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1
Buckler, K. J. "Actions of adrenergic agonists on transmembrane ion exchanges in skeletal and heart muscle." Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380754.
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Mason, M. J. "Mechanisms of entry of L-lactate into frog skeletal muscle : A micro-electrode study." Thesis, University of Bristol, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375026.
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Gramolini, Anthony Orlando. "The effect of modulating ATP-sensitive potassium channels in frog skeletal muscle, in vitro, during fatigue and metabolic inhibition." Thesis, University of Ottawa (Canada), 1996. http://hdl.handle.net/10393/9473.
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The ATP-sensitive potassium (K$\sp+\rm\sb{(ATP)}$) channel is a K$\sp+$ channel which is activated as the energy state of a muscle decreases. It has been hypothesized that once activated, K$\sp+\rm\sb{(ATP)}$ channels decrease the excitability of the cell and cause decreased contractility, such as during fatigue, in order to prevent energy levels from falling to dangerously low levels. The purpose of this study was to test this hypothesis and to determine under which conditions K$\sp+\rm\sb{(ATP)}$ channels can contribute to a decrease in force during a metabolic stress in the sartorius muscle of the frog, Rana pipiens. In the first series of experiments, sartorius muscle fibres were fatigued with 100 msec long tetanic contractions every second for three minutes, a condition known to activate ATP-sensitive potassium channels. So if K$\sp+\rm\sb{(ATP)}$ channels contribute to a decrease in force during fatigue, an activation of K$\sp+\rm\sb{(ATP)}$ channels with channel openers should further decrease membrane excitability and contractility. In a second series of experiments, muscles were subjected to metabolic inhibition which is known to activate a large number of K$\sp+\rm\sb{(ATP)}$ channels in order to better understand the relationship between K$\sp+\rm\sb{(ATP)}$ channel activity, the bioenergetic state, and force. The goal was to determine if K$\sp+\rm\sb{(ATP)}$ channels can contribute to a decrease in force under a bioenergetic state that is within physiological limits. (Abstract shortened by UMI.)
4
Khan, Raheela Nazir. "Ultrastructure and physiology of nerve-muscle cultures from the cockroach." Thesis, Oxford Brookes University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278930.
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Rasanani, Mohammad Reza Hadian. "Electrophysiological studies of spinal reflex pathways from group II muscle afferents." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360304.
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Yao, Yan-Dong. "Acoustic myography : the signal from contracting skeletal muscles." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321718.
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Carroll, Kevin. "Comparison of Muscle Physiology and Performance Outcomes from Either Relative Intensity or Repetition Maximum Training." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3369.
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The main purpose of this dissertation was to compare performance and physiological outcomes of between a repetition maximum (RM) and a relative intensity using sets-and-repetitions (RISR) resistance training (RT) program in well-trained lifters. Fifteen subjects underwent RT 3 d·wk-1 for 10-weeks in either a RM group (n=8) or RISR group (n=7). The RM group achieved a relative maximum each day while the RISR group trained based on percentages. Testing included percutaneous needle biopsies of the vastus lateralis, ultrasonography, unweighted (g to assess within and between-group alterations. RISR from pre-to-post yielded statistically significant increases in Type I CSA (p=0.018), Type II CSA (p=0.012), ACSA (p=0.002), unweighted (p=0.009) and 20 kg SJ JH (p=0.012), unweighted (p=0.003) and 20kg SJ PPa (p=0.026), IPF (ppSR increased in unweighted (p=0.023) and 20kg SJ JH (p=0.014), and 20kg SJ PPa (p=0.026) from pre-to-post taper. RM yielded statistically significant increases from only pre-to-post taper for 20kg SJ JH (p=0.003) and CMJ JH (p=0.031). Additionally, RM had a statistically significant pre-to-post decrease in RFD from 0-50ms (p=0.018) and 0-100ms (p=0.014). Between-group effect sizes supported RISR for Type I CSA (g=0.48), Type II CSA (g=0.50), ACSA (g=1.03), all MYH isoforms (g=0.31-0.87), all SJ variables (g=0.64-1.07), unweighted and 20kg CMJ JH (g=0.76-0.97), unweighted CMJ PPa (g=0.35), IPFa (g=0.20), and all RFD (g=0.31-1.25) time-points except 0-200ms; with all other effects being of trivial magnitude (gSR training yielded greater improvements in vertical jump, RFD and maximal strength compared RM training. These performances results may, in part, be explained mechanistically by the superior physiological adaptations observed in the RISR group within the skeletal muscle. Taken together, these data support the use of RISR training in well-trained populations.
8
Essackjee, Hafejee Cassim. "The influence of contraction, pH and enzyme inhibition on the release of adenosine from rat gracilis muscle." Thesis, Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20565914.
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Fairclough, Valerie Marie. "The role of ornithine decarboxylase in the transformation of skeletal muscle from fast-twitch to slow-twitch type." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333715.
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Alkahtani, Reem. "Changes in the Expression of Thin Filament-Associated Proteins in Colonic Smooth Muscle from Mice During Inflammation." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/220.
