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质疑Frank—Starling心脏定律 总被引：4，自引：4，他引：0
心脏收缩释放的能量（作功）是心肌纤维长度（心室舒张末期容积，EDV）的函数，即Frank—Star一1ing（FS）心脏作功定律，被誉为心脏生理学中的“经典”理论。对此，笔者从各种不同角度进行了探讨：首先分析了Frank伸展离体心肌和Starling及其同事使用心肺制备做的实验与动物生理实际的差异，以及人们在实验中观测到的增加心肌前负荷引起收缩力增强的现象（FS现象），认为：①在正常生理条件下的动物体内，来自心脏以外的、如同心肺制备中那样人工控制心室充盈压力升高、引起EDV增加的那种血液的重力动力是不存在的。②另一方面，人为地增加前负荷，那是改变了心肌收缩时的外环境条件。③由此而激发出的FS现象，是心脏适应其外环境条件变化所作出的反应。④此种心肌收缩力增强的反应，需通过心肌细胞内部与收缩过程发生有关的心肌兴奋一收缩和化学一力学偶联等一系列生化机制（不恒定因素）方能得以实现。⑤根据他们实验中观测到的FS现象，在逻辑上不能得出前负荷这一心肌收缩时的外环境条件变化调控其作功的推论。换言之，所有的在实验中被激发出来的FS现象，都不足以成为支持FS心脏定律的证据。然后，引用国内外公认的计算心脏每搏射血作功（w）的生物物理学公式“w=P×（EDV—ESV）”，证明了w和EDV之间没有函数关系。根据心脏作功的医用物理学和生物数学的基本原理，笔者认为Frank—Starling心脏定律表达的不是心脏作功的规律。 相似文献
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Ranald M. Sutherland Claus Dähne John F. Place Anthony R. Ringrose 《Journal of immunological methods》1984,74(2):253-265
The theoretical basis and instrumental requirements of an optical detection technique for monitoring antibody-antigen reactions at a quartz-liquid interface are described. The antibody is covalently immobilized on the optical surface of a planar, fused-quartz waveguide and reacted with antigen solution. A light beam is internally reflected within the waveguide and penetrates into the solution only a fraction of the wavelength of the incident light. This is the evanescent wave which interacts optically with the growing number of antigen-antibody complexes but minimally with the bulk solution. A two-site immunofluorescent assay for human IgG measurement is described using fluorescein as the label. The assay detection limit is approximately 0.8 micrograms/ml and individual fluorescence measurements are completed within 10 min. It is expected that this evanescent wave immunoassay should have wide applicability in both routine and research fields. 相似文献
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Odaro J. Huckstep Wilby Williamson Fernando Telles Holger Burchert Mariane Bertagnolli Charlotte Herdman Linda Arnold Robert Smillie Afifah Mohamed Henry Boardman Kenny McCormick Stefan Neubauer Paul Leeson Adam J. Lewandowski 《Journal of the American College of Cardiology》2018,71(12):1347-1356
Background
Experimental and clinical studies show that prematurity leads to altered left ventricular (LV) structure and function with preserved resting LV ejection fraction (EF). Large-scale epidemiological data now links prematurity to increased early heart failure risk.Objectives
Echocardiography imaging was performed at prescribed exercise intensities to determine whether preterm-born adults have impaired LV functional response to physical exercise.Methods
A total of 101 normotensive young adults born preterm (n = 47; mean gestational age 32.8 ± 3.2 weeks) and term (n = 54) were recruited for detailed cardiovascular phenotyping. Full clinical resting and exercise stress echocardiograms were performed, with apical 4-chamber views collected while exercising at 40%, 60%, and 80% of peak exercise capacity, determined by maximal cardiopulmonary exercise testing.Results
Preterm-born individuals had greater LV mass (p = 0.015) with lower peak systolic longitudinal strain (p = 0.038) and similar EF to term-born control subjects at rest (p = 0.62). However, by 60% exercise intensity, EF was 6.7% lower in preterm subjects (71.9 ± 8.7% vs 78.6 ± 5.4%; p = 0.004) and further declined to 7.3% below the term-born group at 80% exercise intensity (69.8 ± 6.4% vs 77.1 ± 6.3%; p = 0.004). Submaximal cardiac output reserve was 56% lower in preterm-born subjects versus term-born control subjects at 40% of peak exercise capacity (729 ± 1,162 ml/min/m2 vs. 1,669 ± 937 ml/min/m2; p = 0.021). LV length and resting peak systolic longitudinal strain predicted EF increase from rest to 60% exercise intensity in the preterm group (r = 0.68, p = 0.009 and r = 0.56, p = 0.031, respectively).Conclusions
Preterm-born young adults had impaired LV response to physiological stress when subjected to physical exercise, which suggested a reduced myocardial functional reserve that might help explain their increased risk of early heart failure. (Young Adult Cardiovascular Health sTudy [YACHT]; NCT02103231) 相似文献7.
