Biomedical subjects

Jong-Shyan Wang

Publications and source records attributed to Jong-Shyan Wang.

18 recordsLinked to original sources

PubMed2006

Resveratrol attenuates oxLDL-stimulated NADPH oxidase activity and protects endothelial cells from oxidative functional damages.

trans-Resveratrol (RSV) has been shown to have cardioprotective effect during ischemia-reperfusion through reactive oxygen species (ROS)-scavenging activity. Elevated ROS has been implicated in the initiation and progression of atherosclerosis. The nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a major source of vascular ROS formation. In the present study, we show that exposure of vascular endothelial cells (EC) to oxidized low-density lipoproteins (oxLDL) results in elevations of NOX activity and cellular ROS levels. The oxLDL effects are effectively suppressed by RSV or astringinin (AST), either before or after oxLDL exposure. In this study, we show that RSV or AST treatment appears to suppress NOX activity by reducing the membrane association of gp91(phox) and Rac1, two protein species required for the assembly of active NOX complex. Exposure to RSV or AST protects EC from oxidative functional damages, including antiplatelet activity and mononucleocyte adhesion. In addition, ANG II-induced NOX activation is also attenuated. These results suggest that RSV or AST protects EC from oxLDL-induced oxidative stress by both direct ROS scavenging and inhibition of NOX activity.

Cells, Cultured↗

PubMed2006

Exercise prescription and thrombogenesis.

Lifestyle habits, such as exercise, may significantly influence risk of major vascular thrombotic events. The risk of primary cardiac arrest has been shown to transiently increase during vigorous exercise, whereas regular moderate-intensity exercise is associated with an overall reduced risk of cardiovascular diseases. What are the mechanisms underlying these paradoxical effects of vigorous exercise versus exercise training on thrombotic modification? This review analyzes research regarding effects and their underlying mechanisms of acute exercise, endurance training, and deconditioning on platelets, coagulation, and fibrinolysis. Evidence suggests that (i) light, acute exercise ( < or = 49% VO(2 max)) does not affect platelet reactivity and coagulation and increases fibrinolytic activity; (ii) moderate, acute exercise (50 to approximately 74% VO(2 max)) suppresses platelet reactivity and enhances fibrinolysis, which remains unchanged in the coagulation system; and, (iii) strenuous, acute exercise ( > or = 75% VO(2 max)) enhances both platelet reactivity and coagulation, simultaneously promoting fibrinolytic activity. Therefore, moderate exercise is likely a safe and effective exercise dosage for minimizing risk of cardiovascular diseases by inducing beneficial anti-thrombotic changes. Moreover, moderate-intensity exercise training reduces platelet reactivity and enhances fibrinolysis at rest, also attenuating enhanced platelet reactivity and augmenting hyper-fibrinolytic activity during strenuous exercise. However, these favorable effects of exercise training on thrombotic modification return to a pre-training state after a period of deconditioning. These findings can aid in determining appropriate exercise regimes to prevent early thrombotic events and further hinder the cardiovascular disease progression.

Blood Coagulation↗

PubMed2006

Role of exercise intensities in oxidized low-density lipoprotein-mediated redox status of monocyte in men.

Exercise significantly influences the progression of atherosclerosis. Oxidized LDL (ox-LDL), as a stimulator of oxidative stress, facilitates monocyte-related atherogenesis. This study investigates how exercise intensity impacts ox-LDL-mediated redox status of monocytes. Twenty-five sedentary healthy men exercised mildly, moderately, and heavily (i.e., 40, 60, and 80% maximal oxygen consumption, respectively) on a bicycle ergometer. Reactive oxygen species (ROS) production, cytosolic and mitochondrial superoxide dismutase (c-SOD and m-SOD, respectively) activities, and total and reduced-form gamma-glutamylcysteinyl glycine (t-GSH and r-GSH, respectively) contents in monocytes mediated by ox-LDL were measured. This experiment obtained the following findings: 1) ox-LDL increased monocyte ROS production and was accompanied by decreased c-SOD and m-SOD activities, as well as t-GSH and r-GSH contents, whereas treating monocytes with diphenyleneiodonium (DPI) (a NADPH oxidase inhibitor) or rotenone/2-thenoyltrifluoroacetone (TTFA) (mitochondrial complex I/II inhibitors) hindered ox-LDL-induced monocyte ROS production; 2) production of ROS and reduction of m-SOD activity and r-GSH content in monocyte by ox-LDL were enhanced by heavy exercise and depressed by mild and moderate exercise; and 3) heavy exercise augmented the inhibition of ox-LDL-induced monocyte ROS production by DPI and rotenone/TTFA, whereas these DPI- and rotenone/TTFA-mediated monocyte ROS productions were unchanged in response to mild and moderate exercise. We conclude that heavy exercise increases ox-LDL-induced monocyte ROS production, possibly by decreasing m-SOD activity and r-GSH content in monocytes. However, mild and moderate exercise likely protects individuals against suppression of anti-oxidative capacity of monocyte by ox-LDL.