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The contractility of smooth muscle in inflammatory bowel disease and experimental colitis is reduced due to inhibition of neurotransmitter release and a decrease in the response of smooth muscle to contractile agonists. We and others have shown that inflammation induced by TNBS treatment alters the expression and/or activity of signaling molecules involved in the regulation of Ca2+ mobilization, MLC20 phosphorylation and contraction in colonic smooth muscle. Although, thin filament- associated proteins such as calponin, caldesmon, tropomyosin and smoothelin do not directly participate in contraction, they regulate acto-myosin interaction and thus, muscle contraction. Calponin, caldesmon and tropomyosin inhibit actomyosin interaction and the inhibition is relieved upon phosphorylation of these proteins. Recent studies have shown that visceral smooth muscle from smoothelin knockout mice exhibited decreased contraction. However, the effect of inflammation on the expression of thin filament- associated proteins is not known. The aim of the present study is to determine the changes in the expression of calponin, caldesmon, tropomyosin, and smoothelin in colonic circular smooth muscle from TNBS- and DSS-induced colitis in mice. The animals were euthanized on day 3 and a segment of inflamed distal colon was removed. Colonic muscle strips from colitis mice and control mice were dissected for western blot and real-time RT-PCR analysis; contraction was measured by scanning micrometry in cells isolated from the muscle strips. Contraction in response to acetylcholine in muscle cells isolated from colonic muscle strips derived from mice with TNBS colitis was significantly inhibited compared with the response of cells derived from untreated colon or colon treated with ethanol. Expression of α-actin, γ-actin calponin, caldesmon, smoothelin-A and tropomyosin mRNA in muscle strips from TNBS or DSS colitis was significantly increased compared to control animals. Similarly, expression of α-actin, calponin, caldesmon, smoothelin-A and tropomyosin protein as determined by western blot was significantly increased compared to control animals. We conclude that the expression of α-actin, γ -actin calponin, caldesmon, smoothelin-A and tropomyosin is upregulated in colonic circular smooth muscle from TNBS or DSS colitis. Increase in the expression of calponin, caldesmon and tropomyosin, which act to inhibit acto-myosin interaction, could contribute to decrease in smooth muscle contraction.
11
Kruger, Maria Jacoba. "Antioxidant (Oxiprovin TM) supplementation and muscle recovery from contusion injury - an in vivo study." Thesis, Stellenbosch : Stellenbosch University, 2007. http://hdl.handle.net/10019.1/21670.
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Thesis (MSc)--University of Stellenbosch, 2007.ENGLISH ABSTRACT: Human studies on the response of muscle to contusion injury are limited, probably due to the large variability in injury severity and the non-specificity of clinical symptoms reported. To circumvent this problem, several experimental animal models have been designed to study muscle damage and regeneration after contusion injuries. However, the majority of techniques currently used to induce contusion injury are very invasive and therefore not optimal. Furthermore, published studies regarding clinical treatment of such injuries are limited. The main aims of this study were therefore: a) to establish and characterise an in vivo model of non-invasive contusion injury, and b) to assess the effect of pre-injury chronic administration of the antioxidant supplement Oxiprovin™ - a natural grape seed extract (GSE) - on skeletal muscle recovery after experimentallyinduced injury. Two groups of male Wistar rats were subjected to 14 days of oral administration of isovolaemic placebo (sterile isotonic saline) or GSE (20 mg/kg/day) prior to induced contusion. Contusion injury was induced with the mass-drop technique, and recovery parameters assessed for up to 14 days post-injury. Placebotreated rats on average exhibited a 56 % higher creatine kinase (CK) activity when compared to the GSE-treated rats when area under the curve (AUC) was calculated for 14 days post-injury (p < 0.001). In the placebo group, plasma oxygen radical absorbance capacity (ORAC) was unchanged over time, but muscle ORAC was significantly increased by day 7 post-injury (p < 0.001). In the GSE group, a significant decrease in both plasma (p < 0.01) and muscle ORAC (p < 0.001) was evident 4 hr after injury, followed by a significant increase by day 3 (p < 0.05 and p < 0.001 respectively). CD34+ satellite cell (SC) numbers (quiescent and activated) peaked earlier in GSE-treated rats when compared to placebo-treated rats (4 hours vs. day 7 post-injury). Total satellite cell number (CD56+) also peaked earlier in GSE-treated rats than in placebo-treated rats (4 hours vs. 3 days post-injury), while M-cadherin+ SC numbers (quiescent, activated or proliferating) in both treatment groups were significantly increased 4 hours post-injury (p < 0.001), but more so in the placebo group. In GSE-treated rats when compared to placebo-treated rats, newly generated muscle fibres (displaying central nuclei and MHCf +) both appeared (day 3 vs. day 7 post-injury) and peaked in number (day 3 vs. day 7 post-injury; increase from baseline p < 0.001 for both) earlier. The results of this study demonstrate that we have successfully established an in vivo model for non-invasive contusion injury in rats. Furthermore, we have shown that Oxiprovin™: a) increased the ability to scavenge reactive species generated after injury and b) resulted in the activation of satellite cells and formation of newly generated muscle fibres at an earlier time point, thus accelerating the recovery of skeletal muscle after a standardised contusion injury.
