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心肌内压力:心肌流体压力与纤维应力的相互作用。

Intramyocardial pressure: interaction of myocardial fluid pressure and fiber stress.

作者信息

Rabbany S Y, Kresh J Y, Noordergraaf A

机构信息

Cardiovascular Studies Unit, University of Pennsylvania, Philadelphia 19104.

出版信息

Am J Physiol. 1989 Aug;257(2 Pt 2):H357-64. doi: 10.1152/ajpheart.1989.257.2.H357.

Abstract

Previous measurements of intramyocardial pressure (IMP) have yielded systolic pressures that range from values lower than to far exceeding systolic left ventricular pressure (LVP). This study identifies a possible mechanism underlying these divergent observations by building on established morphology of the ventricular wall. It is hypothesized here that the generation of fiber stress as a manifestation of myocardial contraction increases fluid pressure in the myocytes and the interstitial spaces. This increase in fluid pressure in turn generates the pressure in the ventricular cavity. Thus there are two quantities of interest: intramyocardial fluid pressure (IFP) and intramyocardial fiber stress (IFS). To test the hypothesis, we conducted experiments on conditioned dogs, utilizing a side-mounted catheter-tip strain gauge transducer to sense IMP as the sum of IFP and some component of IFS. In addition, a recessed end-tip fiber-optic transducer with its sensing element shielded from local myocardial fibers was employed to sense IFP. Both IFP and IMP were measured at various depths in the left ventricular free wall. The effects of inotropic interventions by administration of epinephrine and propranolol, mechanical interventions via clamping of the aorta and ligation of the left anterior descending coronary artery, and neural interventions by stimulation of the ansa subclavian of the stellate ganglion and right vagus were recorded. A transmural gradient in the wall for both IMP and IFP was observed. Systolic values of IFP recorded in the endocardium match those of LVP, with peak IMP exceeding both. The results support the hypothesis and offer an interpretation of the long-standing controversy regarding the magnitude of IMP with respect to LVP.

摘要

以往对心肌内压(IMP)的测量所得到的收缩压范围,从低于到远超过左心室收缩压(LVP)。本研究通过基于已确定的心室壁形态学,确定了这些不同观察结果背后的一种可能机制。在此假设,作为心肌收缩表现的纤维应力的产生会增加心肌细胞和间质空间内的流体压力。这种流体压力的增加反过来又会在心室腔内产生压力。因此有两个感兴趣的量:心肌内流体压力(IFP)和心肌内纤维应力(IFS)。为了验证这一假设,我们对经过条件处理的狗进行了实验,使用侧装导管尖端应变片式传感器来感知作为IFP和IFS某一组成部分之和的IMP。此外,还采用了一种凹端光纤传感器,其传感元件免受局部心肌纤维的影响,以感知IFP。在左心室游离壁的不同深度测量了IFP和IMP。记录了通过给予肾上腺素和普萘洛尔进行的变力干预、通过夹闭主动脉和结扎左前降支冠状动脉进行的机械干预,以及通过刺激星状神经节的锁骨下袢和右迷走神经进行的神经干预的效果。观察到IMP和IFP在心室壁上均存在跨壁梯度。在心内膜记录到的IFP收缩值与LVP的收缩值相匹配,IMP峰值超过两者。这些结果支持了该假设,并为关于IMP相对于LVP大小的长期争议提供了解释。

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