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肺损伤通过Starling机制抑制心脏收缩功能。

Pulmonary injury depresses cardiac systolic function through Starling mechanism.

作者信息

Calvin J E, Baer R W, Glantz S A

出版信息

Am J Physiol. 1986 Oct;251(4 Pt 2):H722-33. doi: 10.1152/ajpheart.1986.251.4.H722.

DOI:10.1152/ajpheart.1986.251.4.H722
PMID:3766749
Abstract

To determine whether pulmonary microvascular injury or lung hyperinflation changes left ventricular (LV) performance and whether ventricular interaction plays a role in mediating such changes, we studied seven open-chest, closed-pericardium, anesthetized dogs before and after right ventricular (RV) injections of 150- to 200-micron glass beads. Because people with pulmonary disease are often treated with positive end-expiratory pressure, we also hyperinflated the lungs before and after creating the pulmonary microvascular injury. Measurements of LV and RV pressures and dimensions were taken at end expiration during the basal state, during lung hyperinflation, and after microvascular injury at RV end-diastolic pressures of 5, 10, and 15 mmHg produced by volume loading. Acute volume loading produced upward shifts in the LV diastolic pressure-size curve both before and after microvascular injury. Neither microvascular injury nor lung hyperinflation substantially affected the LV diastolic pressure-size relationship. LV end-diastolic size determined LV stroke work with no consistent independent influence of microvascular injury or lung hyperinflation. Neither microvascular injury nor lung hyperinflation depressed systolic performance beyond that associated with changes in end-diastolic heart size.

摘要

为了确定肺微血管损伤或肺过度充气是否会改变左心室(LV)功能,以及心室相互作用是否在介导此类变化中起作用,我们在向七只开胸、心包封闭、麻醉的犬右心室(RV)注射150至200微米玻璃珠前后进行了研究。由于肺部疾病患者常接受呼气末正压治疗,我们还在造成肺微血管损伤前后使肺过度充气。在基础状态、肺过度充气期间以及在通过容量负荷使RV舒张末期压力达到5、10和15 mmHg时微血管损伤后,于呼气末测量LV和RV压力及尺寸。急性容量负荷在微血管损伤前后均使LV舒张压-尺寸曲线向上移位。微血管损伤和肺过度充气均未显著影响LV舒张压-尺寸关系。LV舒张末期尺寸决定LV每搏功,微血管损伤或肺过度充气无一致的独立影响。微血管损伤和肺过度充气均未使收缩功能降低超过与舒张末期心脏大小变化相关的程度。

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