Daily prickly pear consumption improves platelet function.

Prickly pear is traditionally used by Pima Indians as a dietary nutrient against diabetes mellitus. We examined the effect of daily consumption of 250 g in 8 healthy volunteers and 8 patients with mild familial heterozygous hypercholesterolemia on various parameters of platelet function. Beside its action on lipids and lipoproteins, prickly pear consumption significantly reduced the platelet proteins (platelet factor 4 and beta-thromboglobulin), ADP-induced platelet aggregation and improved platelet sensitivity (against PGI2 and PGE1) in volunteers as well as in patients. Also plasma 11-DH-TXB2 and the WU-test showed a significant improvement in both patients and volunteers. In contrast, collagen-induced platelet aggregation and the number of circulating endothelial cells showed a significant response in patients only. No influence of prickly pear ingestion on peripheral platelet count was monitored. The dietary run-in period did not influence any of the parameters of haemostasis examined. No sex difference was seen. Prickly pear may induce at least part of its beneficial actions on the cardiovascular system via decreasing platelet activity and thereby improving haemostatic balance.

Effect of black tea on (iso-)prostaglandins and platelet aggregation in healthy volunteers.

Flavonoids among others are found in tea. Many of them were shown to exhibit antioxidative action in vitro. We examined the effect of a 1-month consumption of 500 ml black tea containing 2.0 mg quercetin. While single tea consumption 2 h after finishing the intake did not affect any of the parameters (8-epi-PGF(2 alpha) in plasma and serum, 11-DH-TXB(2) and ADP-induced platelet aggregation) examined at all, 1-week consumption and even more than 1 month regular tea intake significantly decreased most of the parameters. The effect was somewhat more pronounced for females as compared with males, the values for 11-dehydro-thromboxane B(2) (11-DH-TXB(2)) and ADP-induced aggregation reached the level of significance in females only. These data show that regular daily black tea consumption for 1 month improves platelet function and decreases thromboxane and 8-epi-PGF(2 alpha) to a varying extent indicating a reduced in vivo oxidation injury.

Regular ingestion of opuntia robusta lowers oxidation injury.

The influence of opuntia robusta (prickly pear), a traditionally used dietary nutrient against diabetes mellitus among the American Indian population, was examined in 15 young patients suffering from familial heterozygous isolated hypercholesterolemia. Oxidation injury was determined via 8-epi-PGF(2 alpha)in plasma, serum and urine. Daily consumption of 250 g broiled edible pulp of prickly pear had no influence on body weight and body fat composition. Total cholesterol was lowered (P<0.01) as was LDL-cholesterol (P<0.04). No significant changes were observed either in triglycerides or in HDL. Prickly pear induced a significant decrease in plasma (27.9+/-3.3-->25.6+/-3.2;P<0.03), serum (302.0+/-11.4-->283.2+/-14.5;P<0.0003) and urinary (355.9+/-18.4-->323.9+/-16;P<0.00002) 8-epi-PGF(2alpha)values. The findings on a decrease of 8-epi-PGF(2alpha)were more pronounced in females than in males, the highest significance being found in urine, while, in contrast, the effects on total- and LDL-cholesterol were more pronounced in males. A prerunning 4 weeks period of dietary counseling had no significant effect on either of the parameters examined. These findings indicate that the regular ingestion of opuntia robusta is able to significantly reduce in-vivo oxidation injury in a group of patients suffering from familial hypercholesterolemia. This traditional food of the American Indians thus may have a significant cardiovascular benefit.

Association of lipoprotein(a), prostaglandin I(2)--synthesis stimulating plasma factor, biological half-life of prostaglandin I(2)and high-density lipoproteins in HIV-1 infection of different stages.

Patients with human immunodeficiency virus show increased atheroembolism and premature arterial events (stroke, myocardial infarction), but no increased venous thromboembolism. This paper describes an association of elevated lipoprotein(a), a decreased prostaglandin I(2)(PGI(2)) synthesis stimulating plasma factor, diminished PGI(2)-stability in plasma and decreased high-density lipoprotein-cholesterol and apolipoprotein A. It is unclear to what extent these biochemical findings represent an acute phase reaction only or a disturbance in the prostaglandin system. Definitely, they are resulting in severe hemostatic imbalance decreasing local PGI(2)-availability with a dramatic reduction in the cytoprotective capacity favouring the onset of premature arterial events seen in some of the patients.

