PubMed Health⌕ Search

Biomedical subjects

H T Yang

Publications and source records attributed to H T Yang.

At least 19 recordsLinked to original sources
PubMed2006

The Y2 receptor mediates increases in collateral-dependent blood flow in a model of peripheral arterial insufficiency.

We have utilized a rat model of peripheral artery disease (PAD) to examine whether the known angiogenic activity of the Y(2) receptor would translate into a meaningful increase in collateral blood flow. The maximal increase in collateral blood flow capacity of approximately 60% (p<0.001) was obtained with a 10microg/kgday (IA infusion, 14 days) of either PYY or PYY(3-36) and did not differ from that obtained with a maximally angiogenic dose of VEGF(165). Pharmacodynamic modeling based upon single dose pharmacokinetic plasma profiles of both agonists suggests that E(max) is reached when the Y(2) receptor is occupied by >or=50%. Furthermore, for PYY(3-36), occupancy of the Y(2) receptor is sufficient to promote a significant benefit in collateral blood flow.

Animals↗
PubMed2006

Exogenous basic fibroblast growth factor increases collateral blood flow in female rats with femoral artery occlusion.

The goal of this study was to determine if extended duration of FGF-2 infusion would further expand collateral blood flow (BF) in female rats with bilateral femoral artery occlusion; rats were infused with either FGF-2 or placebo intra-arterially for 14, 28, and 42 days. Blood flows were measured with isotope labeled microspheres. Blood pressure and heart rate were similar between the treatment groups by ANOVA. In Placebo groups; baseline collateral dependent blood flows to the calf muscle were 11 mL/min/100 g to 17 mL/min/100 g at 4 hours after femoral artery occlusion, calf muscle blood flow increased to 39 +/- 4.2, 49 +/- 4.2, and 48 +/- 3.3 mL/min/100 g following 16, 30, and 44 days femoral artery occlusion respectively. In FGF-2-treated groups, calf muscle blood flows were further increased by 36%, 57%, and 35% over the corresponding time point of Placebo groups (P < 0.001). Exogenous FGF-2 infusion for 28 days showed higher collateral dependent blood flows than the FGF-2 14 days infused group (P < 0.001). Extended duration of exogenous FGF-2 delivery up to 42 days failed to further expand the collateral blood flow. This implies a self-limiting mechanism that might govern the collateral vascular remodeling induced by FGF-2. Our results indicate that female rats can obtain similar extent collateral blood flow expansion as that found in the male rats.

Animals↗
PubMed2004

Time course of changes in collateral blood flow and isolated vessel size and gene expression after femoral artery occlusion in rats.

The objectives of this study were to assess the time course of enlargement and gene expression of a collateral vessel that enlarges following occlusion of the femoral artery and to relate these responses to the increases in collateral-dependent blood flow to the calf muscles in vivo. We employed exercise training to stimulate collateral vessel development. Rats were exercise trained or kept sedentary for various times of up to 25 days postbilateral occlusion (n=approximately 9/time point). Collateral blood flow to the calf muscles, determined with microspheres, increased modestly over the first few days to approximately 40 ml.min(-1).100 g(-1) in sedentary animals; the increase continued over time to approximately 80 ml.min(-1).100 g(-1) in the trained animals. Diameters of the isolated collateral vessels increased progressively over time, whereas an increased vessel compliance observed at low pressures was similar across time. These responses were greater in the trained animals. The time course of upregulation of vascular endothelial growth factor and placental growth factor, and particularly endothelial nitric oxide synthase and fms-like tyrosine kinase 1, mRNAs in the isolated collateral vessel implicates these factors as integral to the arteriogenic process. Collateral vessel enlargement and increased compliance at low pressures contribute to the enlarged circuit available for collateral blood flow. However, modulation of the functioning collateral vessel diameter, by smooth muscle tone, must occur to account for the observed increases in collateral blood flow measured in vivo.

Animals↗
PubMed2004

What makes vessels grow with exercise training?

Exercise and muscle contractions create a powerful stimulus for structural remodeling of the vasculature. An increase in flow velocity through a vessel increases shear stress, a major stimulus for enlargement of conduit vessels. This leads to an endothelial-dependent, nitric oxide-dependent enlargement of the vessel. Increased flow within muscle, in the absence of contractions, leads to an enhanced capillarity by intussusceptive angiogenesis, a process of capillary splitting by intraluminal longitudinal divide. In contrast, sprouting angiogenesis requires extensive endothelial cell proliferation, with degradation of the extracellular matrix to permit migration and tube formation. This occurs during muscle adaptations to chronic contractions and/or muscle overload. The angiogenic growth factor VEGF appears to be an important element in angiogenesis. Recent advances in research have identified hemodynamic and mechanical stimuli that upregulate angiogenic processes, demonstrated a complexity of potent growth factors and interactions with their corresponding receptors, detected an interaction of cellular signaling events, and identified important tissue reorganization processes that must be coordinated to effect vascular remodeling. It is likely that much of this information is applicable to the vascular remodeling that occurs in response to exercise and/or muscle contractions.

