ONTOGENY OF NO ACTIVITY AND RESPONSE TO INHALED NO IN THE DEVELOPING OVINE PULMONARY CIRCULATION

被引:54
作者
KINSELLA, JP
IVY, DD
ABMAN, SH
机构
[1] CHILDRENS HOSP, DEPT PEDIAT, DIV CARDIOL, DENVER, CO 80262 USA
[2] CHILDRENS HOSP, DEPT PEDIAT, DIV PULM MED, DENVER, CO 80262 USA
[3] UNIV COLORADO, SCH MED, DENVER, CO 80262 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1994年 / 267卷 / 05期
关键词
ENDOTHELIUM-DERIVED RELAXING FACTOR; NITRIC OXIDE; FETUS; PREMATURITY; PULMONARY HYPERTENSION; BIRTH; NEWBORN; PERINATAL LUNG; VASODILATION; MECHANICAL VENTILATION;
D O I
10.1152/ajpheart.1994.267.5.H1955
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To determine maturation-related changes in nitric oxide (NO) activity in the developing pulmonary circulation, we studied the hemodynamic effects of endogenous NO inhibition under basal conditions in the premature ovine fetus and the response to birth-related stimuli and exogenous NO in 30 fetal sheep at three different gestational ages. At 0.95 term, pulmonary vasodilation during inhaled NO (20 parts per million) was equivalent to the dilator response to 100% O-2, but at 0.86 term vasodilation during inhaled NO was greater than the dilator response to 100% O-2 (P < 0.05). At 0.78 term, left pulmonary arterial flow (Q(LPA)) did not increase with exposure to either NO or 100% O-2. Intrapulmonary infusion of nitro-L-arginine (L-NA) increased basal pulmonary vascular resistance 38% in the premature fetus at 0.78 term. L-NA treatment decreased the ventilation-induced rise in Q(LPA) by 60% compared with controls (P < 0.05). Inhaled NO but not 100% O-2 increased Q(LPA) after L-NA treatment to levels achieved with ventilation alone in the controls. We conclude that in the premature pulmonary circulation (0.78 term) 1) basal pulmonary vascular resistance is modulated by endogenous NO, 2) pulmonary vasodilation at birth is partly mediated by endogenous NO activity, and 3) inhaled NO causes potent vasodilation.
引用
收藏
页码:H1955 / H1961
页数:7
相关论文
共 34 条
[11]   CHANGES IN THE LUNGS OF THE NEW-BORN LAMB [J].
DAWES, GS ;
MOTT, JC ;
WIDDICOMBE, JG ;
WYATT, DG .
JOURNAL OF PHYSIOLOGY-LONDON, 1953, 121 (01) :141-162
[12]   EFFECT OF LUNG EXPANSION ON FETAL LAMB CIRCULATION [J].
ENHORNIN.G ;
ADAMS, FH ;
NORMAN, A .
ACTA PAEDIATRICA SCANDINAVICA, 1966, 55 (05) :441-&
[13]  
FINEMAN JR, 1991, SEMIN PERINATOL, V15, P58
[14]   MATURATION-RELATED CHANGES IN ENDOTHELIAL NITRIC-OXIDE SYNTHASE IMMUNOLOCALIZATION IN DEVELOPING OVINE LUNG [J].
HALBOWER, AC ;
TUDER, RM ;
FRANKLIN, WA ;
POLLOCK, JS ;
FORSTERMANN, U ;
ABMAN, SH .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1994, 267 (05) :L585-L591
[15]   NORMAL ADAPTATION OF PULMONARY ARTERIAL INTIMA TO EXTRAUTERINE LIFE IN THE PIG - ULTRASTRUCTURAL STUDIES [J].
HALL, SM ;
HAWORTH, SG .
JOURNAL OF PATHOLOGY, 1986, 149 (01) :55-66
[16]   ADAPTATION OF THE PULMONARY CIRCULATION TO EXTRA-UTERINE LIFE IN THE PIG AND ITS RELEVANCE TO THE HUMAN INFANT [J].
HAWORTH, SG ;
HISLOP, AA .
CARDIOVASCULAR RESEARCH, 1981, 15 (02) :108-119
[17]  
JOBE A, 1984, ANIMAL MODELS FETAL, V3, P4
[18]  
JOBE AH, 1993, NEW ENGL J MED, V328, P861
[19]   CLINICAL-RESPONSES TO PROLONGED TREATMENT OF PERSISTENT PULMONARY-HYPERTENSION OF THE NEWBORN WITH LOW-DOSES OF INHALED NITRIC-OXIDE [J].
KINSELLA, JP ;
NEISH, SR ;
IVY, DD ;
SHAFFER, E ;
ABMAN, SH .
JOURNAL OF PEDIATRICS, 1993, 123 (01) :103-108
[20]   LOW-DOSE INHALATIONAL NITRIC-OXIDE IN PERSISTENT PULMONARY-HYPERTENSION OF THE NEWBORN [J].
KINSELLA, JP ;
NEISH, SR ;
SHAFFER, E ;
ABMAN, SH .
LANCET, 1992, 340 (8823) :819-820