Pine bark extract reduces platelet aggregation

Mohsen Araghi-Niknam, Saiid Hosseini, Douglas F Larson, Peter Rohdewald, Ronald R Watson

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

The effects of long-term consumption of the bioflavonoid mixture, French maritime pine bark extract (Pycnogenol®), were assessed on aggregation of platelets from cigarette smokers and nonsmokers. Previously we showed that a single dose of Pycnogenol® 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®/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® consumption. Platelet aggregation was significant when induced in vitro by PAF. However, Pycnogenol® consumption did not change platelet aggregation, suggesting that Pycnogenol®'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®, lowering TxB2 levels to those of nonsmokers. However, Pycnogenol® had no effect on the lower levels of TxB2 in nonsmokers. These observations suggest that Pycnogenol® supplementation reduces a risk factor for cardiovascular diseases, that is, platelet aggregation in smokers. The bioflavonoids in Pycnogenol® reduced platelet aggregation stimulated by tobacco smoke. Copyright (C) 2000 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)73-77
Number of pages5
JournalIntegrative Medicine
Volume2
Issue number2-3
DOIs
StatePublished - 1999

Fingerprint

Platelet Aggregation
Thromboxane B2
Smoking
Tobacco Products
Flavonoids
Smoke
pycnogenols
Pinus
Thromboxane A2
Tobacco
Cardiovascular Diseases
Blood Platelets

Keywords

  • Bioflavonoids
  • Bleeding
  • Platelet reactivity

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Pine bark extract reduces platelet aggregation. / Araghi-Niknam, Mohsen; Hosseini, Saiid; Larson, Douglas F; Rohdewald, Peter; Watson, Ronald R.

In: Integrative Medicine, Vol. 2, No. 2-3, 1999, p. 73-77.

Research output: Contribution to journalArticle

Araghi-Niknam, Mohsen ; Hosseini, Saiid ; Larson, Douglas F ; Rohdewald, Peter ; Watson, Ronald R. / Pine bark extract reduces platelet aggregation. In: Integrative Medicine. 1999 ; Vol. 2, No. 2-3. pp. 73-77.
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abstract = "The effects of long-term consumption of the bioflavonoid mixture, French maritime pine bark extract (Pycnogenol{\circledR}), were assessed on aggregation of platelets from cigarette smokers and nonsmokers. Previously we showed that a single dose of Pycnogenol{\circledR} 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{\circledR}/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{\circledR} consumption. Platelet aggregation was significant when induced in vitro by PAF. However, Pycnogenol{\circledR} consumption did not change platelet aggregation, suggesting that Pycnogenol{\circledR}'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{\circledR}, lowering TxB2 levels to those of nonsmokers. However, Pycnogenol{\circledR} had no effect on the lower levels of TxB2 in nonsmokers. These observations suggest that Pycnogenol{\circledR} supplementation reduces a risk factor for cardiovascular diseases, that is, platelet aggregation in smokers. The bioflavonoids in Pycnogenol{\circledR} reduced platelet aggregation stimulated by tobacco smoke. Copyright (C) 2000 Elsevier Science Inc.",
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