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心肺相互作用的瞬态分析。II. 收缩期事件。

Transient analysis of cardiopulmonary interactions. II. Systolic events.

作者信息

Peters J, Kindred M K, Robotham J L

机构信息

Department of Anesthesiology and Critical Care Medicine, Francis Scott Key Medical Center, Johns Hopkins University Medical Institutions, Baltimore, Maryland 21205.

出版信息

J Appl Physiol (1985). 1988 Apr;64(4):1518-26. doi: 10.1152/jappl.1988.64.4.1518.

Abstract

The etiology of the fall in left ventricular stroke volume (LVSV) and arterial pressure with a negative intrathoracic pressure (NITP) during inspiration is controversial. An increase in LV afterload produced by NITP has been proposed as one explanation but is difficult to evaluate if preload is also altered. To test the hypothesis that a systolic event alone, i.e., a change in LV afterload or contractility, can reduce LVSV during inspiration independent of changes in LV preload, a rapid transient NITP confined to systole was produced by electrocardiogram-triggered phrenic nerve stimulation in eight anesthetized dogs. Intrathoracic descending aortic diameters were measured by sonomicrometry to transduce qualitative changes in aortic transmural pressure. With the airway completely obstructed systolic NITP resulted in a decrease in LVSV (-8.1%, P less than 0.001) but an increase in the systolic anteroposterior (0.54 mm, P less than 0.01) and right-to-left (0.45 mm, P less than 0.01) aortic diameters compared with preceding beat. Similar significant changes were observed with the airway unobstructed. These observations are consistent with an increased afterload imposed on the LV reducing LVSV and egress of blood out of the thorax. Prolonging NITP to include both systole and diastole, a profound fall in LVSV is observed, consistent with the independent influences of systolic and diastolic events combining to diminish LVSV.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

吸气时胸内负压(NITP)导致左心室每搏输出量(LVSV)和动脉压下降的病因存在争议。有人提出NITP导致左心室后负荷增加是一种解释,但如果前负荷也发生改变则难以评估。为了验证仅收缩期事件,即左心室后负荷或收缩力的变化,可在吸气时独立于左心室前负荷变化而降低LVSV这一假设,对8只麻醉犬进行心电图触发的膈神经刺激,产生局限于收缩期的快速短暂NITP。通过超声测微法测量胸内降主动脉直径,以转换主动脉跨壁压的定性变化。在气道完全阻塞的情况下,收缩期NITP导致LVSV下降(-8.1%,P<0.001),但与前一次搏动相比,收缩期前后径(0.54 mm,P<0.01)和右向左径(0.45 mm,P<0.01)的主动脉直径增加。在气道通畅时也观察到类似的显著变化。这些观察结果与左心室后负荷增加导致LVSV降低和血液流出胸腔一致。将NITP延长至包括收缩期和舒张期,可观察到LVSV显著下降,这与收缩期和舒张期事件的独立影响相结合导致LVSV降低一致。(摘要截短于250字)

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