Hyperalphalipoproteinemia and prostaglandin I2 stability.

PGI2 is a powerful regulator of thromboresistance modulating the local platelet/vessel wall interaction. Beside the amount synthesised the availability of the biologically active compound depends on its half-life at the site of action. Plasmatic half-life of PGI2 is extremely shortened during severe infections, but also in acute myocardial infarction with extremely lowered levels of HDL-c and apoAI, the latter being described as a potential PGI2-stabilising factor. These conditions are characterised by an enhanced thrombophilic risk. This study investigated for the first time whether high levels of HDL-c (mean: 95 +/- 13 mg/dl) and apoAI (mean: 179 +/- 13 mg/dl) which have been shown epidemiologically to protect against coronary heart disease in turn might be associated with an increase in PGI2 half-life. Results were obtained from 31 healthy subjects with hyperalpha-LP as compared with 10 controls. The biological half-life of PGI2 (hyperalpha-LP: mean: 915 +/- 118 sec vs. controls: 714 +/- 70 sec; p = 0.001) was positively related to HDL-c (r = 0.8795, p < 0.001) and apoAI levels (r = 0.8025, p < 0.001). The partial correlation coefficient correcting for the association between HDL-c and apoAI levels was also significant (PGI2 to HDL-c: r = 0.6000, p < 0.001). These results suggest that the antiatherosclerotic properties of HDL might be at least partly due to an increase in PGI2 half-life.

Apolipoprotein A and biological half-life of prostaglandin I2 in HIV-1 infection.

Disturbances in lipid and lipoprotein metabolism being reported for HIV-1 infection are a common sign of severe infections. Apolipoprotein A being the main constituent protein of HDL has been described to function as the prostaglandinI2 (PGI2)-stabilising factor. PGI2 is not only one of the most potent biological antiaggregatory substances but seems to exert cell-protective properties in the central nervous system, too. PGI2 half-life as well as lipid [total-cholesterol (total-c), triglycerides] and (apo)lipoprotein [LDL-c, HDL-c and apolipoprotein (apo) AI] levels were investigated in 14 HIV-1 positive patients (13 males, 1 female, aged from 29 to 57 yrs). Patients exhibited decreased levels of total-c, LDL-c, HDL-c and apo AI, respectively, while elevated triglyceride levels were observed. PGI2 half-life was shortened (median 53, range: 15-161 seconds) in the patients' plasma as compared with normal controls ranging from 9-12 minutes. In patients with neurological manifestation (n = 8) the decrease of PGI2 half-life (median: 34 seconds, range: 15-67 seconds) was significantly more pronounced (p < 0.05) than in patients (n = 6) with the absence of any central nervous manifestation (median: 83.5, range: 29-161 seconds). The dramatic changes in both HDL-c and apolipoprotein AI as seen during HIV-1 infection are likely to impair PGI2-stabilisation thus being associated with the presence of peripheral neuropathy, dementia and haemostatic imbalance.

Lipoproteins and prostacyclin stability.

PGI2 is an important local mediator keeping circulating blood cells apart from the vessel wall, thus regulating hemostasis. Alterations of locally available amounts of this compound may be associated with either bleeding or thrombotic events. Factors influencing synthesis, transmission, and degradation coregulate the amount of biologically active PGI2 available at a certain vascular site. Plasmatic T1/2 of PGI2 is shortened either due to an inherited disorder or an acquired disease, its underlying cause being unknown. Generally, this is associated with thrombotic events and extremely low concentrations of both HDL cholesterol and apoA1. In contrast, the only patient we saw with a prolonged PGI2 T1/2 repeatedly experienced extremely severe bleeding complications. Recovery from severe diseases such as shock and malaria, for example, results in normalization of both PGI2 T1/2 and lipoprotein (HDL) and apoA values. Although these findings have not yet been verified at a molecular level, it is likely, that apoA1 contributes to the stabilization of PGI2 in human blood, thus representing one further link between lipid metabolism and hemostasis.