Effects of Birth-Related Events on Blood Flow Distribution

Iwamoto, Harriet S.; Teitel, David; Rudolph, Abraham M.

doi:10.1203/00006450-198712000-00004

Cited by 81 publications

(45 citation statements)

References 28 publications

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“…Alternatively, they could mediate the response to ventilation of the lungs with a gas. Though an increase in oxygen tension alone can increase fetal pulmonary blood flow to newborn values (18), ventilation of the lungs with a gas which does not change oxygen tension also increases fetal pulmonary blood flow to a lesser extent (12,40,41). LeMer et al (39) did find that ventilation of the fetal lungs with such a gas caused them to produce 6-keto-prostaglandin F,,.…”

Section: Resultsmentioning

confidence: 96%

Indomethacin Does Not Diminish the Pulmonary Vascular Response of the Fetus to Increased Oxygen Tension

1988

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ABSTRACT. This study was performed to determineOxygen is one of the major stimuli decreasing pulmonary whether prostaglandins play a role in the increase in pul-vascular resistance at birth (1,(13)(14)(15). Assali et al., (16) and monary blood flow in the fetal lamb caused by an increase Heymann et al., (17) isolated the effect of a rise in oxygen tension in oxygen tension similar to that occurring at birth. To from the effect of ventilation of the lungs with a gas in acutely increase fetal oxygen tension without ventilating the lungs, instrumented fetal lambs by placing pregnant ewes in a hypernine pregnant ewes with chronically instrumented fetuses baric chamber at several atmospheres of pressure. Morin et al.were exposed to 100% oxygen at 3 atmospheres absolute (18) adapted this technique to study chronically instrumented pressure for 20 min in a hyperbaric chamber. This expo-fetal lambs and found that the entire increase in pulmonary sure increased pulmonary arterial oxygen tension in the blood flow that normally occurs at birth could be produced by nine fetuses from 20 f 1 to 54 f 9 torr. It increased an increase in oxygen tension alone. pulmonary blood flow from fetal to newborn values, 31 fThe current study was performed to determine whether the 3 to 295 2 20 ml/kg/min. It did not change pulmonary response of the fetal pulmonary circulation to oxygen is mediated arterial pressure, 52 f 2 torr during normoxia and 50 f 2 by prostaglandins. We measured the ability of prostaglandin torr during hyperoxia. Treating five of these fetuses with synthesis blockade by indomethacin to diminish the increase in 3.2 f 0.4 mg/kg of indomethacin during hyperbaric oxy-fetal pulmonary blood flow caused by an increase in oxygen genation did not alter these effects (Po2 = 51 f 8 torr, tension. pulmonary blood flow = 283 f 13 ml/kg/min, and pulmonary arterial pressure = 48 f 2 torr). We conclude that gestation were prepared for study. A catheter was passed from the maternal jugular vein into the right atrium for sampling of Abbreviations blood and for induction of anesthesia with 700 mg of sodium thiamylal. Surgery was then performed with the pregnant ewe PGD2, prostaglandin D2 under halothane anesthesia. The uterus was exposed through an PGE2, prostaglandin Ez abdominal incision, and the fetal head and neck were delivered 6-keto-PGE2, prostaglandin E2 through a uterine incision. An incision was made in the fetal ATA, atmosphere absolute pressure neck, and catheters were inserted into the carotid artery for measurement of systemic pressure and via the jugular vein into the superior vena cava for injection of radioactive microspheres. A left thoracotomy was performed, and a catheter was inserted into the main pulmonary artery, proximal to the branching of At birth there is a dramatic decrease in pulmonary vascular the right and left pulmonary arteries and the ductus arteriosus, resistance and increase in pulmonary blood flow (1, 2). The for measurement of pressure; sampling of blood gases and withincrease in pulmonary blood f...

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Section: Resultsmentioning

confidence: 96%

Indomethacin Does Not Diminish the Pulmonary Vascular Response of the Fetus to Increased Oxygen Tension

1988

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“…To ventilate the fetus, first, the endotracheal tubing was disconnected from the amniotic cavity catheter to drain the tracheal fluid (3,10). Then, Exosurf™ (10 ml) was instilled into the trachea.…”

Section: Physiologic Studiesmentioning

confidence: 99%

“…Amniotic fluid losses were replaced with warmed 0.9% saline. To ensure unobstructed drainage of the tracheal fluid into the amniotic cavity, the endotracheal tube was connected by tubing to the amniotic cavity catheter (3,10). All catheters and the flow transducer were exteriorized to the left flank of the ewe and placed in a vinyl pouch.…”

Section: Physiologic Studiesmentioning

confidence: 99%

“…After birth, with initiation of ventilation by the lungs, and the subsequent increase in pulmonary and systemic arterial blood oxygen tensions, pulmonary vascular resistance decreases and pulmonary blood flow increases by 8-10-fold to match systemic blood flow (1)(2)(3)(4). This process is regulated by a complex and incompletely understood interplay between mechanical and metabolic factors (5).…”

Section: Introductionmentioning

confidence: 99%

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Ventilation and oxygenation induce endothelial nitric oxide synthase gene expression in the lungs of fetal lambs.