AFRIKAANSE OPSOMMING: Eksperimente aangaande die reaksie van spier op kneusings in mense is beperk, waarskynlik as gevolg van die groot verskeidenheid simptome wat mag voorkom en die verskille in die ernstigheid van beserings. Ten einde hierdie problem te oorbrug, is verskeie eksperimentele diermodelle opgestel om kneusings en die herstel van spier daarna te ondersoek. Die tegnieke wat grootendeels vandag gebruik word om kneusings te veroorsaak, maak inbraak op die spier deur die spier te ontbloot voor besering, en is dus nie ideaal nie. Daar is ook nie baie bewyse aangaande die mees geskikte manier om so ‘n besering klinies te behandel nie. Die doel van hierdie studie was dus om: a) ‘n in vivo model van kneusings op te stel en te omskryf, en b) die effek van chroniese toediening van die antioksidant Oxiprovin™ - ‘n natuurlike druifsaad ekstrak (DSE) – op die herstel van skeletspier na ‘n kneusing te ondersoek. Twee groepe manlike Wistar rotte is onderwerp aan mondelikse toediening van isovolemiese plasebo (steriele isotoniese soutoplossing) of DSE (20 mg/kg/dag) vir ‘n tydperk van 14 dae voor kneusing. Kneusing is geïnduseer met die “massdrop” tegniek, en parameters van herstel is ondersoek tot en met 14 dae na besering. Plasebo-behandelde rotte het gemiddeld 56 % hoër kreatien kinase (KK) aktiwiteit in vergelyking met DSE-behandelde rotte (p < 0.001), toe die oppervlak onder die kurwe (OOK) tot en met 14 dae na besering bereken is. Geen verskil oor tyd is in die plasebo groep opgemerk toe plasma suurstof radikaal absorpsie kapasiteit (SRAK) bepaal is nie, maar ‘n betekenisvolle toename in spier SRAK teen dag 7 (p < 0.001) is waargeneem. ‘n Betekenisvolle afname in beide plasma (p < 0.01) en spier (p < 0.001) SRAK van die DSE is teen 4 hr waargeneem, gevolg deur ‘n betekenisvolle toename teen dag 3 na besering (p < 0.05 en p < 0.001 onderskeidelik). Die aantal CD34+ satelliet selle (SS – rustend en geaktiveerd) het beduidend vroeër in die DSE groep gestyg in vergelyking met die plasebo groep (4 uur vs. 7 dae na besering). Die totale aantal SS (CD56+) het ook vroeër in die DSE-behandelde rotte as die plasebobehandelde rotte gestyg (4 uur vs. 3 dae na besering), terwyl die aantal Mcadherin+ SS (rustend, geaktiveerd of prolifererend) betenisvol gestyg het in beide groepe teen 4 uur (p < 0.001) na besering, maar hoër in die plasebo groep was. Die aantal nuutgevormde spiervesels (met sentraal geleë nukleï en MHCf +) het beide vroeër verskyn en gepiek in die DSE-behandelde rotte in vergelyking met die plasebo-behandelde rotte (dag 3 vs. dag 7 na besering). Die resultate van hierdie studie dui aan dat ons instaat was om ‘n in vivo model van nie-indringende kneusing in rotte op te stel. Verder, het ons ook bewys dat Oxiprovin™ toediening die vermoë verleen het om: a) reaktiewe spesies wat na beserings gevorm word, meer doeltreffend te verwyder en b) satelliet selle vroeër te aktiveer en die vorming van nuwe skeletspiervesels te vervroeg, om sodoende die herstel van skeletspier na ‘n gestandardiseerde kneusing vinniger te bewerkstellig.
12
巫放明 and Fong-ming Mo. "The role of intracellular pH in the control of adenosine output from oxidative skeletal muscle in-vivo and in-vitro." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31235190.
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Nelson, Ian D. "The physiology and pharmacology of muscles from the proboscis of two species of whelk : Buccinum undatum and Busycon caniculatum." Thesis, Lancaster University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358158.
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14
Low, Chee Yong. "Muscle glycogen repletion without food intake during recovery from exercise in humans." University of Western Australia. School of Sport Science, Exercise and Health, 2010. http://theses.library.uwa.edu.au/adt-WU2010.0115.
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[Truncated abstract] It is well established that fish, amphibians and reptiles recovering from physical activity of near maximal intensity can replenish completely their muscle glycogen stores in the absence of food. In contrast, the extent to which these stores are replenished under these conditions in humans has been reported in all but one study to be partial. This implies that a few consecutive bouts of intense exercise might eventually lead to the sustained depletion of the muscle glycogen stores in humans if food is unavailable, thus limiting their capacity to engage in fight or flight behaviors unless mechanisms exist to protect muscle glycogen against sustained depletion. The objective of Study 1 was to test this prediction. Eight participants performed three intense exercise bouts each separated by a recovery period of 75 minutes. Although only 53% of muscle glycogen was replenished after the first exercise bout (postexercise and post-recovery glycogen levels of 246 ± 25 and 320 ± 36 mmol.kg-1 dry mass, respectively), all the glycogen mobilised during the second and third bouts was completely replenished during the respective recovery periods, with glycogen reaching levels of 319 ± 29 mmol.kg-1 dry mass after recovery from the third bout. These findings show that humans are not different from other vertebrate species in that there are conditions where humans have the ability to completely replenish without food intake the muscle glycogen mobilised during exercise. The results of our first study raise the intriguing possibility that humans have pre-set muscle glycogen levels that are protected against sustained depletion, with the extent to which muscle glycogen stores are replenished after exercise being dependent on the amount of glycogen required to attain those protected levels. ... During recovery, glycogen levels in the NORM group increased by more than ~50% and reached levels close to those alleged to be protected (189 ± 21 mmol.kg-1 dry mass), whereas no glycogen was deposited in the HCHO group. The sustained post-exercise activation of glycogen synthase, the transient fall in whole body carbohydrate oxidation rate, the increased mobilisation of body proteins, and the prolonged elevation in NEFA levels most probably played important roles in enabling glycogen synthesis in the NORM group. In conclusion, this thesis shows for the first time that there are some conditions (e.g. low pre-exercise muscle glycogen levels) where humans recovering from intense exercise have the capacity, like other species, to replenish completely their muscle glycogen stores from endogenous carbon sources. This study also suggests that humans protect preset levels of muscle glycogen against sustained depletion and at levels high enough to support at least one maximal sprint effort to exhaustion. Evidence is also provided for the existence of a feedback mechanism whereby glycogen below their protected levels mediate the activation of glycogen synthase to restore the depleted muscle glycogen stores back to their protected levels. Our findings, however, leave us with a number of novel unanswered questions which clearly show that the regulation of glycogen metabolism is far from the simple process generally depicted in most textbooks of biochemistry.
15
Bartels, Else Marie. "Studies of the physiological states of cross-striated muscle with the aim of understanding the underlying processes of the changes from one state to another." Thesis, Open University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276177.
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Cai, Weisong, and 蔡蔚松. "Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49618088.
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Contracting skeletal muscle releases ATP into the interstitial space where it is subsequently broken down to adenosine by the action of ecto-5’-nucleotidase. Both ATP and adenosine are vasodilators that contribute to the exercise hyperaemia. However, the mechanism for the release of ATP from muscle during exercise remains unknown. Cystic fibrosis transmembrane conductance regulator (CFTR) is involved in ATP release from muscle at low intracellular pH: this study was performed to investigate whether CFTR was involved in the ATP release from skeletal muscle during contractions.
