The effects of short-term training on platelet functions and total antioxidant capacity in rats.

The purpose of the present study was to investigate the effect of short-term endurance training on plasma total antioxidant status (TAS) and on in vitro platelet aggregation and ATP release. Blood samples were collected from the abdominal aorta of rats following short-term treadmill exercise (25 m/min, 0 % grade, 30 min) for three consecutive days, as well as in non-exercised control group. Platelet aggregation and platelet ATP release were evaluated by impedance and bioluminescence techniques, respectively. Plasma TAS was measured spectrophotometrically. Plasma TAS was higher and ADP-induced platelet ATP release was lower in the short-term training group with respect to the control group (p<0.001). Significant negative correlation (r = -0.56, p<0.05) was found between plasma TAS and ADP-induced platelet ATP release. Neither ADP- and collagen-induced maximum aggregation rate nor collagen-induced platelet ATP release were significantly different between the groups. According to these results, short-term training caused an alteration in platelet functions limited to the secretion response, which may be related to the oxidant/antioxidant balance changes favoring the antioxidants. The improved plasma total antioxidant capacity was possibly sufficient to prevent exercise-induced oxidative damage, and the adaptive response of platelets might be associated with enhanced antioxidant status.

Effect of submaximal and incremental upper extremity exercise on platelet function and the role of blood shear stress.

INTRODUCTION: Platelets are involved in the pathogenesis of atherosclerosis. Although physical exercise is recommended to prevent atherosclerosis, the effect of exercise on platelet function and the underlying mechanisms of these effects are not completely understood. Accordingly, we aimed to examine the effect of different intensities acute arm exercises on platelet function. In addition, we evaluated the effect of lipid peroxidation and fluid shear rate on platelet response. MATERIALS AND METHODS: Twenty four healthy sedentary male volunteers aged 18-24 years performed submaximal and incremental exercises by upper extremity ergometer. The shear rate in the right artery was measured by Power Doppler Ultrasound (US) at rest and immediately after exercise. Pre and postexercise maximum intensities of ADP and collagen-induced platelet aggregation were measured using the impedance technique. Bioluminescent detection of thrombin-induced platelet ATP release and measurement of thromboxane B(2) (TxB(2)) levels (as a marker of thromboxane A(2) (TxA(2)) formation) by enzyme-linked immunoassay were performed before and after exercise. RESULTS AND CONCLUSION: Shear rate increased after both submaximal and incremental exercise. Collagen-induced platelet aggregation increased after submaximal exercise, while ADP-induced aggregation and thromboxane B(2) levels did not alter with this protocol. Incremental exercise caused increased collagen and ADP-induced platelet aggregation and thromboxane B(2) levels. Neither of the protocols altered platelet ATP release. It was shown that acute upper extremity exercise increased platelet aggregation, without an increase in platelet release. Collagen-induced signalling pathways were more sensitive than those induced by ADP. The increase in thromboxane B(2) after incremental exercise implied increase in thromboxane A(2) formation and lipid peroxidation. Despite a significant correlation between platelet aggregation and thromboxane B(2) levels at rest, we found no clear-cut relationship between thromboxane A(2) formation, blood shear rate and platelet response to exercise.

Effects of platelet-activating factor and hyperbaric oxygenation on antioxidant defense and duodenal contractility.

Platelet-activating factor (PAF) is a phospholipid mediator with potent biological effects on organisms. Some investigators have previously postulated that PAF exerts its effects by producing oxygen free radicals. The aim of this study was to investigate the effects of PAF on intracellular antioxidant enzyme activities and on duodenal muscle contractility. The effects of hyperbaric oxygenation (HBO2) on the response to PAF were also investigated. Two experimental sets were designed. Each experimental set comprised two groups and each group consisted of six animals. The first group of the first experimental set to which only isotonic NaCl solution (serum physiologic, SP) was injected was named the control group. The second group of the first experimental set to which only PAF was administrated was named the PAF group. Blood samples and duodenum segments of both groups were obtained 2 h after the administration of PAF or SP. We observed that acetylcholine (ACh)-induced duodenal muscle contractions were more effective in the PAF group than those in the control group. Erythrocyte catalase and glutathione peroxidase (GPx) activities were found to be lower. In the second experimental set, rats administered PAF, and rats administered SP were exposed to HBO2. In both groups of this set, contractile responses to ACh were found to be significantly increased. We found that erythrocyte GPx activities were lower and erythrocyte superoxide dismutase activities were higher than in the control group. These data support the hypothesis that PAF produces free oxygen radicals and that HBO2 enhances this effect.