Adult↗

PubMed2006

Transcriptional regulation of VCAM-1 expression by tumor necrosis factor-alpha in human tracheal smooth muscle cells: involvement of MAPKs, NF-kappaB, p300, and histone acetylation.

Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce the expression of adhesion molecules in airway resident cells and contribute to inflammatory responses. Here, the roles of mitogen-activated protein kinases (MAPKs) and NF-kappaB in TNF-alpha-induced expression of vascular cell adhesion molecule (VCAM)-1 were investigated in human tracheal smooth muscle cells (HTSMCs). TNF-alpha-enhanced expression of VCAM-1 protein and mRNA as well as phosphorylation of p42/p44 MAPK, p38, and JNK were significantly attenuated by inhibitors of MEK1/2 (U0126), p38 (SB202190), and JNK (SP600125). Transfection with dominant negative mutants of MEK1/2, ERK1, ERK2, p38, and JNK attenuated TNF-alpha-induced VCAM-1 expression. Furthermore, TNF-alpha-induced VCAM-1 expression was significantly blocked by a selective NF-kappaB inhibitor helenalin. TNF-alpha-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha was blocked by helenalin, but not by U0126, SB202190, or SP600125. VCAM-1 promoter activity was enhanced by TNF-alpha in HTSMCs transfected with VCAM-1-Luc, which was inhibited by helenalin, U0126, SB202190, and SP600125. Most surprisingly, VCAM-1 expression was also significantly blocked by a selective inhibitor of p300, curcumin. NF-kappaB transcription factor and p300 were associated with the VCAM-1 promoter, which was dynamically linked to histone H3 acetylation stimulated by TNF-alpha, as determined by chromatin immunoprecipitation assay. Moreover, the resultant enhancement of VCAM-1 expression increased the adhesion of polymorphonuclear cells (PMNs) to monolayer of HTSMCs, which was blocked by helenalin, U0126, SB202190, or SP600125. These results suggest that in HTSMCs, activation of MAPK pathways, NF-kappaB, and p300 is essential for TNF-alpha-induced VCAM-1 expression.

Acetylation↗

PubMed2006

Warm-up exercise suppresses platelet-eosinophil/neutrophil aggregation and platelet-promoted release of eosinophil/neutrophil oxidant products enhanced by severe exercise in men.

Heterotypic platelet-eosinophil/neutrophil aggregation and subsequent release of eosinophil/neutrophil oxidant products contribute to pathogenesis of conditions such as asthma and inflammatory bowel diseases. This study investigates whether warmup exercise (WUE) affects platelet-eosinophil/neutrophil interaction mediated by high-intensity exercise (HIE). Twenty-three healthy sedentary men performed on three occasions light-intensity exercise (LIE, 40%VO(2 max) for 40 min) and HIE (80%VO(2 max) for 40 min) with and without WUE (40%VO(2 max) for 20 min). Before and immediately after exercise, platelet-eosinophil and platelet-neutrophil aggregation (PEA and PNA), reactive oxygen species production of eosinophils and neutrophils (EROS and NROS) enhanced by platelets, and adhesion molecule expression on platelets, eosinophils, and neutrophils were measured. The results of this study demonstrated that HIE enhanced PEA, PNA, and platelet-induced EROS and NROS, was accompanied by increased expressions of Mac-1 on eosinophils and neutrophils and P-selectin on platelets at 5 dyne/cm(2) of shear stress, 100 microg/ml lipopolysaccharide, and 1 microM N-formylmethionyl- leucyl-phenylalanine treatments, whereas the enhancement of HIE on platelet-eosinophil/neutrophil interaction was suppressed by WUE. Conversely, LIE significantly reduced PEA and PNA, suppressed platelet-induced EROS and NROS, and down-regulated eosinophil/neutrophil Mac-1 and platelet P-selectin expressions under various stimuli and shear flow conditions. Moreover, these effects were more pronounced in platelet interaction with eosinophils than with neutrophils. It is concluded that HIE enhances hetero-aggregation, adhesion molecules expressions, and subsequent oxidative bursts mediated by platelets and eosinophils/neutrophils, this effect diminishes after WUE. However, LIE minimizes the risk of thromboinflammation.