Experiments were performed in rats anaesthetised with sodium pentobarbitone and breathing spontaneously. A microdialysis probe was placed in one gastrocnemius muscle: ATP was determined in interstitial microdialysate samples using a bioluminescence assay. The sciatic nerve was stimulated to induce two bouts of muscle contractions, separated by a recovery period of 40 mins; one of the inhibitors was administered prior to the second bout of contractions.
Muscle contractions elevated the interstitial ATP by 1500 to 3000%. In the control experiments, no drug was given: both the contractile force and the increase in interstitial ATP were reproducible in repeated contraction bouts. Infusion of a specific inhibitor of CFTR, CFTRinh-172, did not alter the contractile force, but significantly lowered the interstitial ATP during muscle contractions, suggesting that CFTR was involved in the contraction-induced ATP release. Similarly, infusion of the Protein Kinase A inhibitor, KT5720, significantly reduced interstitial ATP during muscle contractions without altering contractile force, suggesting that CFTR in skeletal muscle is activated through the cAMP/PKA pathway. The increase in interstitial ATP during muscle contraction was also inhibited by the Na/H exchanger inhibitor, amiloride, or the Na/Ca exchanger inhibitor, SN6. It has been also shown that two gap junction hemichannel inhibitors, gadolinium and carbenoxolone, could attenuate the increase of ATP during muscle contraction.
These data suggest that CFTR, activated through the cAMP/protein kinase A pathway, is involved in the ATP release during muscle contraction, and that activation of the Na/H exchanger and Na/Ca exchanger was also required, indicating that the signal transduction mechanism for CFTR activation during muscle contractions may be similar to that which is reported to occur at low pH. The preliminary data showed that the gap junction hemichannels might mediate the ATP release from skeletal muscle cells during muscle contraction.published_or_final_version
Physiology
Master
Master of Philosophy
17
Foreman, III Richard A. "Enzymatic profiles of skeletal muscles from harbor seals (Phoca vitulina) and fin whales (Balaenoptera physalis)." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30808.
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The enzymatic organization of muscle tissue usually is examined in only a select few muscles of any one animal species. However, because the functional demands placed on individual muscles can vary so widely from muscle to muscle, it is inappropriate to generalize findings from one or two muscles to muscle tissue in general. The differences or similarities in metabolic machinery between skeletal muscles of a wide functional range provides crucial information with respect to a particular animals' whole body metabolism. Nowhere is this understanding more important than in the diving marine mammal which must operate as a closed system (with respect to oxygen supply) while submerged. The goals of this thesis are: 1) to provide a broad body of information on the metabolic organization of a large cross-section of marine mammal muscles, both functionally and with regard to location, 2) to assess the implications of the enzyme differences between muscles to the diving habit, and 3) to compare the metabolic organization of skeletal muscle among several species of marine mammal with different diving abilities and habits.
A series of 13 enzymes were measured in 21 skeletal muscles of the harbor seal, Phoca vitulina. In addition, 23 enzyme activity ratios were calculated and analyzed for these muscles. A similar analysis of 22 muscles from fin whales, Balaenoptera physalis. was conducted --including 7 key enzymes and 15 activity ratios. Overall, both the maximum activities and the enzyme activity ratios are consistent with
the idea that marine mammal muscle is typical mammalian muscle, exhibiting few significant differences from terrestrial species with respect to catabolic enzymes. The only obvious exception to this in the species examined is observed with fin whale locomotory muscle which has extremely high activities of lactate dehydrogenase (over 2000 units/gm wet wt at 25°C) due to an apparent scaling phenomenon. Tight control of this high potential glycolytic flux is indicated by pyruvate kinase activities that scale downward.
Comparisons of enzyme relationships between muscles of harbor seals seem to indicate a very aerobically poised metabolic make-up. This is especially true with respiratory and locomotory muscles, which also show a high tendency to utilize fat. This pattern of enzyme activities and activity ratios in the locomotory muscles of harbor seal is evidence that muscle contractile activity while diving is powered primarily through oxidative pathways and largely based on fat as fuel. The majority of non-locomotory muscles appear to be more able to function anaerobically utilizing carbohydrate. This pattern may correlate with circulatory redistributions while diving that preferentially fuel the locomotory muscles with oxygen, leaving the inactive muscles significantly more hypoperfused and, therefore, candidates for energy saving O₂ sparing
(metabolic depression). Fin whales exhibit an opposite pattern, with enzyme profiles more typical of "white" muscle. Unlike harbor seals, the locomotory muscles of fin whales are consistently the least oxidatively poised of the muscles examined. This apparently more anaerobic nature of
fin whale muscle is possibly complicated by scaling adaptations, but appears to be a real phenomenon.
The examination of three to four skeletal muscles from each of three additional phocid seal species from Antarctica, leopard seals (Hydrurga leptonyx). crab-eater seals (Lobodon carcinophagus). and Weddell seals (Leptonychotes weddelli) confirm that the harbor seal pattern of enzyme profiles is fairly consistent among phocid seals. By these criteria skeletal muscles of phocid seals (particularly the locomotory and respiratory muscles) appear to be designed for sustained aerobic metabolism during diving regardless of the habits or diving capabilities of the seal.Science, Faculty of
Zoology, Department of
Graduate
18
Lu, Lin, and 鹿琳. "The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208017.
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The cystic fibrosis transmembrane conductance regulator (CFTR) was identified to be involved in acidosis-induced ATP release from skeletal myocytes in vitro and from contracting muscle in vivo. My PhD studies aimed to investigate the underlying mechanism and identify the pathway for ATP release in acidosis-induced CFTR-regulated ATP release.
