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Muscle metaboreflex control of ventr...
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Sala Mercado, Javier Agustin.
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Muscle metaboreflex control of ventricular contractility during dynamic exercise in normal and heart failure conditions.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Muscle metaboreflex control of ventricular contractility during dynamic exercise in normal and heart failure conditions./
作者:
Sala Mercado, Javier Agustin.
面頁冊數:
67 p.
附註:
Source: Dissertation Abstracts International, Volume: 66-03, Section: B, page: 1244.
Contained By:
Dissertation Abstracts International66-03B.
標題:
Biology, Animal Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3168510
ISBN:
054204725X
Muscle metaboreflex control of ventricular contractility during dynamic exercise in normal and heart failure conditions.
Sala Mercado, Javier Agustin.
Muscle metaboreflex control of ventricular contractility during dynamic exercise in normal and heart failure conditions.
- 67 p.
Source: Dissertation Abstracts International, Volume: 66-03, Section: B, page: 1244.
Thesis (Ph.D.)--Wayne State University, 2005.
This dissertation investigated the effects of muscle metaboreflex activation on left ventricular function in chronically instrumented dogs during mild and moderate dynamic exercise in normal and HF conditions.
ISBN: 054204725XSubjects--Topical Terms:
1017835
Biology, Animal Physiology.
Muscle metaboreflex control of ventricular contractility during dynamic exercise in normal and heart failure conditions.
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Source: Dissertation Abstracts International, Volume: 66-03, Section: B, page: 1244.
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Adviser: Donal S. O'Leary.
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Thesis (Ph.D.)--Wayne State University, 2005.
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This dissertation investigated the effects of muscle metaboreflex activation on left ventricular function in chronically instrumented dogs during mild and moderate dynamic exercise in normal and HF conditions.
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In normal dogs muscle metaboreflex activation during mild and moderate exercise evokes significant increases in MAP, CO and HR. In addition SV may increase slightly or remain constant at mild workloads. At moderate workloads SV increases substantially. However in HF, although blood pressure increases with muscle metaboreflex activation, the rise in CO is vitually abolished which may be due to impaired ability to increase ventricular contractility. Conscious dogs were chronically instrumented to measure HR, CO, MAP, left ventricular pressures and volumes. Unloading of the heart was transiently obtained via caval occlusion and contractility was assessed via pressure-volume loops using the maximal elastance index (Emax, slope of the line intersecting the end systolic pressure-volume relationships). Emax was obtained at rest, during mild and moderate exercise under free flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) in normal animals and after the induction of HF (rapid ventricular pacing, 240 bpm for ∼30 days). In control experiments MMR activation during mild exercise and moderate exercise increased CO and Emax significantly. In contrast, after induction of HF, CO and Emax were significantly lower at rest. Although at both workloads CO increased significantly from rest to exercise, Emax did not change. In addition at either workload MMR caused no significant change in either CO or Emax. We conclude that the activation of the MMR elicits increases in ventricular function in normal animals, whereas those increases in ventricular function are abolished in HF.
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