Adult↗

PubMed2005

Effects of exercise intensity on lymphocyte apoptosis induced by oxidative stress in men.

Exercise is linked with intensity-dependent immune response. Intracellular redox status is important in programmed cell death. This study, by closely examining 18 sedentary men who exercised moderately and severely (ie. 60% and 80% VO2max, respectively) for 40 min, investigated how exercise intensities influence intracellular redox status and oxidative stress-induced apoptosis in lymphocyte. Intracellular superoxide and reduced glutathione (GSH) levels, lipid peroxidation, mitochondrial transmembrane potential (MTP), active caspases contents, phosphotidyl serine (PS) exposure, and DNA fragmentation in lymphocytes were determined. Moreover, sublethal oxidative stress was administered by treating the lymphocyte with H2O2, to closely approximate in vivo pro-oxidative conditions. Immediately or 24 h after severe exercise, (1) lymphocyte GSH level and MTP had diminished while active caspase-8, -9, and -3 contents and DNA fragmentation had risen; and (2) H2O2 induced- lymphocyte PS exposure and DNA fragmentation were enhanced. In contrast, lymphocyte MTP, caspases activation, PS exposure, and DNA fragmentation were unaltered immediately following moderate exercise, whereas GSH level rose, lipid peroxidation diminished, and H2O2 induced- PS exposure and cell damage reduced 24 h after this exercise. These results suggest that heavy exercise diminishes lymphocyte GSH content and subsequently enhances the oxidative stress-induced apoptosis. However, moderate exercise attenuates lymphocyte apoptosis induced by oxidative stress, possibly by improving intracellular anti-oxidative capacity.

Adult↗

PubMed2005

Exercise paradoxically modulates oxidized low density lipoprotein-induced adhesion molecules expression and trans-endothelial migration of monocyte in men.

Physical exercise can affect the risk of cardiovascular disease. Oxidized-low density lipoprotein (ox-LDL) promotes transendothelial migration (TEM) of monocyte, thereby accelerating the pathogenesis of atherosclerosis. This study investigated how exercise intensity affects monocyte/EC interactions under ox-LDL-mediated condition. Light- (LIE), moderate- (MIE) and high- (HIE) intensity exercise (i.e., 40%, 60%, and 80% VO2max, respectively) on a bicycle ergometer in 18 sedentary healthy men were performed on three separate occasions. Before and immediately after exercise, ox-LDL-promoted expressions of monocyte adhesion molecules and TEM of monocyte, as well as oxidation of LDL and amounts of soluble adhesion molecules in plasma were measured. Analytical results showed that (1) ox-LDL furthered monocyte L-selectin shedding and Mac-1 expression, and an attendant increase in TEM of monocyte, while treating the monocyte with Mac-1 antibody inhibited the ox-LDL-promoted TEM of monocyte; (2) under ox-LDL-treated condition, MIE increased monocyte Mac-1 and LFA-1 expressions, enhancing the TEM of monocyte, whereas HIE downregulated monocyte Mac-1 expression, suppressing the TEM of monocyte; (3) LIE decreased basal LFA-1 expression as well as basal and ox-LDL-promoted TEM of monocyte; and (4) MIE and HIE, but not LIE, elevated plasma ox-LDL level, while there were no significant changes in sL-selectin, sE-selectin, sICAM-1, and sVCAM-1 following these exercises. Therefore, we conclude that monocyte activation and subsequent TEM promoted by ox-LDL are changed by short-term exercise in an intensity-dependent manner. These findings provide a new insight into the may aid the development of suitable exercise intensity enable people to prevent early atherogenesis.

