BACKGROUND: Resveratrol has been shown to inhibit platelet aggregation. However, the mechanism for this action of resveratrol remains to be clarified. The purpose of this study was to elucidate the Ca METHODS: Ca RESULTS: Thapsigargin-induced Ca CONCLUSIONS The results suggest that resveratrol inhibits thrombin-induced platelet aggregation through decreasing Ca
Antioxidants/administration & dosage* ; Calcium/physiology* ; Humans ; Platelet Aggregation/drug effects* ; Platelet Aggregation Inhibitors/pharmacology* ; Resveratrol/pharmacology* ; Signal Transduction/drug effects*

Cardiovascular Diseases ; drug therapy ; Humans ; Platelet Aggregation Inhibitors ; administration & dosage ; adverse effects ; therapeutic use

Aspirin ; administration & dosage ; Drug Administration Schedule ; Humans ; Platelet Aggregation Inhibitors ; administration & dosage ; Stroke ; prevention & control ; Time Factors

OBJECTIVETo evaluate the efficacy and safety of anagrelide in essential thrombocythemia (ET).

METHODSPatients who diagnosed as ET according to the World Health Organization classification were enrolled. Each patient was assigned to take anagrelide hydrochloride capsule or hydroxyurea tablet by random 1∶1 ratio. Dose of anagrelide started at 2 mg/d, then increased gradually and the maximum dose was 10 mg/d until the platelet counts dropped to (100-400) × 10⁹/L, one month later gradually reduced to maintain dose. The dose of hydroxyurea was 1000 mg/d at beginning, then increased gradually, when platelet counts dropped to (100-400)×10⁹/L and kept for one month, reduced to maintain dose as 10 mg·kg⁻¹·d⁻¹. The observation period was 12 weeks.

RESULTSA total of 222 patients were enrolled in seventeen centers (including 113 patients treated with anagrelide and 109 with hydroxyurea). Therapy efficacy can be evaluated in 198 patients (including 97 patients administered with anagrelide and 101 with hydroxyurea). At 12th weeks of therapy, the hematologic remission rate was 87.63% (85/97) in anagrelide group and 88.12% (89/107) in hydroxyurea group, the differences between the two groups were not significant (P=0.173). Treatment with anagrelide lowered the platelet counts by a median of 393 (362-1 339) × 10⁹/L from a median of 827 (562-1657) × 109/L at the beginning of the observation to 400(127-1130)×10⁹/L after 12 weeks (P<0.001), which were similar to the treatment result of hydroxyurea by a median drop of 398 (597-1846)× 10⁹/L (P=0.982). The median time to achieving response of anagrelide group was 7 (3-14) days, superior to that of hydroxyurea for 21 (14-28) significantly (P=0.003). Frequency of anagrelide related adverse events was 65.49 % (74/113), including cardiopalmus (36.28% ), headache (21.24% ), fatigue (14.16% ) and dizzy (11.50% ).

CONCLUSIONAnagrelide was effective in patients with ET which had similar hematologic remission rate to hydroxyurea and could take effect more quickly than hydroxyurea. Incidence of adverse events was undifferentiated between anagrelide and hydroxyurea, but anagrelide treatment had tolerable adverse effects and no hematologic toxicity.

Humans ; Hydroxyurea ; administration & dosage ; therapeutic use ; Platelet Aggregation Inhibitors ; administration & dosage ; therapeutic use ; Platelet Count ; Quinazolines ; administration & dosage ; therapeutic use ; Thrombocythemia, Essential ; drug therapy ; Treatment Outcome

OBJECTIVETo explore the in vitro anti-platelet effects of Ginsenoside -2A,a purified extract from Panax notoginseng.

METHODSPlatelet rich plasma (PRP) was prepared routinely from venous blood samples of patients with essential hypertension and normal persons. PRP was incubated with different concentrations of Nifedipine, Ginsenoside-2A ,and SK&F96365. Maximal platelet aggregation rate[ PAG (M) ] induced by 2 micromol/L ADP was taken as the observed index. Five-minute PAG( M) was determined for 5 consecutive times.

