Coronary flow regulation in the fetal sheep.
Coronary flow regulation in the fetal sheep.
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胎羊的冠状动脉血流调节。
DOI：
10.1152/ajpregu.1999.277.5.r1249
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Reller,MD
中科院分区：
文献类型：
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作者：
Thornburg,KL;Reller,MD
绵羊胚胎心脏的两个心室具有解剖和生化差异，这是它们不同的功能能力和血流的原因。在压力负荷和慢性和急性低氧血症的实验中，使用放射性标记的微球[或左心室(LV)血流，通过回旋冠状动脉上的多普勒传感器]测量了流向两个心室的冠脉流量。与右心室(RV)相比，流向较低壁张力的左心室的血流量约为每克血流量的三分之二。RV的急性收缩压负荷达到其最大工作能力时，可刺激流量增加一倍(从∼250ml⋅min−1⋅100g−1)，但低于腺苷刺激的水平(750ml⋅min−1⋅100g−1)。在所有RV工作负荷下，LV流量保持在三分之二的RV流量。慢性低氧胎儿的静息心肌血流水平与正常胎羊的腺苷刺激的最大心肌血流相似。这种血流增加明显是由于血管重塑，因为在腺苷注射过程中，∼500ml⋅min−1⋅100g−1保持了正常的“血流储备”。急性低氧血症可将心肌血流量刺激到非常高的水平(>；1.5 L⋅min−1⋅100 g−1)，这一水平高于单独使用化学扩张所能达到的水平。当一氧化氮合酶被拮抗时，左心室血流不会超过腺苷刺激的血流。我们得出的结论是：1)胎儿RV冠脉流量随着RV工作而增加，但低于腺苷刺激时的水平；2)胎儿心脏被设计为适应极高的流量，以响应急性低氧血症，部分是通过大量产生一氧化氮；以及3)胎儿冠脉树显著重塑，以响应慢性低氧血症。
The two ventricles of the fetal sheep heart have anatomic and biochemical differences that account for their differing functional capabilities and blood flows. Coronary flows to both ventricles have been measured using radiolabeled microspheres [or left ventricular (LV) flow, by Doppler sensor on the circumflex coronary artery] during experiments of pressure loading and chronic and acute hypoxemia. Blood flow to the left ventricle with its lower wall tension is about two-thirds the flow per gram compared with the right ventricle (RV). Acute systolic pressure loading of the RV to its maximal work capability stimulates flow to double (from ∼250 to 500 ml ⋅ min−1⋅ 100 g−1), but to a level less than stimulated by adenosine (750 ml ⋅ min−1⋅ 100 g−1). At all RV work loads, LV flow remains at two-thirds RV flow. Resting myocardial flow levels in fetuses that have been chronically hypoxemic are similar to maximal adenosine-stimulated flows of normal fetal sheep. This flow augmentation is evidently due to vascular remodeling because a normal “flow reserve” of ∼500 ml ⋅ min−1⋅ 100 g−1during adenosine administration remains. Acute hypoxemia stimulates myocardial flow to extraordinary levels (>1.5 l ⋅ min−1⋅ 100 g−1), levels larger than can be obtained with chemical dilation alone. LV flows do not exceed adenosine-stimulated flows when nitric oxide synthase is antagonized. We conclude1) fetal RV coronary flow increases with RV work but to levels less than during adenosine stimulation;2) the fetal heart is designed to accommodate extremely high flows in response to acute hypoxemia, partially through large production of nitric oxide; and3) the fetal coronary tree is dramatically remodeled in response to chronic hypoxemia.