Adult↗

PubMed2004

Effects of exercise training and deconditioning on platelet aggregation induced by alternating shear stress in men.

OBJECTIVE: Alternating shear stress, which resembles the flow condition in stenotic arteries, induces platelet aggregation. This study investigated how exercise training and deconditioning influence alternating shear-induced platelet aggregation (ASIPA) and clarify the mechanisms underlying ASIPA. METHODS AND RESULTS: Thirty healthy male sedentary subjects were randomly divided into control and trained groups. The trained men were trained on a bicycle ergometer at approximately 60% of maximal oxygen consumption for 30 minutes per day, 5 days per week for 8 weeks, and then were deconditioned for 8 weeks. The experimental results indicate the following: (1) short-term strenuous exercise increases the extent of ASIPA and is accompanied by increased the von Willebrand factor (vWF) binding and P-selectin expression on platelets in both the control and trained groups, whereas the enhancement of platelet function decreases after exercise training in trained subjects; (2) at rest and immediately after exercise, ASIPA and the vWF binding and P-selectin expression on platelets are reduced by training, but remain unchanged in the control group; and (3) deconditioning reverses the effects of training on resting and postexercise state. CONCLUSIONS: Exercise training suppresses the extent of ASIPA, probably by reducing vWF binding to platelets and P-selectin expression on platelets. However, deconditioning reverses the training effects. This investigation shows that exercise training decreases resting and severe exercise-promoted platelet aggregation induced by alternating shear stress (ASIPA); moreover, this effect is accompanied by reduced the von Willebrand factor binding and P-selectin expression on platelets. However, the effects of training on ASIPA are reversed to the pretraining state after deconditioning.

Adult↗

PubMed2004

Involvement of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB in IL-1beta-induced VCAM-1 expression in human tracheal smooth muscle cells.

Interleukin-1beta (IL-1beta) has been shown to induce the expression of adhesion molecules on airway epithelial and smooth cells and contributes to inflammatory responses. Here, the roles of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-kappaB) pathways for IL-1beta-induced vascular cell adhesion molecule (VCAM)-1 expression were investigated in human tracheal smooth muscle cells (HTSMC). IL-1beta induced expression of VCAM-1 protein and mRNA in a time-dependent manner, which was significantly inhibited by inhibitors of MEK1/2 (U0126 and PD-98059), p38 (SB-202190), and c-Jun NH(2)-terminal kinase (JNK; SP-600125). Consistently, IL-1beta-stimulated phosphorylation of p42/p44 MAPK, p38, and JNK was attenuated by pretreatment with U0126, SB-202190, or SP-600125, respectively. IL-1beta-induced VCAM-1 expression was significantly blocked by the specific NF-kappaB inhibitors helenalin and pyrrolidine dithiocarbamate. As expected, IL-1beta-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha were blocked by helenalin but not by U0126, SB-202190, or SP-600125. Moreover, the resultant enhancement of VCAM-1 expression increased the adhesion of polymorphonuclear cells to a monolayer of HTSMC, which was blocked by pretreatment with helenalin, U0126, SB-202190, or SP-600125 before IL-1beta exposure or by anti-VCAM-1 antibody. Together, these results suggest that in HTSMC, activation of p42/p44 MAPK, p38, JNK, and NF-kappaB pathways is essential for IL-1beta-induced VCAM-1 gene expression. These results provide new insight into the mechanisms of IL-1beta action that cytokines may promote inflammatory responses in airway disease.

Cell Adhesion↗

PubMed2004

Effects of exercise training and detraining on cutaneous microvascular function in man: the regulatory role of endothelium-dependent dilation in skin vasculature.

