MATERNAL AND FETAL ATRIAL-NATRIURETIC-PEPTIDE LEVELS AT DELIVERY FROM NORMAL AND GROWTH RETARDED PREGNANCIES

被引:19
作者
KINGDOM, JCP [1 ]
MCQUEEN, J [1 ]
CONNELL, JMC [1 ]
WHITTLE, MJ [1 ]
机构
[1] WESTERN INFIRM & ASSOCIATED HOSP,MED RES COUNCIL BLOOD PRESSURE UNIT,GLASGOW G11 6NT,SCOTLAND
来源
BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY | 1992年 / 99卷 / 10期
关键词
D O I
10.1111/j.1471-0528.1992.tb14418.x
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective To determine whether circulating fetal levels of the vasodilator atrial natriuretic peptide (ANP) are reduced in pregnancies complicated by intrauterine growth retardation (IUGR). Design Prospective observational study. Setting University teaching hospital and research laboratory. Subjects 25 normal singleton pregnancies delivered at term by spontaneous vertex delivery (n = 16) or by elective caesarean section (n = 9), and a series of 14 singleton pregnancies complicated by IUGR. Intervention Measurement of ANP by radio-immunoassay in maternal venous, umbilical artery, and umbilical vein plasma from a series of normal, and IUGR pregnancies. Main outcome measures Comparison of plasma ANP levels between the three groups; relation between fetal ANP, Po2 and pH. Results Mode of delivery did not influence either maternal, umbilical artery or umbilical vein plasma ANP levels in normal term singleton pregnancies. Umbilical vein ANP levels were significantly higher in the IUGR group when compared with normal pregnancies at term (mean 66 95%, CI 36-122 vs mean 37, 95% CI 29-47 pg/ml, P = 0.03) and were inversely related to umbilical artery pH (R2 = 65%; P = 0.003). Conclusions These data suggest that umbilical vein ANP levels are elevated in pregnancies complicated by IUGR, and rise appropriately in response to the stress of acidosis. In the absence of any receptor or second messenger defect within fetoplacental vascular smooth muscle, these data suggest that ANP is not directly implicated in the vascular pathophysiology of IUGR.
引用
收藏
页码:845 / 849
页数:5
相关论文
共 31 条
[1]   BIRTH STRESS INCREASES FETAL ATRIAL-NATRIURETIC-FACTOR [J].
ANDERSSON, S ;
HALLMAN, M ;
TIKKANEN, I ;
FYHRQUIST, F .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1990, 162 (03) :872-873
[2]   PERINATAL FACTORS INFLUENCING ATRIAL NATRIURETIC PEPTIDE LEVELS IN UMBILICAL ARTERIAL PLASMA AT THE TIME OF DELIVERY [J].
CASTRO, LC ;
ARORA, CP ;
ROLL, KE ;
SASSOON, DA ;
HOBEL, CJ .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1989, 161 (03) :623-627
[3]   FETAL HYPOXIA ELEVATES PLASMA ATRIAL NATRIURETIC FACTOR CONCENTRATION [J].
CHEUNG, CY ;
BRACE, RA .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1988, 159 (05) :1263-1268
[4]   A MEMBRANE FORM OF GUANYLATE-CYCLASE IS AN ATRIAL NATRIURETIC PEPTIDE RECEPTOR [J].
CHINKERS, M ;
GARBERS, DL ;
CHANG, MS ;
LOWE, DG ;
CHIN, HM ;
GOEDDEL, DV ;
SCHULZ, S .
NATURE, 1989, 338 (6210) :78-83
[5]   MATERNAL AND FETAL PLASMA ATRIAL-NATRIURETIC-PEPTIDE CONCENTRATIONS DURING ELECTIVE CESAREAN-SECTION [J].
DATTA, S ;
MURPHY, MT ;
CARR, DB ;
BADER, AM ;
JOHNSON, MD .
ACTA ANAESTHESIOLOGICA SCANDINAVICA, 1991, 35 (02) :93-96
[6]   ATRIAL-NATRIURETIC-PEPTIDE IN FETAL DISEASE [J].
FISK, NM ;
TANNIRANDORN, Y ;
NICOLINI, U ;
HUBINONT, C ;
RODECK, CH ;
MELIAGROS, L .
BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY, 1990, 97 (06) :545-546
[7]  
FOK RY, 1990, OBSTET GYNECOL, V75, P578
[8]  
FORBES JF, 1982, CENTILE VALUES BIRTH
[9]   EXPRESSION OF THE ATRIAL NATRIURETIC PEPTIDE GENE IN HUMAN-FETAL HEART [J].
GARDNER, DG ;
HEDGES, BK ;
WU, J ;
LAPOINTE, MC ;
DESCHEPPER, CF .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1989, 69 (04) :729-737
[10]   FETAL UMBILICAL ARTERY FLOW VELOCITY WAVEFORMS AND PLACENTAL RESISTANCE - PATHOLOGICAL CORRELATION [J].
GILES, WB ;
TRUDINGER, BJ ;
BAIRD, PJ .
BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY, 1985, 92 (01) :31-38