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Adaptations of coronary smooth muscl...
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Heaps, Cristine Lynn.
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Adaptations of coronary smooth muscle to chronic occlusion and exercise training.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Adaptations of coronary smooth muscle to chronic occlusion and exercise training./
作者:
Heaps, Cristine Lynn.
面頁冊數:
187 p.
附註:
Source: Dissertation Abstracts International, Volume: 61-02, Section: B, page: 0629.
Contained By:
Dissertation Abstracts International61-02B.
標題:
Biology, Animal Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9962530
ISBN:
0599665572
Adaptations of coronary smooth muscle to chronic occlusion and exercise training.
Heaps, Cristine Lynn.
Adaptations of coronary smooth muscle to chronic occlusion and exercise training.
- 187 p.
Source: Dissertation Abstracts International, Volume: 61-02, Section: B, page: 0629.
Thesis (Ph.D.)--University of Missouri - Columbia, 1999.
We hypothesized that exercise training produces beneficial adaptations in vascular smooth muscle of both normal and diseased hearts that ultimately results in reduced resistance and increased blood flow in the coronary vascular bed. Chronic occlusion was produced by surgically placing an ameroid constrictor around the proximal left circumflex coronary artery (LCX) of female Yucatan miniature swine 8 weeks before initiating sedentary (pen-confined) or exercise training (treadmill run, 5 days·wk-1 for 16 wks) protocols. Twenty-four weeks following ameroid placement, segments of nonoccluded left anterior descending (LAD) and collateral-dependent LCX arteries (0.8--1.2 mm ID) were isolated from sedentary and exercise trained animals for subsequent in vitro evaluation of smooth muscle function. Additional normal, nonoccluded groups of swine underwent similar sedentary and exercise training protocols and subsequent in vitro evaluation of coronary smooth muscle function.
ISBN: 0599665572Subjects--Topical Terms:
1017835
Biology, Animal Physiology.
Adaptations of coronary smooth muscle to chronic occlusion and exercise training.
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Source: Dissertation Abstracts International, Volume: 61-02, Section: B, page: 0629.
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We hypothesized that exercise training produces beneficial adaptations in vascular smooth muscle of both normal and diseased hearts that ultimately results in reduced resistance and increased blood flow in the coronary vascular bed. Chronic occlusion was produced by surgically placing an ameroid constrictor around the proximal left circumflex coronary artery (LCX) of female Yucatan miniature swine 8 weeks before initiating sedentary (pen-confined) or exercise training (treadmill run, 5 days·wk-1 for 16 wks) protocols. Twenty-four weeks following ameroid placement, segments of nonoccluded left anterior descending (LAD) and collateral-dependent LCX arteries (0.8--1.2 mm ID) were isolated from sedentary and exercise trained animals for subsequent in vitro evaluation of smooth muscle function. Additional normal, nonoccluded groups of swine underwent similar sedentary and exercise training protocols and subsequent in vitro evaluation of coronary smooth muscle function.
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Results revealed impaired relaxation responses to the sympathomimetic vasodilator, isoproterenol, and the metabolic vasodilator, adenosine, in collateral-dependent LCX versus nonoccluded LAD coronary arterial rings of sedentary pigs, which were associated with attenuated reductions in myoplasmic Ca2+ levels. Exercise training reversed the attenuated reductions in both contractile tension and myoplasmic Ca2+.
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Further studies examined myoplasmic Ca2+ regulation (fura-2) in dissociated smooth muscle cells of LCX and LAD arteries of sedentary and exercise trained occluded pigs and suggest SERCA activity is impaired in smooth muscle cells isolated distal to chronic occlusion. Exercise training did not correct the impaired SERCA activity in smooth muscle cells of collateral-dependent vasculature. SERCA protein expression was not different between LCX and LAD coronary arteries of either sedentary or exercise trained animals.
520
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Additional studies in normal, nonoccluded pigs demonstrate that Ca 2+ influx through voltage-gated Ca2+ channels is enhanced in smooth muscle cells isolated from exercise trained animals. Furthermore, these studies document that the enhanced rate of Ca2+ entry is compensated by other cellular Ca2+ regulatory mechanisms to limit net Ca2+ accumulation in smooth muscle cells of exercise trained animals.
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These studies document that chronic occlusion and exercise training produce alterations in myoplasmic Ca2+ regulation in coronary smooth muscle cells of miniature swine. However, the impact of the specific adaptations in myoplasmic Ca2+ handling demonstrated in these studies on vascular reactivity and the resultant alterations in coronary blood flow capacity remain to be determined.
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