ABSTRACT
The effect of 2,2'-dipyridyl (DP) on cerebral vasospasm was investigated in a double-injection rabbit model of subarachnoid haemorrhage (SAH). Thirty-six animals were divided between four groups: control (sham-operated), SAH (model alone), SAH + DP (the SAH model in which DP dissolved in dimethyl sulphoxide [DMSO] was injected once daily for 5 days into the cisterna magna), and SAH + DMSO (the SAH model in which DMSO [vehicle] was injected daily for 5 days). There were significant differences in the basilar artery luminal area, wall thickness, neurological deficit score and vasospasm index between the SAH + DP and SAH groups. There was a significant negative correlation between arterial luminal area and arterial wall thickness, and also between the neurological deficit score and vasospasm index. Cells that were positive for terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labelling (TUNEL) and p53 expression were significantly increased in the SAH + DMSO and SAH groups, but not in the SAH + DP group, versus controls. Thus, DP may attenuate cerebral vasospasm after SAH by suppressing p53-induced apoptosis in the cerebral vessels.
Subject(s)
2,2'-Dipyridyl/pharmacology , Chelating Agents/pharmacology , Disease Models, Animal , Subarachnoid Hemorrhage/drug therapy , Vasospasm, Intracranial/prevention & control , Animals , Apoptosis/drug effects , Blotting, Western , Immunoblotting , Immunoenzyme Techniques , Male , Rabbits , Tumor Suppressor Protein p53/metabolismABSTRACT
Thiofedrine inhibited rat platelet aggregation and intraplatelet thromboxane B2 (TxB2) generation induced by arachidonic acid. The IC50 values were 0.18 and 0.21 mmol/l, respectively. Thiofedrine, 1.25-5.00 mg/kg i.v., showed a significant inhibition of rat platelet aggregation and intraplatelet TxB2 generation induced by arachidonic acid, with ID50 values of 2.4 and 3.3 mg/kg. Thiofedrine, 0.5-2.0 mg/kg i.v., reduced TxB2 generation but increased 6-keto-PGF1 alpha formation in rat plasma.
Subject(s)
6-Ketoprostaglandin F1 alpha/blood , Antithrombins/pharmacology , Oxyfedrine/analogs & derivatives , Platelet Aggregation Inhibitors/pharmacology , Platelet Aggregation/drug effects , Thromboxane B2/biosynthesis , Animals , Arachidonic Acid/pharmacology , Depression, Chemical , Female , Male , Oxyfedrine/pharmacology , Rats , Rats, Wistar , Thromboxane B2/bloodABSTRACT
This paper introduced a new method applied to repair cleft palate,in which,the bilateral buccal mucosal muscle flaps were shaped T forms and turned over to cover the fissure of palate,instead of common mucopriostrum excision and of retro-pushing method.It may push the soft palate back.The advantage is avoiding wide tearing of the mucoperiosteum of the palate,which results in the disformation of maxilla.Also we can reconstruct the suspension of levetor veli palatini,so as to repair the palate cleft functionally.
ABSTRACT
Platelet aggregation and cyclic adenosine monophosphate (cAMP) production were studied by turbidimetry and competitive protein binding assay, respectively, in rats. Thiofedrine (Thi) significantly inhibited adenosine diphosphate (ADP)-induced and thrombin-induced platelet aggregation in vitro, with IC50 values of 0.56 and 0.16 mmol/l, respectively. In vivo, Thi 1.25-5.0 mg/kg i.v. significantly inhibited ADP-induced platelet aggregation at rate of 17.1-40.3%. Thi caused a dose-dependent increase in cAMP levels in rat washed platelets. Malondialdehyde (MDA) levels in rat platelets were measured by colorimetry. Thi had an inhibitory effect on thrombin-induced platelet MDA production. The results suggest that the antiaggregatory action of Thi may be related to metabolism of arachidonic acid (AA) and elevation of cAMP levels.