Lactic acid (10 mM) decreased the intracellular pH of L6 skeletal myocytes to 6.87 ± 0.12 after 3 hours, and the lowered pH resulted in the elevation of ATP release from skeletal myocytes. The acidosis-induced ATP release was totally abolished by GlyH-101 (40 μM), an open-channel CFTR blocker, suggesting that CFTR was involved. The cAMP/PKA signaling pathway was involved in the CFTR-regulated ATP release from skeletal myocytes: 1). Forskolin increased the extracellular ATP and the phosphorylation of CFTR; IBMX, a phosphodiesterase inhibitor, further enhanced the forskolin-induced extracellular ATP and phosphorylation of CFTR; 2). Inhibition of PKA by its selective inhibitor KT-5720 abolished the acidosis-induced ATP release and the forskolin-induced phosphorylation of CFTR. In addition, the inhibition of Na+/H+ exchanger (NHE) by amiloride, or inhibition of Na+/Ca2+ exchanger (NCX) by its specific inhibitors SN-6 and KB-R7943 abolished the lactic-acid-induced ATP release from skeletal myocytes, indicating that NHE and NCX might be involved.
Previous studies demonstrated that Connexin hemichannels and Pannexin channels were able to conduct ATP in response to stimuli. This study found that connexin 43 (Cx43) was strongly expressed on skeletal myocytes, while Pannexin 1 (Panx1) showed a strong expression in gastrocnemius muscle. Investigation of the role that Cx43 may play in acidosis-induced cAMP/PKA-activated CFTR-regulated ATP release from myocytes showed that: 1). Cx43 was immunoprecipitated with CFTR suggesting a physical interaction; 2). The opening of Cx hemichannels was increased by lactic acid and this lactic-acid-induced opening was inhibited by CFTRinh-172, suggesting the mediation of CFTR; 3). Inhibition of Cxs and Panxs with carbenoxolone abolished the acidosis-induced ATP release; moreover, specific silencing of the Cx43 gene using siRNA decreased both basal and acidosis-induced ATP release, suggesting that Cx43 was involved; 4). Overexpression of CFTR alone did not elevate the acidosis-induced ATP release, while overexpression of Cx43 alone doubled the acidosis-induced ATP, and co-overexpression of CFTR and Cx43 further elevated the acidosis-induced ATP release, supporting the concept that Cx43 functionally interacted with CFTR to induce the acidosis-induced ATP release.
Panx1 was studied in native skeletal muscle, and found to be coimmunoprecipitated with CFTR. Inhibition of Panxs with gadolinium or probenecid abolished the muscle-contraction-induced ATP release, while inhibition with carbenoxolone or quinine reduced it to less than 10% of control, suggesting that Panx1 may be involved in the acidosis-induced ATP release during muscle contraction.
All the in vitro and in vivo studies suggested that Cxs and Panx were involved in the acidosis-induced CFTR-regulated ATP release from skeletal myocytes and skeletal muscle.published_or_final_version
Physiology
Doctoral
Doctor of Philosophy
19
Donaldson, Judith Margaret. "Respiratory properties of mitochondria from heart and mosaic muscle of rainbow trout (Salmo gairdneri) : substrate utilization and response to temperature and extramitochondrial pH." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24630.
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Mitochondria were isolated from heart and mosaic muscle of rainbow trout (Salmo qairdneri R.). State 3 respiratory rates were determined at 5 and 15°C using pyruvate, malate, lactate, glutamate or acetyl—carnitine as substrate. The final three substrates were used to generate pH profiles. Pyruvate was oxidized at high rates in all cases, indicating good potential for aerobic carbohydrate metabolism. At 15°C, malate was an equally good substrate for heart mitochondria, while all substrates were oxidized at similar rates to pyruvate in muscle mitochondria. Maximal oxidation rates of heart mitochondria were greater than or equal to those of muscle. State 3 Q₁₀ for oxidation of most substrates in heart was approximately 2, except for malate which had a Q₁₀ of 3. Mitochondrial oxidation tended to be more sensitive to decreased temperature in muscle than in heart, particularly with respect to acetyl—carnitine and glutamate oxidation which in muscle had Q₁₀ values of 4 and 7, respectively. Based on RCR values at 5 and 15°C, there was no indication that membrane permeability to H⁺ ions was altered by a 10°C change in temperature in mitochondria from either tissue. At pH above 7.6 respiratory rates decreased with increasing pH. State 3 respiratory rate increased in heart
mitochondria as pH decreased, below 7.6 while in muscle mitochondria, no such pH dependence was observed. RCR values were above 4 in all experiments except at high pH. Muscle mitochondria were the more sensitive to extreme pH with respect to RCR. Heart mitochondria had higher
oxidative rates than those of muscle and were less sensitive to decreased temperature, in keeping with the greater oxidative demands of that tissue relative to mosaic muscle. Muscle mitochondria which typically face larger fluctuations in extramitochondrial pH in vivo than do those of heart, were less sensitive to pH in vitro. It was concluded that substrate utilization patterns and response to changes in temperature and extramitochondrial pH in the two mitochondrial populations was different and reflected both the intracellular environment of the mitochondria and the different needs of each tissue for aerobic energy supply.Science, Faculty of
Zoology, Department of
Graduate
20
Kaiser, Jennifer L. "The effects of polyunsaturated phosphatidylcholine supplementation on body composition and muscle recovery from repeated bouts of resistance exercise." Virtual Press, 2002. http://liblink.bsu.edu/uhtbin/catkey/1231346.
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The purpose of this study was to examine the influence of a supplement containing polyunsaturated phoshphatidylcholine (PPC) on physical performance, delayed muscle soreness (DOMS), markers of membrane damage, and lipid peroxidation after repeated bouts of whole body resistance on men ages 18-35 years. Subjects were randomly assigned to receive either PPC or placebo supplements for 31 days. After 3 weeks of supplementation, subjects were to perform 3 whole body resistance exercise sessions with 3 days of recovery between sessions. In order to document the effects of supplementation on recovery, fasting blood samples for determination of creatine kinase (CK) and malondialdehyde (MDA), and muscle soreness ratings were obtained each day in the morning after the initial 3 weeks of supplementation. The data was analyzed using a two-way ANOVA. The results indicate notable trends favoring PPC supplementation, such as lower ratings of perceived muscle soreness, lower CK and MDA responses to repeated bouts, improved maintenance of upper body strength and power, and increased lean body mass. However, these findings were not statistically different when compared to the placebo group.School of Physical Education
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Davies, Thomas. "Investigating the role of the extracellular calcium-sensing receptor (CaSR) in vascular pathophysiology using a novel mouse model of selective ablation of CaSR from mouse vascular smooth muscle cells." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/47503/.
