UMBILICAL AND HEPATIC VENOUS RESPONSES TO CIRCULATING VASOCONSTRICTIVE HORMONES IN FETAL LAMB

被引:41
作者
PAULICK, RP
MEYERS, RL
RUDOLPH, CD
RUDOLPH, AM
机构
[1] UNIV CALIF SAN FRANCISCO, CARDIOVASC RES INST, BOX 0544, HSE 1403, SAN FRANCISCO, CA 94143 USA
[2] UNIV CALIF SAN FRANCISCO, DEPT PEDIAT, SAN FRANCISCO, CA 94143 USA
[3] UNIV CALIF SAN FRANCISCO, DEPT SURG, SAN FRANCISCO, CA 94143 USA
[4] UNIV CALIF SAN FRANCISCO, DEPT OBSTET GYNECOL & REPROD SCI, SAN FRANCISCO, CA 94143 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1991年 / 260卷 / 04期
关键词
ANGIOTENSIN-II; EPINEPHRINE; NOREPINEPHRINE; VASOPRESSIN; UMBILICAL-PLACENTAL BLOOD FLOW; UMBILICAL-PLACENTAL VASCULAR RESISTANCE;
D O I
10.1152/ajpheart.1991.260.4.H1205
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Acute fetal hypoxemia increases the vascular resistance of the umbilical veins as well as that of the liver. Because, at least in the human, the umbilical-placental circulation has no autonomic innervation, circulating hormones could well be responsible for this increase in umbilical-placental outflow resistance. In chronically instrumented fetal sheep, norepinephrine, epinephrine, vasopressin, and angiotensin II were infused in sequentially increasing doses into the descending aorta and vascular resistance to umbilical-placental blood flow was measured. Norepinephrine and epinephrine increased the vascular resistance of the umbilical veins in a dose-dependent manner. Both catecholamines also increased the vascular resistance of the liver, resulting in an increase in ductus venosus blood flow. In contrast, vasopressin and angiotensin II had no effect on umbilical-placental outflow resistance. Thus catecholamines may be responsible for the increase in the vascular resistance of the umbilical veins and liver in response to acute fetal hypoxemia.
引用
收藏
页码:H1205 / H1213
页数:9
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