ischemia. Ninety minutes after ligation of both common carotid arteries the erythrocyte deformability coefficient decreased by 11+/-2% in experimental group in comparison with the baseline level and by 12% in comparison with sham-operated animals and remained 16% decreased after 4 days.
Subject(s)
Brain Ischemia/blood , Erythrocyte Deformability , Animals , Hemorheology , Interferometry/methods , Rats , Rats, WistarABSTRACT
This work investigates whether nitric oxide production and lipid peroxidation contribute to the pathophysiology of ischemia and whether glycine and a novel Russian compound, Semax are neuroprotective via a mechanism involving the regulation nitric oxide (NO) and lipid peroxidation. In brief, nitric oxide and indices of lipid peroxidation were elevated following global ischemia. While glycine proved ineffective in reducing NO levels or ameliorating the neurological deficits following global ischemia, Semax proved to be highly effective in abating the rise in nitric oxide and restoring neurologic functioning.