Mario Kasner Aleksandar S. Aleksandrov Dirk Westermann Dirk Lassner Michael Gross Stephan von Haehling Stefan D. Anker Heinz-Peter Schultheiss Carsten Tschöpe 《International journal of cardiology》2013
Background
Functional iron deficiency (FID) is an independent risk factor for poor outcome in advanced heart failure with reduced EF, but its role in heart failure with preserved EF (HFPEF) remains unclear. We aimed to investigate the impact of FID on cardiac performance determined by pressure–volume loop analysis in HFPEF.Methods
26 HFPEF patients who showed an increase in LV stiffness by pressure–volume (PV) loop analysis obtained by conductance-catheterization, performed exercise testing, echocardiographic examination including tissue Doppler and determination of iron metabolism: serum iron, ferritin and transferrin saturation. HFPEF patients who provided ferritin < 100 μg/l or ferritin of 100–299 μg/l in combination with transferrin saturation < 20% were defined as having FID. In 14 patients the expression of transferrin receptor was determined from available endomyocardial biopsies.Results
Fifteen out of 26 HFPEF patients showed FID without anemia. Compared to control subjects and HFPEF patients without FID, HFPEF patients with FID showed an up-regulation of the myocardial transferrin receptor expression (p < 0.05). No differences between HFPEF patients with and without iron deficiency were found in heart dimensions, systolic and diastolic function obtained by PV-loop and echocardiography analysis. According to the linear regression analysis, LV stiffness was correlated with peak oxygen uptake (r = − 0.636, p < 0.001) but not with the ferritin level or transferrin saturation. No relation was found between FID and exercise capacity. The association of LV stiffness with exercise performance was independent from the level of iron deficiency.Conclusion
In non-anemic HFPEF patients, cardiac dysfunction and impaired exercise capacity occur independently of FID. 相似文献8.
Akihisa Kataoka Xin Zeng J. Luis Guerrero Adam Kozak Gavin Braithwaite Robert A. Levine Gus J. Vlahakes Judy Hung 《The Journal of thoracic and cardiovascular surgery》2018,155(4):1485-1493
Objectives
Ischemic mitral regurgitation (IMR) results from ischemic left ventricular (LV) distortion and remodeling, which displaces the papillary muscles and tethers the mitral valve leaflets apically. The aim of this experimental study was to examine efficacy of an adjustable novel polymer filled mesh (poly-mesh) device to reverse LV remodeling and reduce IMR.Methods
Acute (N = 8) and chronic (8 weeks; N = 5) sheep models of IMR were studied. IMR was produced by ligation of circumflex branches to create myocardial infarction. An adjustable poly-mesh device was attached to infarcted myocardium in acute and chronic IMR models and compared with untreated sham sheep. Two- and 3-dimensional echocardiography and hemodynamic measurements were performed at baseline, post IMR, and post poly-mesh (humanely killed).Results
In acute models, moderate IMR developed in all sheep and decreased to trace/mild (vena contracta: 0.50 ± 0.09 cm to 0.26 ± 0.12 cm; P < .01) after poly-mesh. In chronic models, IMR decreased in all sheep after poly-mesh, and this reduction persisted over 8 weeks (vena contracta: 0.42 ± 0.09 cm to 0.08 ± 0.12 cm; P < .01) with significant increase in the slope of end-systolic pressure–volume relationship (1.1 ± 0.5 mm Hg/mL to 2.9 ± 0.7 mm Hg/mL; P < .05). There was a significant reduction in LV volumes from chronic IMR to euthanasia stage with poly-mesh compared with sham group (%end-diastolic volume change ?20 ± 11 vs 15% ± 16%, P < .01; %end-systolic volume change ?14% ± 19% vs 22% ± 22%, P < .05; poly-mesh vs sham group) consistent with reverse remodeling.Conclusions
An adjustable polymer filled mesh device reduces IMR and prevents continued LV remodeling during chronic follow-up. 相似文献9.
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