RESULTS(1) PAG (M) in essential hypertension group was 0. 89 +/- 0. 06, which was higher than that in the normal group (0. 68 +/-0. 07 ) with significant difference (P <0.01). (2)Nifedipine of two concentrations (10 p.mol/L,20 pVmol/L) had no effect on PAG(M) in either essential hypertension group or normal group(P >0. 05). (3)Different concentrations of SK&F96365 (2.5 micromol/L,5 micromol/L,10 micromol/L and 20 micromol/L) could inhibit the PAG(M) in essential hypertension group; (4) Differen concentrations of Ginsenoside -2A (2. 5 micromol/L, 5 micromol/L, 10 micromol/L and 20 micromol/L) could inhibit PAG ( M) in essential hypertension group; three concentrations of Ginsenoside -2A (5 micromol/L, 10 micromol/L, 20 micromol/L) could inhibit the PAG(M) in the normal group (all P <0.05).

CONCLUSIONPlatelet aggregating function in essential hypertension patients was obviously higher than that in the normal persons and platelets was in the high reactive status. Nifedipine had no inhibitive effect on platelet aggregation. SK&F96365 could inhibit the platelet aggregation. Ginsenoside-2A could inhibit platelet aggregation, and had the definite anti-platelet action.

Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; Ginsenosides ; administration & dosage ; pharmacology ; Humans ; Imidazoles ; administration & dosage ; pharmacology ; Nifedipine ; administration & dosage ; pharmacology ; Platelet Aggregation Inhibitors ; administration & dosage ; pharmacology

OBJECTIVETo investigate the effect of early high-loading-dose tirofiban on platelet activity for patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention.

METHODSA total of 120 acute STEMI patients were treated with 300 mg aspirin and 600 mg loading dose clopidogrel and randomized to high-dose tirofiban (25 µg/kg bolus followed by 0.15 µg×kg(-1)×min(-1) infusion for 36 hours, n = 40), standard-dose tirofiban (10 µg/kg bolus followed by 0.15 µg×kg(-1)×min(-1) infusion for 36 hours, n = 40) or control (no tirofiban, n = 40) before angiography. Inhibition of platelet aggregation (IPA) was assessed before angiography, at 10 min and 24 hours after tirofiban infusion, and at 12 and 24 hours after stopping tirofiban infusion by the thrombelastography assay.

RESULTSThere was no significant difference in baseline of IPA between the 3 groups (P > 0.05). IPA was significantly higher in high-dose tirofiban group compared with standard-dose tirofiban and no tirofiban group at 10 minutes after tirofiban infusion [(84.2 ± 12.0)% vs. (67.8 ± 26.8)% and (31.5 ± 21.9)%, all P < 0.01]. At 24 hours after tirofiban infusion, the IPA of high-dose and standard-dose tirofiban was similar [(93.0 ± 9.8)% vs. (88.5 ± 18.1)%, P > 0.05] and was significantly higher than no tirofiban group [(40.4 ± 22.8)%, all P < 0.01]. IPA was similar at 12 and 24 hours after stopping tirofiban use among the 3 groups (all P > 0.05). The maximum amplitude of high-dose tirofiban and standard-dose tirofiban groups at different time points was similar (all P > 0.05), and maximum amplitude in both tirofiban groups was significantly lower than in no tirofiban group at 10 min [(47.2 ± 7.6) mm and (50.0 ± 9.8) mm vs. (57.7 ± 6.5) mm, all P < 0.01] and at 24 hours after stopping tirofiban infusion [(54.6 ± 5.6) mm and (54.3 ± 9.0) mm vs. (59.6 ± 4.0) mm, all P < 0.01].

CONCLUSIONEarly use of high-loading-dose of tirofiban on top of 600 mg loading dose clopidogrel is more efficient on inhibiting platelet activity than standard dose of tirofiban in patients with acute STEMI undergoing primary primary percutaneous coronary intervention.

Aged ; Blood Platelets ; Emergency Treatment ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; drug therapy ; physiopathology ; Percutaneous Coronary Intervention ; Platelet Activation ; Platelet Aggregation ; Platelet Aggregation Inhibitors ; administration & dosage ; therapeutic use ; Treatment Outcome ; Tyrosine ; administration & dosage ; analogs & derivatives ; therapeutic use

Acute Coronary Syndrome ; drug therapy ; Angioplasty, Balloon, Coronary ; Aspirin ; administration & dosage ; Humans ; Platelet Aggregation Inhibitors ; administration & dosage ; Thrombelastography ; Ticlopidine ; administration & dosage ; analogs & derivatives ; Tyrosine ; administration & dosage ; analogs & derivatives

OBJECTIVETo observe the effect of Tongxinluo Capsule (TXL) on platelet aggregation in patients with cerebral infarction, and to explore its underlying mechanisms.