This study investigated how exercise training and detraining affect the cutaneous microvascular function and the regulatory role of endothelium-dependent dilation in skin vasculature. Ten healthy sedentary subjects cycled on an ergometer at 50% of maximal oxygen uptake (VO(2max)) for 30 min daily, 5 days a week, for 8 weeks, and then detrained for 8 weeks. Plasma nitric oxide (NO) metabolites (nitrite plus nitrate) were measured by a microplate fluorometer. The cutaneous microvascular perfusion responses to six graded levels of iontophoretically applied 1% acetylcholine (ACh) and 1% sodium nitroprusside (SNP) in the forearm skin were determined by laser Doppler. After training, (1) resting heart rate and blood pressure were reduced, whereas VO(2max), skin blood flow and cutaneous vascular conductance to acute exercise were enhanced; (2) plasma NO metabolite levels and ACh-induced cutaneous perfusion were increased; (3) skin vascular responses to SNP did not change significantly. However, detraining reversed these effects on cutaneous microvascular function and plasma NO metabolite levels. The results suggest that endothelium-dependent dilation in skin vasculature is enhanced by moderate exercise training and reversed to the pretraining state with detraining.

Adaptation, Physiological↗

PubMed2004

Intense exercise increases shear-induced platelet aggregation in men through enhancement of von Willbrand factor binding, glycoprotein IIb/IIIa activation, and P-selectin expression on platelets.

Vigorous exercise transiently enhances the risk of primary cardiac arrest. Shear-induced platelet aggregation (SIPA) is an important mechanism in arterial thrombogenesis. This study investigates whether intense exercise affects SIPA, and elucidates mechanisms that underlie SIPA. Eighteen sedentary healthy men engaged in intense exercise (about 80% of maximal oxygen consumption) for 40 min on a bicycle ergometer. Platelet aggregation, binding of von Willebrand factor (vWF) to platelets, and activation of glycoprotein (GP) IIb/IIIa and expression of P-selectin on platelets induced by shear stress were analyzed both before and immediately after exercise. Analytical results demonstrated that: (1). the levels of plasma vWF antigen and activity were enhanced after intense exercise, (2). intense exercise increased either shear- or ristocetin-induced platelet aggregation and was accompanied by an increase in vWF binding to platelets and vWF-mediated GP IIb/IIIa activation at high shear flow, and (3). shear-induced P-selectin expression in the absence or the presence of exogenous vWF was enhanced by intense exercise. Therefore, we conclude that intense exercise promotes the extent of SIPA, possibly by enhancing the ability of vWF to bind to platelets and the subsequent activation of GP IIb/IIIa complexes, as well as the expression of P-selectin in response to shear stress, which in turn may augment the risk of vascular thrombosis.

Adult↗

PubMed2004

Effects of exercise training and detraining on oxidized low-density lipoprotein-potentiated platelet function in men.

OBJECTIVE: To investigate how exercise training and detraining affect oxidized low-density lipoprotein (Ox-LDL)-potentiated platelet function in men. DESIGN: Cohort study. SETTING: Department of physical medicine and rehabilitation. PARTICIPANTS: Ten sedentary men (mean age +/- standard error of the mean, 21.6+/-0.2 y) who did not engage in any regular physical activity for at least 1 year before the study. INTERVENTIONS: Subjects cycled on an ergometer at about 50% of maximal oxygen consumption for 30 minutes daily, 5 days a week, for 8 weeks, then detrained for 12 weeks. MAIN OUTCOME MEASURES: During the experimental period, blood samples from the subjects were collected before and immediately after a progressive exercise test (ie, strenuous, acute exercise) every 4 weeks. The following measurements were taken when the subjects were at rest and immediately after exercise: plasma lipid profile, plasma Ox-LDL level, and platelet aggregation and intracellular calcium concentration ([Ca2+]i) elevation induced by adenosine disphosphate (ADP) alone or simultaneous ADP and Ox-LDL addition. RESULTS: Analytical results indicated that: (1) plasma total cholesterol and LDL levels were reduced after exercise training from 151+/-7 mg/dL and 58+/-2 mg/dL to 133+/-6 mg/dL and 46+/-2 mg/dL (P<.05), respectively, whereas the plasma Ox-LDL level remained unchanged; (2) platelet aggregation and [Ca2+]i elevation promoted by 100 microg/mL of Ox-LDL were significantly increased from 70%+/-5% and 91%+/-7% of resting level to 108%+/-4% and 125%+/-3% after strenuous, acute exercise (P<.05); (3) exercise training decreased resting and postexercise 100 microg/mL Ox-LDL-potentiated platelet aggregation (ie, 31%+/-4% and 82%+/-4%, respectively; P<.05) and [Ca2+]i elevation (ie, 35%+/-6% and 71%+/-4%, respectively; P<.05); (4) detraining reversed the training effects on lipid profile and platelet function; and (5) treating the platelet with L-arginine-inhibited Ox-LDL-potentiated platelet activation during the experimental period. CONCLUSIONS: Our results suggest that 8 weeks of exercise training decreased the plasma LDL level, but failed to influence production of plasma Ox-LDL. Importantly, resting and exercise-induced Ox-LDL-potentiated platelet activation was decreased by exercise training. However, this was reversed by detraining to the pretraining level.