Adaptation, Physiological↗
PubMed2003

Modeling and measurement of electrostatic spray behavior in a rectangular throat of Pease-Anthony venturi scrubber.

This paper presents the simulation and experimental results of the distribution of droplets produced by electrostatic nozzles inside a venturi scrubber. The simulation model takes into account initial liquid momentum, hydrodynamic, gravitational and electric forces, and eddy diffusion. The velocity and concentration profile of charged droplets injected from an electrostatic nozzle in the scrubber under the combined influence of hydrodynamic and electric fields were simulated. The effects of operating parameters, such as gas velocity, diameter of the scrubbing droplets, charge-to-mass ratio, and liquid-to-gas ratio on the distribution of the water droplets within the scrubber, were also investigated. The flux distribution of scrubbing liquid in the presence of electric field is improved considerably over a conventional venturi scrubber, and the effect increases with the increase in charge-to-mass ratio. Improved flux distribution using charged droplets increases the calculated overall collection efficiency of the submicron particles. However, the effect of an electric field on the droplet distribution pattern for small drop sizes in strong hydrodynamic field conditions is negligible. Simulated results are in good agreement with the experimental data obtained in the laboratory.

Air Movements↗
PubMed2003

Basic fibroblast growth factor increases collateral blood flow in spontaneously hypertensive rats.

Ischemia-induced angiogenic response is reduced in spontaneously hypertensive rats (SHR). To study whether exogenous basic fibroblast growth factor (bFGF) infusion is effective in expanding collateral circulation in frankly hypertensive SHR, femoral arteries of male SHR (weighing approximately 250 g) were kept intact (nonoccluded control; n = 9) or occluded for 4h(n = 12) or for 16 days with vehicle (n = 14) or bFGF [0.5 (n = 17), 5.0 (n = 13), and 50.0 (n = 14) microg. kg-1. day-1 for 14 days] intraarterially. Maximal collateral-dependent blood flows (BF) to the hindlimbs were determined with 85Sr- and 141Ce-labeled microspheres during running at 20 and 25 m/min (15% grade). Preexercise heart rates (approximately 530 beats/min) and blood pressures (BP; approximately 200 mmHg) were similar across groups except in the high-dose bFGF group, where BP was reduced by approximately 12% (P < 0.05). Femoral artery occlusion for 4 h resulted in approximately 95% reduction of BF in calf muscles [199 +/- 18.7 (nonoccluded group) to 10 +/- 1.0 ml. min-1. 100 g-1; P < 0.001]. BF to calf muscles of the vehicle and low-dose bFGF (0.5 microg. kg-1. day-1) groups increased to 36 +/- 3.2 and 45 +/- 2.0 ml. min-1. 100 g-1, respectively (P < 0.001). bFGF infusion at 5.0 and 50.0 microg. kg-1. day-1 further increased (P < 0.001) BF to calf muscles (62 +/- 4.6 and 62 +/- 2.2 ml. min-1. 100 g-1, respectively). Our results show that bFGF can effectively increase BF in hypertensive rats. The reduced hypertension with high-dose bFGF suggests that a critical signal in arteriogenesis (nitric oxide bioavailability) may be restored. These findings suggest that the dulled endothelial nitric oxide synthase of SHR does not preempt collateral vessel remodeling.

Animals↗
PubMed2003

Arteriogenesis: role of nitric oxide.

Arteriogenesis is an important process for adapting the pre-existing circuit of vessels into functional collateral conduits for delivery of oxygen enriched blood to tissue distal to occlusion of a large, peripheral conduit artery. Recent evidence has shown that arteriogenesis is regulated by nitric oxide (NO), angiogenic factors and shear stress. NO significantly impacts vasomotor tone to enhance conductance of the newly recruited collateral arteries, and this effect is augmented by exercise training prior to arterial occlusion. NO-mediated increases in vascular conductance allows for greater collateral dependent blood flow to the tissue distal to occlusion. NO production is also critical to the efficacy of therapeutic arteriogenesis achieved by delivery of exogenous angiogenic growth factors (VEGF, FGF-2) or by exercise training. The critical role of NO in therapeutic arteriogenesis is independent of NO-mediated changes in vascular conductance and implies a central role in arteriogenic signaling events. Maintenance, or improvement, of NO production and signaling, such as with regular exercise, may improve endothelial cell function and thus may help preserve the arteriogenic potential of preexisting collateral networks.