Does the platelet-activating factor affect the antioxidant defense system? The possible role of hyperbaric oxygenation.

The platelet-activating factor (PAF) is an inflammatory mediator and it may exert some of its effects by reactive oxygen species (ROS). We investigated the effects of PAF and hyperbaric oxygenation (HBO) on copper (Cu) and zinc (Zn) levels in plasma and the intracellular antioxidant enzyme activities of rats. PAF administration caused a decrease in erythrocyte catalase (CAT) and glutathione peroxidase (GPx) activities and in the plasma zinc level. Following PAF administration, exposure to HBO also caused a decrease in erythrocyte GPx activity. These results support the hypothesis that PAF may produce free oxygen radicals and HBO enhances this effect. The enzyme activities of the antioxidant defense system were found to be affected by these oxidative processes. This is likely to be the result of excessive production of ROS or overutilization and/or inhibition of the antioxidant enzymes.

Platelet aggregation in traumatic spinal cord injury.

STUDY DESIGN: Collagen-induced platelet aggregation and platelet count of ten paraplegic patients (four females, six males, aged 16 - 42 years) with traumatic spinal cord injury (SCI) (posttraumatic 12 - 48 weeks) and of ten age-matched healthy volunteers (control group; five females, five males, aged 18 - 37 years) were investigated. OBJECTIVES: Investigation of platelet aggregation in the whole blood of the patients with SCI. SETTING: Ankara/Turkey. METHODS: Platelet aggregation was evaluated by impedance technique using Chrono Log Model 560 WB aggregometer in whole blood. Platelet count was determined by Medonic Cell Analyser 610. RESULTS: Maximal intensity of collagen-induced platelet aggregation of the patients was 18.50+/-8.28 ohm (mean+/-SD) and of the controls was 7.60+/-4.25 ohm. Maximal rate of collagen-induced aggregation of platelets from the patients was 3.98+/-1.59 ohm/min, maximal rate of aggregation of platelets from the controls was 1.57+/-1.01 ohm/min. Platelet counts of the patients and controls were 290 500+/-50 357/mm3 and 273 000+/-48 343/mm3 respectively. It was determined that both maximal rate (P<0.001) and maximal intensity (P<0.01) of collagen-induced platelet aggregation of the patients were significantly higher than those of the controls. There was no significant difference between the two groups in respect to platelet counts. CONCLUSION: Collagen-induced platelet aggregation of patients with traumatic SCI 12 - 48 weeks after the trauma was significantly higher than that of the controls. Our results indicate that increased tendency of platelet aggregation, which is probably induced by free radicals, may have a great impact on the late thromboembolic complications reported in patients with traumatic SCI.

Platelet aggregation and release function in hyperbaric oxygenation.

The aim of the study was to investigate the acute and chronic effects of hyperoxygenation on platelet aggregation and adenosine triphosphate (ATP) release. To observe the acute effects of hyperbaric oxygen (HBO2), seven New Zealand rabbits were exposed to 2.4 atm abs oxygen for 90 min (group 1). Eight other rabbits were further exposed to O2 daily for 20 days (group 2) to observe the chronic effects of HBO2. Adenosine diphophate (ADP) and collagen-induced platelet aggregation and ATP release were evaluated before and after oxygenation in groups 1 and 2. It was found that the maximal rate of ADP and collagen-induced platelet aggregation decreased after hyperbaric oxygenation in group 1. No significant alteration was observed in platelet responses at the end of 20 days of oxygenation in group 2. The adaptation of platelets of 2.4 atm abs O2 after 20 days of exposure seems to need further investigation.