Adenosine Diphosphate↗

PubMed2004

Neuromuscular electric stimulation enhances endothelial vascular control and hemodynamic function in paretic upper extremities of patients with stroke.

OBJECTIVE: To investigate the effects of neuromuscular electric stimulation (NMES) on endothelial vascular control and hemodynamic function in patients in rehabilitation after acute stroke. DESIGN: Before-after trial. SETTING: Inpatients in a tertiary hospital. PARTICIPANTS: Sixteen stroke patients (11 women, 5 men) with a mean age of 60.6+/-19.5 years. INTERVENTIONS: All patients received NMES for paretic wrist extensor and flexor muscles 30 minutes daily, 5 days a week, for 4 weeks. The nonparetic upper extremities, which served as controls, did not receive NMES. MAIN OUTCOME MEASURES: Laser Doppler perfusion testing was conducted to measure cutaneous microcirculatory responses to transdermal iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), as specific endothelium-dependent and -independent vasodilators, respectively. Arterial and venous hemodynamic function was also measured by impedance plethysmography. RESULTS: Before NMES treatment, the venous capacity and compliance of the paretic extremities did not differ significantly from those of the nonparetic extremities. However, hyperemic arterial inflow, ACh-induced cutaneous perfusion, and the ratio of ACh- to SNP-induced cutaneous perfusion were lower in the paretic than in the nonparetic extremities. After NMES treatment, hyperemic arterial inflow and venous outflow increased by 21.5% and 57.2%, respectively, in the paretic extremities (P<.05). ACh-induced cutaneous perfusion and the ratio of ACh- to SNP-induced cutaneous perfusion were also significantly enhanced in the paretic extremities. In contrast, hyperemic arterial inflow decreased by 39.6% in the nonparetic extremities (P<.05), and endothelium-dependent cutaneous vasodilation also decreased significantly. CONCLUSIONS: NMES therapy may enhance the hyperemic arterial response and endothelium-dependent dilation in skin vasculature in the paretic upper extremities of patients with stroke.

Acetylcholine↗

PubMed2004

Moderate-intensity exercise suppresses platelet activation and polymorphonuclear leukocyte interaction with surface-adherent platelets under shear flow in men.

The reciprocal modulation of platelet and polymorphonuclear leukocyte (PMN) activities is important in the pathogenesis of thrombosis and inflammation. This study investigated how moderate exercise affects shear-induced platelet activation and subsequent PMNs interaction with platelet-related thrombi under shear flow. Sixteen sedentary healthy men engaged in moderate exercise (about 60% VO(2max)) on a bicycle ergometer. Platelet activation, PMNs interaction with surface-adherent platelets, and PMN-dependent inhibition of platelet activation under shear flow were measured both before and immediately after exercise. The results of this study can be summarized as follows: (1) moderate exercise was associated with lower extents of shear-induced platelet adhesion and aggregation, binding of von Willbrand factor (vWF) to platelets, and glyco-protein IIb/IIIa activation and P-selectin expression on platelet than at rest; (2) the velocity and percentage of rolling PMNs increased while the number of PMNs remaining bound to surface-adherent platelets decreased after moderate exercise; (3) although treating the PMNs with oxidized-low density lipoprotein (Ox-LDL) enhanced PMNs interaction with surface-adherent platelets, moderate exercise suppressed the enhancement of platelet-PMN interaction by Ox-LDL; (4) moderate exercise decreased platelet [Ca (2+)](i) elevation induced by ADP and platelet [Ca(2+)](i) levels mediated by PMN and Ox-LDL-treated PMN; and (5) plasma and PMN-derived nitric oxide metabolites and plasma vWF antigen and activity increased after moderate exercise, whereas plasma and platelet-derived soluble P-selectin levels remained unchanged in response to exercise. Therefore, we conclude that moderate-intensity exercise suppresses shear-induced platelet activation and subsequent PMNs adhesion to platelets deposited at sites of vascular injury under flow, thereby reducing the risks of vascular thrombosis and inflammation.

