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围产期氧输送与心功能。

Perinatal oxygen delivery and cardiac function.

作者信息

Teitel D, Rudolph A M

出版信息

Adv Pediatr. 1985;32:321-47.

PMID:3909777
Abstract

In this review, we have considered interrelationships between blood flow and oxygen requirements of the body during fetal and neonatal development. During fetal life, blood is oxygenated in the placenta and returns to the fetus through the umbilical vein. The ductus venosus serves as a bypass of umbilical venous blood from the hepatic microcirculation. Preferential streaming of blood in the inferior vena cava facilitates delivery of well-oxygenated ductus venosus blood to the brain and heart. During fetal stress of hypoxia or umbilical cord compression, flow through the liver and ductus venosus is modified to facilitate oxygen delivery to the fetal body and local organ vascular responses, and to maintain blood flow and oxygen delivery to vital organs, such as the brain, heart, and adrenal gland. During fetal life, immaturity of the fetal myocardium accounts for limited ability for cardiac output to be augmented when ventricular filling pressure is increased above the resting level; yet immediately after birth, cardiac output increases dramatically. Experimental evidence points to an important role of prenatal thyroid hormone in maturation of the myocardium for postnatal requirements. In association with the increase in oxygen requirements after birth, cardiac output increases, but because resting requirements for blood flow are high, there is a limited ability for cardiac output to be increased further. With postnatal development, cardiac output requirements in relation to body weight decrease, partly in parallel with reduced oxygen requirements related to body weight, but also as a result of rightward shift of the oxygen dissociation curve as fetal hemoglobin is replaced by adult hemoglobin. Understanding the circulatory and metabolic changes that occur in the perinatal period and the mechanisms of response to stress is important in management of the newborn infant with cardiorespiratory distress.

摘要

在本综述中,我们探讨了胎儿和新生儿发育过程中身体血流与氧需求之间的相互关系。在胎儿期,血液在胎盘进行氧合,然后通过脐静脉返回胎儿体内。静脉导管可使脐静脉血绕过肝脏微循环。下腔静脉中血液的优先流动有助于将氧合良好的静脉导管血输送至大脑和心脏。在胎儿发生缺氧或脐带受压等应激情况时,流经肝脏和静脉导管的血流会发生改变,以促进向胎儿身体输送氧气以及局部器官的血管反应,并维持向大脑、心脏和肾上腺等重要器官的血流和氧气输送。在胎儿期,胎儿心肌不成熟,当心室充盈压高于静息水平时,心输出量增加的能力有限;然而出生后即刻,心输出量会急剧增加。实验证据表明产前甲状腺激素在使心肌成熟以满足出生后需求方面发挥着重要作用。随着出生后氧需求的增加,心输出量会增加,但由于静息时的血流需求较高,心输出量进一步增加的能力有限。随着出生后的发育,与体重相关的心输出量需求会降低,部分原因与体重相关的氧需求降低平行,但也是由于胎儿血红蛋白被成人血红蛋白替代后氧解离曲线右移所致。了解围生期发生的循环和代谢变化以及应激反应机制对于管理患有心肺窘迫的新生儿至关重要。

相似文献

1
Perinatal oxygen delivery and cardiac function.围产期氧输送与心功能。
Adv Pediatr. 1985;32:321-47.
2
Effects of reducing uterine blood flow on fetal blood flow distribution and oxygen delivery.减少子宫血流对胎儿血流分布及氧输送的影响。
J Dev Physiol. 1991 Jun;15(6):309-23.
3
The transition from fetal to neonatal circulation: normal responses and implications for infants with heart disease.从胎儿循环到新生儿循环的转变:正常反应及其对患心脏病婴儿的影响。
Semin Perinatol. 1993 Apr;17(2):106-21.
4
Reference values of fetal ductus venosus, inferior vena cava and hepatic vein blood flow velocities and waveform indices during the second and third trimester of pregnancy.妊娠中晚期胎儿静脉导管、下腔静脉及肝静脉血流速度和波形指数的参考值
Arch Gynecol Obstet. 2004 Jul;270(1):46-55. doi: 10.1007/s00404-003-0586-6. Epub 2004 Mar 12.
5
Effects of ductus venosus obstruction on liver and regional blood flows in the fetal lamb.静脉导管阻塞对胎羊肝脏及局部血流的影响。
Pediatr Res. 1991 Apr;29(4 Pt 1):347-52. doi: 10.1203/00006450-199104000-00004.
6
Blood circulation and oxygen transport in the fetal guinea pig.豚鼠胎儿的血液循环与氧气运输
J Dev Physiol. 1983 Jun;5(3):181-93.
7
Fetal circulatory responses to oxygen lack.胎儿对缺氧的循环反应。
J Dev Physiol. 1991 Oct;16(4):181-207.
8
Effects of birth-related events on blood flow distribution.与出生相关事件对血流分布的影响。
Pediatr Res. 1987 Dec;22(6):634-40. doi: 10.1203/00006450-198712000-00004.
9
Effects of cord compression on fetal blood flow distribution and O2 delivery.脐带受压对胎儿血流分布及氧输送的影响。
Am J Physiol. 1987 Jan;252(1 Pt 2):H100-9. doi: 10.1152/ajpheart.1987.252.1.H100.
10
Circulatory adjustments at birth.出生时的循环系统调整。
Obstet Gynecol Annu. 1975;4:99-118.

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