Animals↗
PubMed2003

Exercise-induced vascular remodeling.

Exercise produces a powerful angiogenic stimulus within the active muscle that leads to a functionally important increase in capillarity. Further, exercise can increase flow capacity by enlarging the caliber of arterial supply vessels. These adaptations are achieved by the processes of angiogenesis and arteriogenesis, respectively.

Animals↗
PubMed2002

Muscle blood flow and mitochondrial function: influence of aging.

Skeletal muscle mitochondrial capacity (mito), tissue blood flow (BF) capacity, and oxygen exchange capacity (e.g., DO2) appear to be well matched. The different skeletal muscle fiber types and muscle remodeled, due to inactivity (e.g., related to aging or disease) or exercise training, exhibit widely differing aerobic capacities (VO2max). Yet, there are remarkably coordinated alterations in these 3 parameters in each of these conditions. With such a balance, there is likely shared control among these parameters in limiting VO2max of muscle, although this is a matter of considerable debate. The reduction in aerobic capacity in elderly can be improved by submaximal aerobic exercise training; this is related to increases in muscle mitochondria concentration and capillarity, but probably not BF capacity, as this is limited by central cardiovascular function. Thus, exercise-induced biochemical adaptations and angiogenesis occur in the elderly. The increase in muscle capillarity likely contributes to the increased oxygen exchange capacity, typical of endurance type training. The increase in [mito] appears essential to realize the increased in muscle VO2max with training and amplifies the rate-limiting influence of the muscles oxygen exchange capacity. Further, vascular remodeling induced by exercise in the elderly could be effective at improving flow capacity, if limited by peripheral obstruction. Thus, the limits to aerobic function specific to aged muscle appear most influenced by inactivity, whereas central cardiovascular changes impact whole body performance. Some may consider the aged myocyte as a small, inactive, normal myocyte in need of activity!

Aging↗
PubMed2002

Prior exercise training produces NO-dependent increases in collateral blood flow after acute arterial occlusion.

We previously reported that prior training improves collateral blood flow (BF) to the calf muscles after acute-onset occlusion of the femoral artery (Yang HT et al. Am J Physiol Heart Circ Physiol 279: H1890-H1897, 2000). The purpose of this study was to test the hypothesis that increased release of nitric oxide (NO) by NO synthase (likely endothelial NOS) contributes to the increased BF to calf muscles of trained rats after acute femoral artery occlusion. Adult male Sprague-Dawley rats (~325 g) were limited to cage activity and were sedentary (SED; n = 28) or exercise trained (TR; n = 30) for 6 wk by treadmill running. On the day of the investigation, rats were anesthetized with ketamine-acepromazine and instrumented for determination of BF (using (141)Ce- and (85)Sr-labeled microspheres) and distal limb arterial pressure, and femoral arteries were occluded bilaterally. Four hours after surgery, collateral BF was determined twice during treadmill running: first at a demanding speed (20 m/min, 15% grade) and second, after a brief rest and at a faster running speed (25 m/min, 15% grade). The fact that BF did not increase further at the higher running speed indicated that maximal collateral BF was measured. Approximately half of the rats in each group received 20 mg/kg body wt N(G)-nitro-L-arginine methyl ester (L-NAME) intra-arterially 30 min before treadmill exercise and BF measurement to block production of NO by NOS. Results indicate that prior training improved collateral-dependent BF to the skeletal muscle of rats after acute femoral artery occlusion due primarily to an increase in the conductance of the upstream collateral circuit. Blockade of NOS with L-NAME produced decreased vascular conductance, both in the upstream collateral circuit and in the distal skeletal muscle microcirculation, and the difference between collateral vascular conductance in TR and SED rats was abolished. Our results indicate that the primary determinant of the increased collateral BF with prior training is the resistance of the upstream collateral circuit and imply that enhanced endothelium-mediated dilation induced by training serves to increase collateral BF following acute arterial occlusion.

Analysis of Variance↗
PubMed2001

Genetic linkage analysis of the antibody responses to myelin basic protein and myelin oligodendrocyte glycoprotein in rats immunized with rat spinal cord homogenate.