Blood Platelets↗

PubMed2004

Strenuous, acute exercise suppresses polymorphonuclear leukocyte respiratory burst under adherence to surface-adherent platelets in men.

Interaction between polymorphonuclear leukocyte (PMN) and platelets is important in the pathogenesis of thrombosis and inflammation. This study investigates how strenuous, acute exercise affects PMN oxidative burst activity under adherence to surface-adherent platelets. Thirty sedentary healthy men exercised strenuously (up to maximal oxygen consumption) on a bicycle ergometer. Before and immediately after exercise, the kinetics of oxidant production, phosphorylation of various protein kinase C (PKC) isoforms, and translocation of p47(phox) in PMNs under adherence to surface-adherent platelets were measured using fluorescence microscopy combined with computerized image analysis. Analytical results can be summarized as follows: (i) either treating the platelet with P-selectin (CD62P) and glycoprotein IIb/IIIa (CD41) antibodies or treating the PMN with beta 2-integrin (CD18) and Mac-1 (CD11b) anti-bodies and PKC zeta pseudosubstrate effectively inhibits platelet-promoted oxidant production of PMN; (ii) PMNs adhesion to surface-adherent platelets is associated with a higher amount of phospho-PKC zeta and a larger ratio of membrane to cytosolic p47(phox) than suspended PMNs; (iii) strenuous, acute exercise decreases platelet-promoted oxidant production of PMN and is accompanied by suppressed phosphorylation of PKC zeta, translocation of p47(phox), and inhibition of PKC zeta pseudosubstrate to oxidant production; (iv) no significant changes occur in PKC alpha/beta II and delta phosphorylation of adherent PMNs following this exercise. Therefore, we conclude that strenuous, acute exercise suppresses platelet-promoted oxidative burst of PMN, possibly by reducing phosphorylation of PKC zeta and translocation of the cytosolic p47(phox) to the plasma membrane, thus inhibiting the assembly and activation of NADPH oxidase in PMN.

Adult↗

PubMed2002

Tai Chi Chuan training is associated with enhanced endothelium-dependent dilation in skin vasculature of healthy older men.

OBJECTIVES: The vascular endothelium modulates vascular tone by synthesizing and metabolizing vasoactive substances. Endothelium-dependent vasodilation declines with age. This study investigated whether Tai Chi Chuan (TCC) training could enhance endothelial function in the skin vasculature of older men. SETTING: Community setting. DESIGN: Basic hemodynamic characteristics and skin vascular response to endothelium-dependent and -independent vasodilators were studied. PARTICIPANTS: Ten older men who practiced TCC, 10 older healthy sedentary men, and 12 younger healthy sedentary men. The older TCC subjects had practiced classical Yang TCC for a mean +/- standard deviation of 11.2 +/- 3.4 years; mean attendance was 5.1 +/- 1.8 times weekly. Sedentary subjects had not participated in any regular exercise training for at least 5 years. MEASUREMENTS: Different doses of 1% acetylcholine (ACh) and 1% sodium nitroprusside (SNP) were iontophoretically applied to the skin of subjects' lower legs, and cutaneous microvascular perfusion responses were determined by laser doppler measurements. Additionally, arterial and venous hemodynamic variables were measured by impedance plethysmograph. RESULTS: The older TCC group had higher lower leg arterial blood flow (LABF); LABF in response to reactive hyperemia; and lower leg venous capacity, tone and blood flow than their sedentary counterparts, but the older TCC group displayed similar arterial and venous hemodynamic variables to the younger sedentary group. The younger sedentary group had a higher ACh-induced cutaneous perfusion and a higher ratio of ACh- to SNP-induced cutaneous perfusion than the two older groups. The older TCC group showed a higher ACh-induced cutaneous perfusion and a higher ratio of ACh- to SNP-induced cutaneous perfusion than the older sedentary group. Skin vascular responses to SNP did not differ significantly between the three groups. CONCLUSIONS: Regular practice of TCC is associated with enhanced endothelium-dependent dilation in skin vasculature of older individuals. Moreover, TCC training may delay the age-related decline of venous compliance and hyperemic arterial response.

