Cardiovascular and Catecholamine Responses to Successive Episodes of Hypoxemia in the Fetus

Lewis, Alan B.; Wolf, Wendy J.; Sischo, William M.

doi:10.1159/000241883

Cited by 22 publications

(11 citation statements)

References 10 publications

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“…This effect is consistent with other studies in which fetal hypoxia was produced by a reduction in uterine blood flow [5,6,9] or secondarily by maternally inspired, low-oxygen gas mixtures [13,14]. The rebound tachycardia has been reported previously [5,15] and is postulated to occur as a result of the increased circulating cate cholamines released by the fetus in response to hypoxic stress [6,16,17].…”

Section: Discussionsupporting

confidence: 91%

Fetal Beta-Endorphin Levels in Response to Reductions in Uterine Blood Flow

Skillman¹,

Clark²

1987

Neonatology

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Fetal β-endorphin release has been associated with fetal hypoxia. The purpose of this study was to assess the degree of uterine blood flow reduction needed to elicit fetal β-endorphin release in the sheep since there is a large reserve of oxygen supply to the fetus. Uterine blood flow was reduced by 26 ± 2, 46 ± 3 and 66 ± 2%, producing fetal oxygen content concentrations of 5.7 ± 0.6, 4.4 ± 0.7 and 2.6 ± 0.3 ml/dl, respectively. Although fetal oxygen concentrations were significantly decreased in the groups with a reduction in uterine blood flow of 46 and 66%, β-endorphin was elevated only in the latter group. It is speculated that fetal β-endorphin is released at a level of hypoxia which leads to a decrease in fetal oxygen consumption. A reduction in uterine blood flow of 66% appears to produce a stressful environment for the fetus as measured by fetal plasma β-endorphin levels.

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Section: Discussionsupporting

confidence: 91%

Fetal Beta-Endorphin Levels in Response to Reductions in Uterine Blood Flow

Skillman¹,

Clark²

1987

Neonatology

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“…As reported by others for partial cord occlusions (Giussani et al, 1997), we observed that following the initial bradycardia fetal heart rate stabilized or even increased slightly only to fall again during the last minute of occlusion. This transient increase in heart rate parallels the increase in arterial pressure and thus may also be the result of increased sympathetic drive (Lewis et al, 1984). In contrast to the bradycardia of the first minute, fetal heart rate in pre-existing hypoxia fetuses was significantly lower than in normoxic fetuses during the last minute only in the last three occlusions.…”

Section: Discussionmentioning

confidence: 85%

Mild chronic hypoxia modifies the fetal sheep neural and cardiovascular responses to repeated umbilical cord occlusion

et al. 2007

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We have shown that five days of mild hypoxia has significant effects on fetal ECoG activity, heart rate and blood pressure. We now studied if mild prolonged hypoxemia had an adverse effect on the fetal cardiovascular and neural responses to repeated cord occlusion and on the magnitude of neuronal damage. Fetal and maternal catheters were placed at 120 days' gestation and animals allocated at random to receive intratracheal maternal administration of nitrogen (n=8) or compressed air in controls (n=7). Five days after surgery, nitrogen infusion was adjusted to reduce fetal brachial artery pO 2 by 25%. After 5 days of chronic hypoxemia the umbilical cord was completely occluded for 5 minutes every 30 minutes for a total of four occlusions. Data are presented as mean ± SEM and were analyzed by Two Way ANOVA or two sample t test. Nitrogen infusion decreased fetal pO 2 by 26% (20.5±1.7 vs. 14.3±0.8 mmHg) without changing fetal pCO 2 or pH. Pre-existing hypoxia fetuses had a greater terminal fall in heart rate in occlusions II, III and IV, and also had a more severe terminal hypotension in the final occlusion. Pre-existing hypoxia was associated with a greater fall in spectral edge frequency during occlussions from 14.4±0.9 Hz to 6.9±0.4 Hz vs. 13.6±1.64 Hz to 10.6±0.77 Hz in controls, p<0.05. In addition, during the three-day post-occlusion period the contribution of theta and alpha band frequencies to total ECoG activity was significantly lower in the pre-existing hypoxia fetuses (p<0.05). These effects were associated with increased neuronal loss in the striatum (p<0.05). In summary, the cardiovascular and neural response indicate a detrimental effect of preexisting mild hypoxia on fetal outcome following repeated umbilical cord occlusions.

