Pine bark extract reduces platelet aggregation due to tobacco smoking
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Araghi-Niknam
M , Hosseini
S , Larson
D , Rohdewald
P , Watson
RR The effects of long-term consumption of the bioflavonoid mixture, French maritime pine bark extract (Pycnogenol(R)), were assessed on aggregation of platelets from cigarette smokers and nonsmokers. Previously we showed that a single dose of Pycnogenol(R) reduced platelet aggregation in cigarette smokers in a dose-response fashion. Cigarette smoking increased platelet reactivity aggregation when measured 2 h after smoking the first cigarette of the day. Blood was collected immediately before and 5 min after smoking three cigarettes each. Smoking increased platelet aggregation (1.17 +/- 0.04). However 200 mg Pycnogenol(R)/day, taken 3 h prior to first cigarette for the day for 2 months, significantly (p <.0023) reduced smoke-induced platelet aggregation (0.98 +/- 0.05) to the level of nonsmokers. In a group of 19 nonsmokers, platelet aggregation was measured during in vitro stimulation by platelet aggregation factor (PAF) after 4 or 8 weeks of 200 mg/day of Pycnogenol(R) consumption. Platelet aggregation was significant when induced in vitro by PAF. However, Pycnogenol(R) consumption did not change platelet aggregation, suggesting that Pycnogenol(R)'s regulation of aggregation is by another mechanism. Thromboxane A2 (TxA2) is increased in smokers by release from platelets and rapidly becomes thromboxane B2 (TxB2). Smoking increased TxB2, which was prevented by Pycnogenol(R), lowering TxB2 levels to those of nonsmokers. However, Pycnogenol(R) had no effect on the lower levels of TxB2 in nonsmokers. These observations suggest that Pycnogenol(R) supplementation reduces a risk factor for cardiovascular diseases, that is, platelet aggregation in smokers. The bioflavonoids in Pycnogenol(R) reduced platelet aggregation stimulated by tobacco smoke. Inhibition of smoking-induced platelet aggregation by aspirin and pycnogenol. Pätter
M , Grotemeyer
KH , Wärthwein
G , Araghi-Niknam
M , Watson
RR , Hosseini
S , Rohdewald
P The effects of a bioflavonoid mixture, Pycnogenol, were assessed on platelet function in humans. Cigarette smoking increased heart rate and blood pressure. These increases were not influenced by oral consumption of Pycnogenol or Aspirin just before smoking. However, increased platelet reactivity yielding aggregation 2 hours after smoking was prevented by 500 mg Aspirin or 100 mg Pycnogenol in 22 German heavy smokers. In a group of 16 American smokers, blood pressure increased after smoking. It was unchanged after intake of 500 mg Aspirin or 125 mg Pycnogenol. In another group of 19 American smokers, increased platelet aggregation was more significantly reduced by 200 than either 150 mg or 100 mg Pycnogenol supplementation. This study showed that a single, high dose, 200 mg Pycnogenol, remained effective for over 6 days against smoking-induced platelet aggregation. Smoking increased platelet aggregation that was prevented after administration of 500 mg Aspirin and 125 mg Pycnogenol. Thus, smoking-induced enhanced platelet aggregation was inhibited by 500 mg Aspirin as well as by a lower range of 100-125 mg Pycnogenol. Aspirin significantly (p<0.001) increased bleeding time from 167 to 236 seconds while Pycnogenol did not. These observations suggest an advantageous risk-benefit ratio for Pycnogenol. Product Source: http://www.suvida.com Disclaimer: The
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