Black¹,

Johengen²,

Dong³

et al. 1997

J. Clin. Invest.

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At birth, ventilation and oxygenation immediately decrease pulmonary vascular resistance (PVR) and increase pulmonary blood flow (PBF); more gradual changes occur over the next several hours. Nitric oxide, produced by endothelial nitric oxide synthase (eNOS), mediates these gradual changes. To determine how ventilation and oxygenation affect eNOS gene expression, 12 fetal lambs were ventilated for 8 h without changing fetal descending aortic blood gases or pH (rhythmic distension) or with 100% oxygen (O 2 ventilation). Vascular pressures and PBF were measured. Total RNA, protein, and tissue sections were prepared from lung tissue for RNase protection assays, Western blotting, and in situ hybridization. O 2 ventilation increased PBF and decreased PVR more than rhythmic distension ( P Ͻ 0.05). Rhythmic distension increased eNOS mRNA expression; O 2 ventilation increased eNOS mRNA expression more and increased eNOS protein expression ( P Ͻ 0.05). To define the mechanisms responsible for these changes, ovine fetal pulmonary arterial endothelial cells were exposed to 1, 21, or 95% O 2 or to shear stress. 95% O 2 increased eNOS mRNA and protein expression ( P Ͻ 0.05). Shear stress increased eNOS mRNA and protein expression ( P Ͻ 0.05). Increased oxygenation but more importantly increased PBF with increased shear stress induce eNOS gene expression and contribute to pulmonary vasodilation after birth. (

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“…To ensure a maximal decrease in pulmonary vascular resistance, 100% oxygen was used. The ventilation settings were initially adjusted to deliver an inspiratory:expiratory ratio of 0.8:I, a respiratory rate of 55-60/min, and a tidal volume of about 20-30 mL, similar to that used in our previous experiments (3,39). Positive endexpiratory pressure was applied to counterbalance amniotic pressure.…”

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confidence: 99%

In Utero Ventilation Augments the Left Ventricular Response to Isoproterenol and Volume Loading in Fetal Sheep

et al. 1991

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The basis of this limitation in the ability of the fetal left ventricle to greatly increase output (systolic performance) is controversial. Several studies point to myocardial immaturity: incomplete development of sarcomeres (17-21), decreased functioning of {J-receptors (22, 23), and myofibrillar disarray (24,25) have all been implicated. Although fetal myocardium is certainly immature relative to that of the adult, none of these factors have been shown to change immediately at birth. In addition, many indices of systolic performance are increased in the newborn left ventricle relative to that of the adult (11,12), so that myocardial immaturity may not necessarily be associated with impaired ventricular function. It is remarkable that both the prematurely born animal (26-28) and human (29), which have not been exposed to prenatal hormone surges and labor to accelerate myocardial maturation, are capable of greatly increasing left ventricular output in response to a patent ductus arteriosus. In addition, recent studies of fetal sheep undergoing oxygen ventilation in utero have shown a doubling of left ventricular output (3,30), and other determinants of output such as septal compliance (31) have been shown to change in the perinatal period.Thus, left ventricular output may be limited in the fetus more because of its "circulatory environment" (the combination of a parallel circulation with central shunts, a dominant hypertrophied right ventricle that ejects more output and fills under similar pressures, a pulmonary vascular bed that is markedly constricted and that returns a very limited amount of blood to the left atrium and ventricle, and a highly compliant fetoplacental vascular bed that can absorb increases in volume that would otherwise increase left ventricular filling volume) than because of myocardial immaturity. For example, the fetal left ventricle has a very limited ability to increase output via the Frank-Starling mechanism (13), with a plateau occurring at 5-7 mm Hg. However, Hawkins et at.(32) have shown that some of this limitation is caused by a concomitant increase in afterload; if afterload is controlled, left ventricular output continues to rise at filling pressures of 10 mm Hg. In addition, high right ventricular filling and ejecting pressures may constrain left ventricular performance both in diastole and systole (33-36).We undertook the present study to determine whether the near-term (approximately 0.9 gestation) fetal left ventricle, functioning in a simulated "postnatal circulatory environment" (abolition of most central shunts with a small left to right shunt through the ductus arteriosus, a dominant left ventricle ejecting somewhat more blood than the right under higher filling pressures, a dilated pulmonary vascular bed returning a large amount of blood to the left atrium and ventricle, and a decrease in the fetoplacental vascular bed), is capable of increasing its output to levels similar to those seen in the newborn. We simulated the immediate postnatal circulatory environment in ute...

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Effects of Birth-Related Events on Blood Flow Distribution

Cited by 81 publications

References 28 publications

Indomethacin Does Not Diminish the Pulmonary Vascular Response of the Fetus to Increased Oxygen Tension

Indomethacin Does Not Diminish the Pulmonary Vascular Response of the Fetus to Increased Oxygen Tension

Ventilation and oxygenation induce endothelial nitric oxide synthase gene expression in the lungs of fetal lambs.

In Utero Ventilation Augments the Left Ventricular Response to Isoproterenol and Volume Loading in Fetal Sheep

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