Neonatal Adaptation: Sympatho-Adrenal Response to Umbilical Cord Cutting

Padbury, Jamés F.; Diakomanolis, Emmanuel; Hobel, Calvin J.; Perelman, Alvin; Fisher, Delbert A.

doi:10.1203/00006450-198112000-00005

Cited by 79 publications

(41 citation statements)

References 13 publications

(19 reference statements)

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“…Catecholamines do not cross the placenta and in the fetal lamb increase after hypothermia (S), hypoxia (33), hemorrhage (34), labor (32), and umbilical cord cutting (35). The surge in catecholamine that occurs at birth is associated with a rise in plasma FFA levels.…”

Section: Discussionmentioning

confidence: 99%

“…The surge in catecholamine that occurs at birth is associated with a rise in plasma FFA levels. It has been suggested by Padbury et al (35,36) that this is the primary signal for the initiation of nonshivering thermogenesis. In previous studies (8,23), the initial surge in plasma catecholamines after cooling without ventilation or cord snare was not accompanied by nonshivering thermogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Reversible Umbilical Cord Occlusion: Effects on Thermogenesis In Utero

1991

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A rapid fall in environmental temperature accompanies the transition from intrauterine to extrauterine existence, and effective thermogenesis is essential to neonatal adaptation. Studies on temperature regulation have shown the importance of thermal homeostasis in reducing the mortality rate of low birth weight infants. The mortality in preterm infants subjected to cold stress is dependent upon the degree and duration of hypothermia (1, 2).The demand for heat production is often maximal at the moment of birth, and the brown adipose tissue thermogenic response to chilling in newborn infants and precocial species such as the lamb is mediated by the sympathetic nervous system. Norepinephrine may increase oxygen consumption and heat production more than 3-fold (3, 4). The mammalian fetal environment is relatively thermostable, and the fetus does not appear to regulate its temperature independently of the mother (5). We

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Reversible Umbilical Cord Occlusion: Effects on Thermogenesis In Utero

1991

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“…I). The order of oxygen ventilation and isoproterenol to simulate the important catecholamine surge at birth (28,37), and volume loading. We measured left ventricular output, vascular pressures, and heart rate, and determined the individual and combined effects of each intervention on these variables.…”

Section: Methodsmentioning

confidence: 99%

“…We have previously shown that oxygen ventilation in utero creates a central circulatory pattern that is identical to the immediate postnatal circulation (3). In addition, the newborn left ventricle functions under significant fJ-adrenergic stimulation (8,37), which is essential to the increase in output at birth (28), and at higher filling pressures (6, 11) than before birth, so we performed the studies during isoproterenol infusion and volume loading in addition to oxygen ventilation. We found that oxygen ventilation and isoproterenol increased left ventricular output, but not volume infusion, and that the effect of oxygen ventilation far exceeded that of isoproterenol.…”

Section: Ascendingaortic Bloodjlow Mean Ascending Aortic Blood Flowmentioning

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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“…It is also interesting to speculate on the mechanisms supporting the LV contraction during the transition from fetal to neonatal circulation. One mechanism can be attributable to the presence of neuroendocrines, especially catecholamines which increase markedly in the circulation at birth (Eliot et al 1980;Padbury et al 1981Padbury et al , 1985, along with the supersensitivity of newborn myocardium to circulating catecholamines (Friedman 1972). In addition, we suggest that the low afterload condition may be one mechanism supporting the LV adaptation to various loading changes shortly after birth.…”

Section: Discussiqnmentioning

confidence: 99%

Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus.

Harada

Shiota

Tamura

et al. 1994

Tohoku J. Exp. Med.

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A. and TAKADA, G. Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus. Tohoku J. Exp. Med., 1994, 172 (2), 155-161 Using echocardiographic technique, we studied the left ventricular (LV) contractile state in 32 full-term infants within 24 hr after birth. They were divided into 2 groups based on the timing of the examinations; the group 1(n -17), < 3 hr after birth; the group 2 (n=15), > 3 and <24 hr after birth, and the additional examinations were performed on day 5. The patency of the ductus arteriosus and its internal diameter were determined by pulsed Doppler and two-dimensional echocardiography. The left atrial to aortic root ratio was obtained from M-mode echocardiography, and the LV contractile state was estimated by the relationship between heart rate-corrected velocity of circumferential fiber shortening (mVcfc) and end-systolic meridional wall stress (ESS). The ductus arteriosus was open in all cases of group 1 and in 83% of the cases of group 2, but the ductal diameter and the left atrial to aortic root ratio significantly decreased in group 2. The relationship between mVcfc and ESS showed no significant differences between 2 groups and the control. Afterload, represented as ESS, was significantly lower in group 1 than the control. We suggest that the low afterload condition helps the adequate LV contraction even under the increased preload through the left-to-right ductus arteriosus shunting after birth. left ventricle; patent ductus arteriosus; neonate; end-systolic meridional wall stress During the transition from fetal to neonatal circulation, the left-to-right ductus arteriosus shunting acts as a preload to the left ventricle (LV). In animal research on newborn lambs, some investigators demonstrated the less capacity of LV response to an increased preload (Klopfenstein and Rudolph 1978;Romero and Friedman 1979;Baylen et al. 1985), whereas, others demonstrated the capa-

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Neonatal Adaptation: Sympatho-Adrenal Response to Umbilical Cord Cutting

Cited by 79 publications

References 13 publications

Reversible Umbilical Cord Occlusion: Effects on Thermogenesis In Utero

Reversible Umbilical Cord Occlusion: Effects on Thermogenesis In Utero

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

Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus.

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