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“…Acute hypoxemia increases plasma concentrations of norepinephrine, epinephrine, and vasopressin (20), and also increases plasma glucagon concentrations (2 1) in fetal lambs. Acute cord compression similarly increases norepinephrine and epinephrine (22); however, changes in glucagon, vasopressin, and angiotensin I1 have not been studied. Determination of the specific role of each of these hormones as stimuli for fetal hepatic glucose release during hypoxemia or cord compression will require further study using specific antagonists.…”

Section: Discussionmentioning

confidence: 98%

Effect of Acute Umbilical Cord Compression on Hepatic Carbohydrate Metabolism in the Fetal Lamb

1989

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ABSTRACT. Although the liver plays a central role in UV, umbilical vein glucose homeostasis in the adult, its importance in fetal C(:(substrate)~~~, concentraton of substrate in right hepatic vein glucose homeostasis during acute reductions of substrate QUV, total umbilical venous blood flow delivery is unknown. To examine this, we studied eight QUVe,,,, blood flow to the liver from the umbilical vein fetal lambs at 121 f 2 d gestation. We placed catheters in V(substrate), substrate flux across the liver the descending aorta, inferior vena cava umbilical vein and the left (n = 6) or right (n = 2) hepatic vein, and a balloon occluder around the umbilical cord. At least 4 d after surgery, before and during umbilical cord compression, we measured blood oxygen saturation, glucose, lactate, and Hb concentrations, and blood flows using the radiolabeled microsphere technique. Gluconeogenesis was assessed by infusion of [U14C]lactate. Reducing umbilical flow by 50-60% from a control value of 181 f 20 mL/min/kg (mean* SD) caused a dramatic decrease in hepatic blood flow from 332 f 99 to 94 f 77 mL/min/100 g (p ~0.05). Oxygen delivery to the fetus fell by 50% and that to the liver by 73%. However, hepatic 0 2 consumption was maintained by increased extraction. Glucose delivery to the liver fell from 67 f 24 to 20 f 13 mg/min/100 g (p <0.001), but lactate delivery did not change. In spite of the maintenance of lactate delivery, net hepatic lactate uptake fell significantly from 3.3 2 1.7 to 1.4 f 0.9 mg/min100 g (p ~0.05). This could account, in part, for the increase of blood lactate concentration from 16 f 4 to 27 f 7 mg/dl. Although hepatic glucose delivery fell markedly, net glucose production by the liver increased from 0.1 f 2.4 to 3.9 f 7.3 mg/ min/100 g (p ~0.05). Presumably, this glucose production is from glycogenolysis because no hepatic gluconeogenesis from labeled lactate could be detected. During umbilical cord compression, hepatic glycogenolysis contributed 1.5 f 2.8 mg/min/kg (30%) of total glucose utilized by the fetus. The mechanisms responsible for fetal hepatic glycogenolysis are yet to be delineated. (Pediatr Res 25228-233,1989 Acute umbilical cord compression, which causes hypoxemia and acidemia, is one of the most common causes of fetal distress. The homeostatic mechanisms invoked by the fetus to supply adequate oxygen to the brain and heart have been well characterized (I). As placental blood flow decreases, regional blood flows alter to maintain brain and heart flow. An increased proportion of the oxygen-rich blood from the UV is shunted away from the liver through the ductus venosus to the brain and heart, with blood flow and oxygen delivery to the liver decreasing by 50--75%.Changes in fetal substrate delivery and utilization have not been studied during umbilical cord compression. In the unstressed fetal lamb, 40% of the energy substrates to the fetus are provided by glucose and 20% by lactate (2). Glycogen is synthesized by the liver (3), but no gluconeogenesis or glycogenolysis occurs (4). We ...

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Cardiovascular and Catecholamine Responses to Successive Episodes of Hypoxemia in the Fetus

Cited by 22 publications

References 10 publications

Fetal Beta-Endorphin Levels in Response to Reductions in Uterine Blood Flow

Fetal Beta-Endorphin Levels in Response to Reductions in Uterine Blood Flow

Mild chronic hypoxia modifies the fetal sheep neural and cardiovascular responses to repeated umbilical cord occlusion

Effect of Acute Umbilical Cord Compression on Hepatic Carbohydrate Metabolism in the Fetal Lamb

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