Davis L, Roullet J B, Thornburg K L, Shokry M, Hohimer A R, Giraud G D
Department of Obstetrics and the Heart Research Center, Oregon Health Sciences University, Portland, OR 97239-3098, USA.
J Physiol. 2003 Feb 15;547(Pt 1):53-9. doi: 10.1113/jphysiol.2002.023283. Epub 2002 Oct 18.
Maximal coronary conductance with adenosine in anaemic fetal sheep is twice that of non-anaemic fetuses. To investigate whether this increase in conductance persists into adulthood we studied twin sheep as fetuses and again as adults. Nine anaemic fetuses (118 days gestation) underwent isovolaemic haemorrhage for 18.0 +/- 4.6 days (means +/- S.D.) during which time the haematocrit was reduced from 39.9 +/- 5.2 % to 16.3 +/- 3.4 % and oxygen content from 8.6 +/- 1.3 to 2.3 +/- 0.2 ml dl-1. At 138 days the anaemic fetuses were transfused; at delivery the haematocrit was 29.3 +/- 6.8 % compared to nine control fetuses in which the haematocrit was 38.5 +/- 4.3 %. The weight at delivery was 3.5 +/- 0.36 kg in the anaemic fetuses vs. 4.2 +/- 0.83 kg in controls. Twenty-eight weeks later, we placed an occluder on the descending thoracic aorta and inferior vena cava, a flow probe around the proximal left circumflex coronary artery, and catheters in the left atrial appendage, jugular and carotid vessels. Maximal coronary conductance was determined in the adults by recording coronary blood flow as driving pressure was altered by inflating the occluders while adenosine was infused into the left atrium. Right atrial, left atrial, systolic and mean arterial pressures, systemic vascular resistance and haematocrit were not different between 'in utero anaemic' and control adults. The adults that were anaemic in utero weighed less than the controls 39.4 +/- 4.6 kg vs. 45.0 +/- 5.6 kg. Maximal conductance was greater in the adults that were anaemic in utero: 11.2 +/- 4.0 ml min(-1) (100 g)(-1) mmHg-1 as compared to 6.1 +/- 1.8 ml min(-1) (100 g)(-1) mmHg(-1) in the controls. Vascular reactivity of the mesenteric arteries was not different. These data suggest that coronary conductance can be modified in utero by anaemia (high flow and hypoxaemia) and that the remodelled coronary tree persists to adulthood.
贫血胎羊在使用腺苷时的最大冠状动脉传导率是非贫血胎儿的两倍。为了研究这种传导率的增加是否会持续到成年期,我们对双胞胎绵羊进行了研究,从胎儿期一直跟踪到成年期。9只贫血胎儿(妊娠118天)进行了18.0±4.6天(平均值±标准差)的等容性失血,在此期间,血细胞比容从39.9±5.2%降至16.3±3.4%,氧含量从8.6±1.3降至2.3±0.2 ml dl-1。在138天时,对贫血胎儿进行输血;分娩时,贫血胎儿的血细胞比容为29.3±6.8%,而9只对照胎儿的血细胞比容为38.5±4.3%。贫血胎儿分娩时的体重为3.5±0.36 kg,而对照组为4.2±0.83 kg。28周后,我们在胸降主动脉和下腔静脉上放置了封堵器,在左回旋支冠状动脉近端周围放置了流量探头,并在左心耳、颈静脉和颈动脉中插入了导管。在成年绵羊中,通过记录冠状动脉血流量来测定最大冠状动脉传导率,在向左心房注入腺苷的同时,通过充气封堵器改变驱动压力。“宫内贫血”成年绵羊和对照成年绵羊的右心房压力、左心房压力、收缩压和平均动脉压、全身血管阻力和血细胞比容没有差异。宫内贫血的成年绵羊体重低于对照组,分别为39.4±4.6 kg和45.0±5.6 kg。宫内贫血的成年绵羊的最大传导率更高:为11.2±4.0 ml min-1(100 g)-1 mmHg-1,而对照组为6.1±1.8 ml min-1(100 g)-1 mmHg-1。肠系膜动脉的血管反应性没有差异。这些数据表明,贫血(高流量和低氧血症)可在子宫内改变冠状动脉传导率,并且重塑的冠状动脉树会持续到成年期。