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Cardiac systolic and diastolic function during whole body heat stress

机译:全身热应力期间心脏收缩和舒张功能

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摘要

During a whole body heat stress, stroke volume is either maintained or slightly elevated despite reduced ventricular filling pressures and central blood volume, suggestive of improved cardiac diastolic and/or systolic function. Heat stress improves cardiac systolic and diastolic function in patients with congestive heart failure, although it remains unknown whether similar responses occur in healthy individuals, which is the hypothesis to be tested. Nine male volunteers underwent a whole body heat stress. Echocardiographic indexes of diastolic and systolic function were performed following a supine resting period, and again following an increase in internal temperature of ~1.0°C via passive heat stress. Despite previous reports of heat stress-induced decreases in ventricular filling pressures and central blood volume, no changes in indexes of diastolic function were identified during heating [i.e., unchanged early diastolic mitral annular tissue velocity (E'), mitral inflow during the early diastolic phase (E), the E/E' ratio, and isovolumetric relaxation time]. Heat stress increased late diastolic septal (P = 0.03) and lateral (P = 0.01) mitral annular tissue velocities (A'), mitral inflow velocity during atrial contraction (P > 0.001), and the relative contribution of atrial contraction to left ventricular filling during diastole (P = 0.01), all indicative of improved atrial systolic function. Furthermore, indexes of ventricular systolic function were increased by heat stress [i.e., increased septal (P = 0.001) and lateral (P = 0.01) mitral annular systolic velocities and isovolumic acceleration at the septal (P = 0.03) and lateral (P > 0.001) mitral annulus]. These data are suggestive of improved atrial and ventricular systolic function by the heat stress. Together these data support previous findings, which used the less precise measure of ejection fraction, that heat stress improves indexes of systolic ? 2009 the American Physiological Society.
机译:尽管心室灌浆压力和中枢血量减少,但暗示了改善的心脏舒张和/或收缩功能,因此在整个体温应激期间保持或稍微升高,既暗示了暗示的心脏抑制和/或收缩功能。热应激改善了充血性心力衰竭患者的心脏收缩和舒张功能,尽管仍然未知是否在健康个体中发生类似的反应,这是要测试的假设。九个男性志愿者经历了全身热应激。在仰卧静息时期进行舒张和收缩功能的超声心动图指标,并通过被动热应力增加〜1.0℃的内部温度的增加。尽管先前对心室填充压力和中枢血容量的热应激诱导的报告降低,但在加热期间没有鉴定舒张功能的指标的变化[即,早期舒张期间的二尖瓣流入(E'),二有二尖瓣流入相(e),E / E'比和离子抑制时间。热应力增加晚期舒张间隔(P = 0.03)和横向(P = 0.01)二尖瓣环状组织速度(A'),心房收缩期间二尖瓣流入速度(P> 0.001),以及心房收缩到左心室填充的相对贡献在肺渗透(P = 0.01)期间,所有指示性细胞收缩功能的均表明。此外,通过热应激增加室性收缩功能的指数[即,在隔膜(p = 0.03)和横向(p> 0.001)和横向(p> 0.001 )二尖瓣环。这些数据暗示通过热应力改善的心房和心室收缩功能。这些数据支持以前的发现,它使用了少量射入分数的精确度,热应力提高了收缩的指标? 2009年美国生理社会。

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