CHANGES IN LEFT-VENTRICULAR GEOMETRY DURING SPONTANEOUS BREATHING

CHANGES IN LEFT-VENTRICULAR GEOMETRY DURING SPONTANEOUS BREATHING
复制标题

DOI:
10.1152/jappl.1987.63.2.803
复制
发表时间:
1987-08-01
影响因子:
3.3
通讯作者:
RAMANATHAN, M
RAMANATHAN, M
中科院分区:
医学2区
文献类型:
--
作者:
CASSIDY, SS;WEAD, WB;RAMANATHAN, M

文献摘要

被引文献

相似文献

这些实验的目的是确定自发产生的吸气对麻醉仰卧犬左室(LV)大小和形状的影响。我们在LV内植入标志物以建立三个垂直轴,并在60赫兹的双平面电影透视下记录这些标志物的运动。伴随吸气的LV大小的主要变化发生在舒张末(ED)。LVED内径的最大变化是间隔-侧壁内径缩小了2.46 mm,但心尖-基底部内径也减少了0.74 mm。前后径实际增宽1.07 mm。间隔-侧壁狭窄是由间隔标记物和心尖基底轴之间的1.0 mm狭窄以及尖底标记物和侧壁标记物之间的1.4 mm狭窄引起的。间隔部分的缩小似乎是意料之中的,因为假定在吸气时右室充盈增强。LV外侧部分变窄,而前后径变宽,这是令人惊讶的,因为LVEDV形状的改变是隐含的。假设室壁是同质的,左心室形态的这种变化意味着施加在心外膜表面的力是不均匀的。在前、后表面一定有一种左室壁所没有的回缩。这些舒张末LV的尺寸变化(由三个ED轴的乘积估计)的净影响是LVED体积减少3.5cm3。吸气对收缩末期内径没有明显影响(0.3 mm),左心室收缩末期容量也没有明显变化(增加了0.5厘米3)。因此,吸气对左心室功能的净影响似乎主要是前负荷的减少。导致预负荷减少的机制是复杂的,不能完全从这些数据中推断出来。
The purpose of these experiments was to determine the effects of a spontaneously generated inspiration on the size and shape of the left ventricle (LV) in anesthetized supine dogs. We implanted markers in the LV to establish three perpendicular axes and recorded the motion of these markers using biplane cinefluoroscopy at 60 Hz. The primary changes in LV size that accompanied inspiration occurred at end diastole (ED). The largest change in LVED dimension was a 2.46-mm narrowing of the septal-lateral wall dimension, but the apex-base dimension decreased also, by 0.74 mm. The anteroposterior dimension actually widened by 1.07 mm. The septal-lateral narrowing was caused by both a 1.0-mm narrowing of the disease between the septal marker and the apex-base axis, as well as by a 1.4-mm narrowing between the apex-base axis and the lateral wall marker. Narrowing of the septal portion seemed expected because of presumed enhanced right ventricular filling during inspiration. Narrowing of the lateral portion of the LV, while the anteroposterior dimension widened, was surprising because a change in LVEDV shape is implied. Assuming ventricular homogeneity, this change in LVED shape implies that the forces applied to the epicardial surface were not uniform. There must have been a retraction on the anterior and posterior surface that was not experienced by the lateral LV wall. The net effect of these dimensional changes of the LV at end diastole (estimated from the product of the three ED axes) was a 3.5-cm3 reduction in LVED volume. Inspiration did not alter end-systolic dimensions appreciably (< 0.3 mm), and left ventricular end-systolic volume did not change significantly (increasing by < 0.5 cm3). Thus the net effect of inspiration on the LV function appeared to be predominantly a reduction in preload. The mechanisms responsible for this reduction in preload were complex and could not be inferred entirely from these data.