The genetic control of the antibody response to myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG) was analysed in F1 and F2 crosses of DA and E3 rats, immunized with rat spinal chord homogenate. The DA rats were highly susceptible to encephalomyelitis and made antibody responses to both MBP and MOG, whereas the E3 rats were disease-resistant and responded only to MOG. The anti-MBP response was mainly controlled by the disease-promoting MHC region of the DA strain together with several disease loci outside MHC. In contrast, the anti-MOG response was associated with loci not related to or actually conferring resistance to disease.

Animals↗
PubMed2001

[Radiofrequency catheter abaltion of right atrioventricular accessory pathway by superior vena cava approach].

The radiofrequency ablation effect was observed in 21 patients with single right atrioventricular accessory pathway by superior vena cava approach. Because of many factors, radiofrequency ablation by routine inferior vena cava approach failed. However, all of these accessory pathways were successfully ablated by the superior vena cava approach with could significantly reduce operation and radiofrequency ablation time and exposed time in x-ray, and there were not any complications. The success was probably related to the good contact between the ablation catheter tip and ablation target point. It is suggested that radiofrequency ablation of right atrioventricular accessory pathways by superior vena cava approach is effective and safe when the routine inferior vena cava approach is difficult or unsuccessful.

Adolescent↗
PubMed2001

A distant upstream region of the rat multipartite Na(+)-Ca(2+) exchanger NCX1 gene promoter is sufficient to confer cardiac-specific expression.

The Na(+)-Ca(2+) exchanger (NCX) regulates intracellular calcium homeostasis. We report on an upstream region of the rat NCX1 multipartite promoter that is active in cardiac myocytes. Although inactive in most non-cardiac cell lines, its activity can be rescued by cotransfection with GATA-4 and -6, but not GATA-5 transcription factors. In transgenic mice and similar to endogenous NCX1 mRNA expression, the upstream promoter region directs uniform beta-galactosidase expression in cardiac myocytes from approximately 7.75dpc. In adult mouse hearts, promoter activity is, however, significantly reduced and heterogeneous, except in the conduction system (sinoatrial and atrioventricular node, atrioventricular bundles). The upstream NCX1 promoter region thus directs appropriate spatial and temporal control of cardiac expression throughout development.

Animals↗
PubMed2001

VEGF(121)- and bFGF-induced increase in collateral blood flow requires normal nitric oxide production.

The angiogenic proteins basic fibroblast growth factor (bFGF; FGF-2) and vascular endothelial growth factor 121 (VEGF(121)) are each able to enhance the collateral-dependent blood flow after bilateral femoral artery ligation in rats. To study the effect of nitric oxide (NO) synthase (NOS) inhibition on bFGF- or VEGF(121)-induced blood flow expansion, the femoral arteries of male Sprague-Dawley rats were ligated bilaterally, and the animals were given tap water [non-N(G)-nitro-L-arginine methyl ester (L-NAME) group; n = 36] or water that contained L-NAME (L-NAME group; 2 mg/ml, n = 36). Animals from each group were further divided into three subgroups: vehicle (n = 12), bFGF (5 microg x kg(-1) x day(-1), n = 12), or VEGF(121) (10 microg x kg(-1) x day(-1), n = 12). Growth factors were delivered via intra-arterial infusion with osmotic pumps over days 1-14. On day 16, after a 2-day delay to permit clearance of bFGF and VEGF from the circulation, maximal collateral blood flow was determined by (85)Sr- and (141)Ce-labeled microspheres during treadmill running. L-NAME (approximately 137 mg x kg(-1) x day(-1)) for 18 days increased systemic blood pressure (approximately 26%, P<0.001). In the absence of L-NAME, collateral-dependent blood flows to the calf muscles were greater in the VEGF(121)- and bFGF-treated subgroups (85 +/- 4.5 and 80 +/- 2.9 ml x min(-1) x 100 g(-1), respectively) than in the vehicle subgroup (49 +/- 3.0 ml x min(-1) x 100 g(-1), P<0.001). In the presence of NOS inhibition by L-NAME, blood flows to the calf muscles were essentially equivalent among the three subgroups (54 +/- 3.0, 56 +/- 5.1, and 47 +/- 2.0 ml x min(-1) x 100 g(-1) in the bFGF-, VEGF(121)-, and vehicle-treated subgroups, respectively) and were not different from the blood flow in the non-L-NAME vehicle subgroup. Our results therefore indicate that normal NO production is essential for the enhanced vascular remodeling induced by exogenous bFGF or VEGF(121) in this rat model of experimental peripheral arterial insufficiency. These results imply that a blunted endothelial NO production could temper vascular remodeling in response to these angiogenic growth factors.