Full textAbstract:
The extracellular calcium-sensing receptor (CaSR) is a G-protein coupled receptor central to systemic Ca2+ homeostasis in mammals. We have previously shown that CaSR is expressed in primary bovine aortic vascular smooth muscle cells (VSMCs). Furthermore, dominant-negative adenoviral knockdown of this receptor in bovine VSMCs in vitro causes enhanced calcification in the presence of culture conditions which mimic vascular calcification in vivo. Using mineralising conditions in vitro, we have also previously demonstrated that positive pharmacological allosteric activation of CaSR using the calcimimetic, R-568, significantly reduces calcification of bovine VSMCs. These findings now implicate the CaSR, not just in systemic Ca2+ homeostasis, but also in potential protection against vascular calcification; a condition associated with increased blood pressure, left ventricular hypertrophy, chronic kidney disease and cardiovascular morbidity. Using a specific targeted deletion strategy, we have developed CaSR-specific knockout in VSMCs driven by the SM22α promoter. Using in vitro, ex vivo and in vivo approaches, here, I have characterised the cardiovascular phenotype of this novel transgenic mouse model. In vivo data demonstrate that ablation of CaSR from VSMCs causes hyperkalaemia at 3 months of age and hypercalcaemia throughout life. 3 month old CaSR-VSMC Knockout (KO) mice also exhibit reduced bone mineral integrity and increased heart weight at the age of 18 months. Ex vivo analysis implicates the VSMC-CaSR as a modulator of blood vessel tone. CaSR-VSMC KO mice exhibit reduced luminal diameters of the aorta and mesenteric arteries. CaSR-VSMC KO also reduces contractile tone in addition to evoking Ca2+-dependent relaxation only, compared to CaSR-wild-type (WT) mice which exhibit both Ca2+-dependent contraction and relaxation of the aorta. In vitro analyses confirm that CaSR expression and activation reduces Ca2+-dependent proliferation and mineralisation. In conclusion, the VSMC CaSR is a modulator of vascular tone ex vivo and of VSMC proliferation and calcification in vitro.
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Schulte, Patricia Marita. "Recovery from exhaustive exercise in rainbow trout white muscle : a model for studies of the control of energy metabolism in vivo." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29874.
Full textAbstract:
Recovery from exhaustive exercise in the white muscle of rainbow trout (Oncorhynchus mykiss) was used to examine the role of the adenylates in the control of energy metabolism and to assess the validity of equilibrium models of the behaviour of the high energy phosphates.
The difficulty of obtaining muscle samples from fish makes detailed analysis of the behaviour of the labile high energy phosphates complex. The use of a new sampling procedure, the infusion of a lethal dose of anaesthetic via an indwelling cannula, minimized this problem.
At exhaustion [ATP] and [PCr] were depressed by 75 and 80% respectively relative to the resting values. [ATP] depletion was mirrored by a stoichiometric increase in [IMP]. During recovery [PCr] returned to the resting level within 2 hours, but [ATP] recovery was slow and not complete until 24 hours post exercise. In contrast, energy charge and RATP(the proportion of the free adenylate pool phosphorylated to ATP) were, if anything, higher than the resting values by 2 hours post exercise. Therefore, [ATP] and energy status can be dissociated in tissues like fish white muscle because of the action of the purine nucleotide cycle.
At 2 hours post exercise the calculated free ADP concentration dropped to less than one tenth the value at rest. As a result the [ATP] / [ADP] free ratio increased by nearly 6 fold. This condition may be required for glycogen resynthesis from lactate in muscle.
Several similar equilibrium models of the behaviour of the adenylates and PCr were applied to the fish white muscle system. In general, the models well describe the relationship between the high energy phosphates. However, the definition of the high energy phosphate pool introduces some complications since this includes the total [ATP]. Because of the action of AMP deaminase the [ATP] concentration can change without measurable changes in the energy status, which is not considered in any of the models. As long as the extent of IMP formation is known the models can be applied, but since the formation of IMP may vary from fish to fish or with exercise regime the models lose much of their predictive power.Science, Faculty of
Zoology, Department of
Graduate
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Foster, Aurora. "Mechanisms and Mitigation of Skeletal Muscle Fatigue in Single Fibers from Older Adults." 2019. https://scholarworks.umass.edu/masters_theses_2/772.