Adult↗

PubMed2002

Effect of strenuous arm crank exercise on platelet function in patients with spinal cord injury.

OBJECTIVE: To investigate the effects of arm crank exercise on various platelet functions and prostacyclin in individuals with spinal cord injury (SCI). DESIGN: Case-control study. SETTING: Research project at a hospital-based exercise physiology laboratory. PARTICIPANTS: Seven men (with lesions at levels T11, n = 1; T12, n = 2; L1, n = 2; L2, n = 2) and 3 women (T12, n = 1; L1, n = 2) in the SCI group had SCI for at least 6 weeks. Ten age- and gender-matched healthy people who had not engaged in any regular physical activity for at least 1 year were selected as the control group. INTERVENTION: All subjects exercised strenuously by using an arm crank engometer. MAIN OUTCOME MEASURE: Platelet adhesiveness on fibrinogen-coated surface and epinephrine-induced aggregation in vitro, plasma soluble P-selectin (sP-selectin), and urinary 6-keto-prostaglandin F(1alpha) (6-keto PGF(1alpha)) levels. RESULTS: The SCI group had higher platelet adhesiveness and aggregability and plasma sP-selectin level, but lower urinary 6-keto PGF(1alpha) level than the control group. Platelet adhesiveness and aggregability were enhanced by strenuous arm exercise in all subjects, but only in the SCI group was sP-selectin level increased by exercise. Strenuous exercise raised the levels of 6-keto PGF(1alpha) in control group subjects, but not in subjects with SCI. CONCLUSIONS: Individuals with SCI had more extensive basal and exercise-induced platelet activation and sP-selectin release than people without SCI. Moreover, strenuous arm exercise, which enhanced the release of prostacyclin in healthy subjects, failed to do so in those with SCI.

6-Ketoprostaglandin F1 alpha↗

PubMed2002

Suppressed cutaneous endothelial vascular control and hemodynamic changes in paretic extremities with edema in the extremities of patients with hemiplegia.

OBJECTIVE: To investigate peripheral circulatory function and its underlying mechanisms in the paretic upper extremity after a stroke. DESIGN: Case-control study. SETTING: A department of physical medicine and rehabilitation in Taiwan. PARTICIPANTS: A total of 53 hemiplegic patients (28 men, 25 women; mean age +/- standard deviation; 58.2+/-3.8y) were studied. Subjects were divided into edema and nonedema groups. The edema group included 29 hemiplegic patients with edematous paretic upper extremities. Twenty-four hemiplegic patients in the nonedema group did not suffer from limb edema in the paretic upper extremity. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Cutaneous microvascular perfusion responses to 3 grade levels of iontophoretically applied 1% acetylcholine (ACh), 1% ACh plus 1% N(G)-monomethyl-L-arginine (L-NMMA), and 1% sodium nitroprusside (SNP) in the skin of subjects' forearms were determined by laser Doppler perfusion measurements. Moreover, hemodynamic characteristics in the arterial and venous vessels were measured by impedance plethysmography. RESULTS: Resting arterial inflow and venous capacity, tone, and outflow in paretic extremities did not significantly differ from nonparetic extremities, but the hyperemic arterial inflow was lower in paretic extremities than in nonparetic extremities, and paretic extremities were associated with lower ACh- and ACh plus L-NMMA-induced cutaneous perfusions than nonparetic extremities. ACh-induced cutaneous perfusions also decreased much more significantly in edematous paretic extremities than in nonedematous paretic extremities, and skin vascular responses to SNP do not differ significantly between paretic and nonparetic extremities. CONCLUSION: Cutaneous microcirculatory function in the paretic upper extremity after stroke may be impaired. The impairment may occur because of decreased endothelium-dependent dilation in skin vasculature. Dysfunction in cutaneous microcirculation tends to be more pronounced in the edematous than in the nonedematous extremities.

Adult↗