Animals↗
PubMed2001

Arteriogenesis and angiogenesis in rat ischemic hindlimb: role of nitric oxide.

Nitric oxide (NO) has been implicated in both collateral expansion (arteriogenesis) and capillary growth (angiogenesis). Exercise training increases collateral-dependent blood flow to tissues at risk of ischemia and enhances capillarity in active skeletal muscle. Exercise also acutely elevates NO. Thus we assessed the role of NO in training-induced arteriogenesis and angiogenesis. These studies utilized a rat model of peripheral vascular disease (bilateral femoral artery ligation). Untreated rats (control) and rats treated with the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME; 65-70 mg x kg(-1) x day(-1), via drinking water) were divided into sedentary or exercise-trained subgroups. After approximately 3 wk, L-NAME treatment had elevated preexercise mean arterial pressure approximately 39-58%, confirming NO synthesis inhibition. The training program (treadmill exercise twice per day, 20-25 m/min, 15% grade, approximately 18 days) increased collateral-dependent blood flow to the distal hindlimb, with the greatest increase (approximately 59%) in the calf (P < 0.001). This increase was inhibited by L-NAME. In contrast, the training-induced increase in muscle capillarity was not blocked by L-NAME. Thus arteriogenesis and angiogenesis appear to differ in their requirement for NO.

Animals↗
PubMed2000

Evidence for common autoimmune disease genes controlling onset, severity, and chronicity based on experimental models for multiple sclerosis and rheumatoid arthritis.

The pathogenicity of multiple sclerosis is still poorly understood, but identification of susceptibility genes using the animal model experimental allergic encephalomyelitis (EAE) could provide leads. Certain genes may be shared between different autoimmune diseases, and identification of such genes is of obvious importance. To locate gene regions involved in the control of EAE and to compare the findings with the susceptibility loci recently identified in a model for rheumatoid arthritis (pristane-induced arthritis), we made crosses between the encephalomyelitis- and arthritis-susceptible rat strain DA and the resistant E3 strain. Genetic analysis of animals produced in a F2 intercross identified 11 loci associated with specific EAE-associated traits. Interestingly, five of these loci were situated at the same position as major loci controlling pristane-induced arthritis and showed similarities in inheritance pattern and subphenotype associations. Our results show that different phases of EAE are controlled by different sets of genes and that common genes are likely to be involved in different autoimmune diseases.

Animals↗
PubMed2000

bFGF increases collateral blood flow in aged rats with femoral artery ligation.

We tested the hypothesis that aged animals are as responsive as the young adult animals in expanding collateral vasculature under a similar treatment of basic fibroblast growth factor (bFGF). Two age groups of male Fischer 344 rats (11 mo old; n = 32, 23 mo old; n = 43) weighing approximately 385 g were subdivided into normal, acute ligation [femoral artery (FA) ligated 3 days before blood flow (BF) measurement] or ligated groups for 16 days and received recombinant human bFGF intra-arterial infusion at doses of 0, 0.5, 5, and 50 microg x kg(-1) x day(-1). BF was determined with (85)Sr- and (141)Ce-labeled microspheres during treadmill running at 15 and 20 m/min at 15% grade. Blood pressure (BP) values were approximately 149 and approximately 163 mmHg (p < 0.05); heart rates were approximately 496 and approximately 512 beats/min in the aged and young adult groups during running, respectively. Maximal collateral BF values were confirmed by no additional BF increase in the calf muscle at the higher speed. Ligation of the FA for 3 days reduced the BF reserve to the calf muscle by approximately 90%. Calf muscle BF was modestly greater (10 ml x min(-1) x 100 g(-1)) by 16 days in the carrier group. bFGF infusion expanded collateral BF in a dose-dependent manner with an increase of 33 and 42 ml x min(-1) x 100 g(-1) (P < 0.001) in the 5 and 50 microg x kg(-1) x day(-1) bFGF groups, respectively. Aged animals showed similar BF improvements as observed with the adult groups in response to ligation surgery and bFGF treatment. Our data indicate that the aged rats (approximately 23 mo old) remain responsive to exogenous bFGF induced in developing collateral-dependent BF as the young adult (approximately 11 mo old) controls. This suggests that the influence of bFGF in expanding collateral BF should not be preempted in the aged group, the population most affected by peripheral arterial insufficiency.

Aging↗