Full textAbstract:
Skeletal muscle fatigue is the contraction-induced decline in whole muscle force or power, and can be greater in older versus young adults. Fatigue primarily results from increased metabolism elevating phosphate (Pi) and hydrogen (H+), which alters myosin-actin interactions; however, which steps of the myosin-actin cross-bridge cycle are changed and their reversibility are unclear. PURPOSE: This study sought to: 1) Examine the effects of elevated Pi and H+ on molecular and cellular function, and 2) Test the ability of deoxyadenosine triphosphate (dATP), an alternative energy to adenosine triphosphate (ATP), to reverse the contractile changes induced with high Pi and H+. METHODS: Maximal tension (force/cross-sectional area), myofilament mechanics and myosin-actin cross-bridge kinetics were measured in 214 single fibers (104 type 1) from the vastus lateralis of eight (4 men) healthy, sedentary older adults (71±1.3 years) under normal (5 mM Pi, pH 7.0), simulated fatigue (30 mM Pi, pH 6.2) and simulated fatigue with dATP conditions. RESULTS: Tension declined with high Pi and H+ in slow- (type I, 23%) and fast-contracting (type II, 28%) fibers due to fewer strongly bound myosin heads (28-48%) and slower cross-bridge kinetics (longer myosin attachment times (ton) (18-40%) and reduced rates of force production (18-30%)). Type I myofilaments became stiffer with high Pi and H+ (48%), which may have partially mitigated fatigue-induced tension reduction. Elevated Pi and H+ with dATP moderately improved force production similarly in both fiber types (8-11%) compared to high Pi and H+ with ATP. In type I fibers, high Pi and H+ with dATP returned the number of myosin heads strongly bound and ton to normal, while the rate of force production became faster than normal (16%). In type II fibers, high Pi and H+ with dATP did not change the number of myosin heads bound, but cross-bridge kinetics were 16-23% faster than normal. CONCLUSION: These results identified novel fiber-type specific changes in myosin-actin cross-bridge kinetics and myofilament stiffness that help explain fatigue-related force reduction in human single skeletal muscle fibers as well as an alternative energy source that partially to fully reverses contractile changes of elevated Pi and H+ that occur with fatigue.
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Foulis, Stephen A. "Recovery from muscle fatigue in young and older adults: Implications for physical function." 2013. https://scholarworks.umass.edu/dissertations/AAI3603082.
Full textAbstract:
As adults age, skeletal muscles become smaller and weaker, which can ultimately lead to declines in physical function and disability. In general, older adults produce less isometric force and dynamic power than younger adults. The effects of this weakness are amplified following a series of muscle contractions that result in muscle fatigue. Since daily routines consist of repeated series of activity followed by rest, it is important to understand how muscle recovers from fatigue. In particular, muscle power has been shown to be related to physical function and balance. Thus, understanding the process of recovery from muscle fatigue will help in preventing declines in physical function in older adults. This dissertation consisted of two studies designed to understand how muscle recover following fatigue and the implications of that recovery on physical function. Study one examined recovery from muscle fatigue following a constrained task. Young and older adults were fatigued to a similar degree using a dynamometer, and recovery of power at 4 velocities, central activation, pre-motor signaling, neural efficiency and contractile properties were recorded over an hour. To evaluate the functional implications of the recovery, ratings of perceived exertion were collected and the amount of fatigue following a second fatigue bout was also recorded. The second study associated changes in physical function and balance with power following an ecologically-relevant fatiguing exercise. Following a 30 minute treadmill walk, chair rise time and balance were measured during the period of recovery from this task. As a result of fatigue, we saw increased power loss at high-velocities that did not recover over the course of an hour in older adults. . This finding was concurrent with other velocity specific changes in rates of force development, muscle acceleration, and pre-motor neural signaling. Functionally, we saw an increased in perceived effort during contraction in older adults, and an increased fatigue during a second fatigue bout. While chair rise didn't differ as a group with fatigue, there was a significant relationship with loss of high-velocity power and change in chair rise time over the hour recovery period. Balance declined immediate post-fatigue but appeared to recover to a point of greater stability over an hour. This dissertation provides novel insight about alterations in the recovery process following an acute bout of muscle fatigue, and ultimately provides data that may be useful for developing strategies to prevent disability in older adults.
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Mbong, Nathan. "Hydrogen peroxide enhances the expression and function of Giα proteins in aortic vascular smooth muscle cells from Sprague-Dawley rats : role of growth factor receptors transactivation." Thèse, 2010. http://hdl.handle.net/1866/12757.
Full textAbstract:
Nous avons récemment démontré que les espèces réactives oxygénées induisent une augmentation de l’expression des protéines Giα dans les cellules du muscle lisse vasculaire (CMLV) provenant d’aortes de rats spontanément hypertendus (SHR, de l’anglais spontaneously hypertensive rats). La présente étude a pour but d’étudier les effets du peroxyde d’hydrogène (H2O2), un oxydant qui induit le stress oxydatif, sur l’expression de Giα et sur l’activité de l’adénylate cyclase, et d’explorer les voies de signalisation sous-jacentes responsables de cette réponse.
Nos résultats montrent que H2O2 induit une augmentation de l’expression des protéines Giα-2 et Giα-3 de manière dose- et temps-dépendante avec une augmentation maximale de 40-50% à 100 µM après 1 heure, sans affecter l’expression de Gsα. L’expression des protéines Giα a été maintenue au niveau normal en presence de AG 1478, AG1295, PD98059 et la wortmannine, des inhibiteurs d’EGF-R (de l’anglais epidermal growth factor receptor), PDGFR-β (de l’anglais platelet-derived growth factor receptor β), de la voie de signalisation ras-ERK1/2 (de l’anglais extracellular regulated kinase1/2), et de la voie de la PI3Kinase-AKT (de l’anglais phosphatidyl inositol-3 kinase), respectivement. En outre, le traitement des CMLV avec H2O2 a induit une augmentation du degré de phosphorylation d’EGF-R, PDGF-R, ERK1/2 et AKT; et cette expression a été maintenue au niveau témoin par leurs inhibiteurs respectifs. Les inhibiteurs d’EGF-R et PDGF-R ont aussi induit une diminution du degré de phosphorylation de ERK1/2, et AKT/PKB. En outre, la transfection des cellules avec le siRNA (de l’anglais, small interfering ribonucleic acid) de EGF-R et PDGFR-β a atténué la surexpression des protéines Giα-2 et Giα-3 induite par le traitement au H2O2.
