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心室等容收缩期间的冠状动脉-主动脉相互作用。

Coronary-aortic interaction during ventricular isovolumic contraction.

机构信息

Experimental Cardiology, Thoraxcenter, Cardiovascular Research Institute COEUR, Erasmus MC, University Medical Center Rotterdam, Dr Molewaterplein 50, P.O. Box 2040, 3000 CA, Rotterdam, The Netherlands.

出版信息

Med Biol Eng Comput. 2011 Aug;49(8):917-24. doi: 10.1007/s11517-011-0770-y. Epub 2011 Apr 13.

Abstract

In earlier work, we suggested that the start of the isovolumic contraction period could be detected in arterial pressure waveforms as the start of a temporary pre-systolic pressure perturbation (AIC(start), start of the Arterially detected Isovolumic Contraction), and proposed the retrograde coronary blood volume flow in combination with a backwards traveling pressure wave as its most likely origin. In this study, we tested this hypothesis by means of a coronary artery occlusion protocol. In six Yorkshire × Landrace swine, we simultaneously occluded the left anterior descending (LAD) and left circumflex (LCx) artery for 5 s followed by a 20-s reperfusion period and repeated this sequence at least two more times. A similar procedure was used to occlude only the right coronary artery (RCA) and finally all three main coronary arteries simultaneously. None of the occlusion protocols caused a decrease in the arterial pressure perturbation in the aorta during occlusion (P > 0.20) nor an increase during reactive hyperemia (P > 0.22), despite a higher deceleration of coronary blood volume flow (P = 0.03) or increased coronary conductance (P = 0.04) during hyperemia. These results show that the pre-systolic aortic pressure perturbation does not originate from the coronary arteries.

摘要

在早期的工作中,我们提出可以在动脉压力波形中检测到等容收缩期的开始,作为一个暂时的收缩前期压力扰动的开始(AIC(start),即动脉检测到的等容收缩期),并提出逆行冠状动脉血流结合反向传播压力波作为其最可能的起源。在这项研究中,我们通过冠状动脉阻塞方案来验证这一假设。在六头约克夏×长白猪中,我们同时阻塞左前降支(LAD)和左回旋支(LCx)动脉 5 秒,然后进行 20 秒的再灌注期,并至少重复两次这个序列。类似的程序用于阻塞右冠状动脉(RCA),最后同时阻塞所有三条主要冠状动脉。在阻塞期间,没有任何阻塞方案导致主动脉中动脉压力扰动减少(P > 0.20),在反应性充血期间也没有增加(P > 0.22),尽管在充血期间冠状动脉血流速度下降(P = 0.03)或冠状动脉传导性增加(P = 0.04)。这些结果表明,收缩前期主动脉压力扰动不是起源于冠状动脉。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/542f/3139876/50ff76404b0c/11517_2011_770_Fig1_HTML.jpg

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