METHODSSeventy-four patients with cerebral infarction at the rehabilitation stage were assigned to two groups according to taking or not taking aspirin at hospitalization, the 30 patients in group A were administered with TXL alone and the 44 in group B with TXL combined with aspirin. Platelet aggregation tests induced by adenosine diphosphate, epinephrine, collagen and arachidonic acid were conducted in all patients to evaluate the effect of TXL on platelet aggregation.

RESULTSPlatelet aggregation rate induced by adenosine diphosphate and epinephrine decreased after treatment in Group A from 88.5 +/- 4.9 and 92.9 +/- 3.1 to 80.9 +/- 16.5 and 91.8 +/- 4.0 respectively (P <0.05 ); that induced by adenosine diphosphate and arachidonic acid decreased after treatment in Group B from 66.9 +/- 13.5 and 22.7 (13.5 - 32.6) to 62.0 +/- 16.3 and 17.7 (10.2 - 23.7) respectively (P < 0.05 and P < 0.01). Cases of aspirin resistance reduced in Group B from 20 (45%) to 10 (23%), also showing statistical difference (P <0.05). No obvious increase of side effect was found after combined use of TXL with aspirin.

CONCLUSIONTXL has anti-platelet aggregation effect, its mechanism may be related with the inhibition of adenosine diphosphate and arachidonic acid path. It is relatively safe when used in combination with aspirin.

Aged ; Aged, 80 and over ; Aspirin ; administration & dosage ; Capsules ; Cerebral Infarction ; drug therapy ; physiopathology ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Humans ; Male ; Middle Aged ; Platelet Aggregation ; drug effects ; Platelet Aggregation Inhibitors ; administration & dosage ; Treatment Outcome

Using sustained release tablets of Ginkgo bibolia extract as model drug,discuss technical feasibility of using biotic index to evaluate sustained release tablets. Chosing two pharmacological indicatrix: antioxidant ability and inhibition of platelet aggregation, to investigate the influence factors on experimental result, optimize the method and experiment condition, and set up pharmacological indicatrix evaluation method. Using those methods to determinate biological effects of dissolved liquid. Drawing release curves and biological effects curves, discussing their correlation. A good correlation was observed, illustrating that pharmacological indicatrix could evaluate sustained release tablets.
Animals ; Antioxidants ; administration & dosage ; chemistry ; Delayed-Action Preparations ; Female ; Ginkgo biloba ; chemistry ; Male ; Plant Extracts ; administration & dosage ; chemistry ; Platelet Aggregation Inhibitors ; administration & dosage ; chemistry ; Rabbits ; Tablets

OBJECTIVETo observe the protective effect of Kang Naoxueshuan Tablet (KNT) on ischemic brain injury in rats, and explore its possible mechanism.

METHODSRats were administrated with KNT twice per day for successive 14 days. Rat model of acute focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO) with a nylon suture inserted through the right internal carotid artery to occlude the beginning of middle cerebral artery. After 24 hrs MCAO, the neurological deficit and the volume of cerebral infarct were observed, and the effect of KNT on the thrombosis of rats in vitro, platelet aggregation and blood viscosity were also determined.

RESULTSKNT could alleviate volume of cerebral infarct caused by focal cerebral ischemia in a dose-dependent manner and improve neurological symptoms. The volume of cerebral infarct was 11. 18 +/- 3. 35% , 14. 60 +/- 7.00% and 15. 37 +/- 7. 21% in the high, middle and low-dose groups, respectively, and they were decreased 59. 36% , 46. 93% and 44. 13% than that in the model group 27. 51 +/- 4. 71% (P <0. 01 ). The wet and dry weigh of thrombosis in vitro of the three different dose groups were significantly decreased, and they were significantly different than that of the model group (P <0. 05, P <0. 01). KNT could significantly inhibit platelet aggregation induced by ADP and decrease blood viscosity, but it had no effect on plasma viscosity and hematocrit.

CONCLUSIONKNT has significant protective effect on ischemia, the mechanism is relateed to the improvement of blood viscosity and inhibiti on of platelet aggregation. But the exact mechanisms need to be probed into deeply.

Animals ; Blood Viscosity ; drug effects ; Brain Ischemia ; blood ; drug therapy ; Medicine, Chinese Traditional ; Platelet Aggregation ; drug effects ; Platelet Aggregation Inhibitors ; administration & dosage ; therapeutic use ; Protective Agents ; administration & dosage ; therapeutic use ; Rats ; Tablets