La surexpression des protéines Giα induite par H2O2 a été corrélée avec une augmentation de la fonction de la protéine Giα. L’inhibition de l’activité de l’adénylate cyclase par de faibles concentrations de GTPγS après stimulation par la forskoline a augmenté de 20% dans les cellules traitées au H2O2. En outre, le traitement des CMLV au H2O2 a aussi accru l’inhibition de l’activité de l’adénylate cyclase par les hormones inhibitrices telles que l’angiotensine II, oxotrémorine et C-ANP4-23. D’autre part, la stimulation de l’adénylate cyclase induite par GTPγS, glucagon, isoprotérénol, forskoline, et le fluorure de sodium (NaF) a été atténuée de façon significative dans les cellules traitées au H2O2. Ces résultats suggèrent que H2O2 induit la surexpression des protéines Giα-2 and Giα-3 via la transactivation des récepteurs des facteurs de croissance EGF-R, PDGFR-β et l’activation des voies de signalisation ras-ERK1/2 et PI3K-AKT
Mot-cles: Protéines Giα, peroxyde d’hydrogène, stress oxydant, récepteurs des facteurs de croissance, MAP kinases, adénylate cyclase, hypertensionWe recently have shown that reactive oxygen species contribute to the enhanced expression of Giα proteins in vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR). The present study was undertaken to examine if H2O2, an oxidant that induces oxidative stress could also enhance the expression of Giα proteins and associated adenylyl cyclase signalling in aortic VSMC and to further explore the underlying signaling pathways responsible for this response. Treatment of cells with H2O2 increased the expression of Giα-2 and Giα-3 proteins but not that of Gsα proteins in a concentration- and time-dependent manner. A maximal increase of 40-50% was observed at 100µM and 1h. The enhanced expression of Giα proteins was restored to control levels by AG 1478, AG1295, PD98059 and wortmannin, inhibitors of epidermal growth factor receptor (EGF-R), platelet-derived growth factor receptor (PDGFR-β), the mitogen-activated protein kinase (MEK1/2), and PI3 kinase respectively. In addition, treatment of VSMC with H2O2 also increased the phosphorylation of EGF-R, PDGF-R, ERK1/2 and AKT and this increased phosphorylation was attenuated to control levels by the respective inhibitors, whereas the inhibitors of EGF-R and PDGE-R also attenuated the enhanced phosphorylation of ERK1/2 and AKT to control levels. Transfection of cells with EGF-R and PDGFR-β siRNA followed by H2O2 treatment restored the H2O2-induced enhanced expression of Giα-2 and Giα-3 proteins to control levels. The increased expression of Giα proteins by H2O2 was reflected in the increased Gi functions. The inhibition of forskolin (FSK)-stimulated AC activity by low concentration of GTPγS (receptor- independent Gi functions) was increased by about 20% by H2O2 treatment. Moreover, treatment of cells with H2O2 also resulted in an increased Ang II-, C-ANP4-23, and oxotremorine-mediated inhibition of AC (receptor-dependent functions of Gi). On the other hand, Gsα-mediated stimulation of AC by GTPγS, glucagon, isoproterenol, FSK, and NaF was significantly decreased in H2O2-treated cells. These results suggest that H2O2 increases the expression of Giα-2 and Giα-3 proteins in VSMC through the transactivation of EGF-R, PDGFR-β and associated ERK1/2 and PI3K signalling pathways. Keywords: Giα proteins, hydrogen peroxide, adenylyl cyclase, oxidative stress, MAP kinase, growth factor receptors, hypertension.
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"Neural engineering: modeling bioelectric activities from neuromuscular system with its applications." 2004. http://library.cuhk.edu.hk/record=b6073667.
Full textAbstract:
Ma Ting."July 2004."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2004.
Includes bibliographical references (p. 181-196).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstracts in English and Chinese.
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Almajdoob, Sara. "The Effect of Resveratrol on the Hyperproliferation of Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats : Molecular Mechanisms." Thèse, 2017. http://hdl.handle.net/1866/20526.
Full text
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Myler, Heather Ann. "Heparanase and platelet factor-4 induce smooth muscle cell proliferation and migration via basic fibroblast growth factor release from the extracellular matrix: Implications in the restenosis process." Thesis, 2003. http://hdl.handle.net/1911/18597.
Full textAbstract:
Basic fibroblast growth factor (bFGF) plays an instrumental role in the cascade of events leading to restenosis, vascular re-occlusion due to excessive smooth muscle cell (SMC) proliferation, migration and extracellular matrix (ECM) deposition following arterial intervention procedures such as balloon angioplasty. The mechanism of bFGF activation following vascular injury has remained elusive. bFGF is stored bound to heparan sulfate proteoglycans in the ECM of the arterial media; release from extracellular sequestration may activate bFGF and initiate SMC proliferation and migration. bFGF mobilization at injured sites may be induced by platelet degranulation products. We have carried out in vitro studies demonstrating that platelet-derived heparanase and platelet factor-4 (PF4) liberate bFGF from the ECM of vascular SMCs, resulting in the induction of SMC proliferation and migration. Increases in proliferation and migration were inhibited by treatment with a bFGF-neutralizing antibody, suggesting that proliferation and migration in response to heparanase or PF4 are mediated by bFGF activation. When platelets were seeded on top of SMCs, degranulation products were found to release bFGF from the ECM, increasing cell proliferation and cell migration. These increases in SMC proliferation and migration were completely inhibited by the addition of a bFGF-neutralizing antibody. In order to investigate the role of heparanase and PF4 in vivo, each was delivered to the uninjured rat carotid artery. Heparanase and PF4 were both found to release bFGF, induce substantial SMC proliferation and increase the expression of several growth factor receptors thought to promote restenosis. An antibody that neutralizes platelet-derived heparanase was developed and evaluated in a rat carotid balloon injury model. Perivascular delivery of anti-heparanase IgG was found to inhibit bFGF depletion from the arterial wall by approximately 60% (p < 0.001) at 4 days. This correlated with the reduction in intimal thickening observed at 14 days. Platelet degranulation products, such as heparanase and PF4, may liberate bFGF from extracellular sequestration, activating the growth factor and inducing the SMC proliferation and migration that contribute to luminal narrowing following vascular injury. In addition, platelet-derived heparanase is likely to play a key role in initiating events leading to restenosis via bFGF mobilization.