Fetal heart rate patterns in postasphyxiated fetal lambs with brain damage

Ikeda, Tomoaki; Murata, Yuji; Quilligan, Edward J.; Parer, Julian T.; Theunissen, Ingrid; Cifuentes, P.; Doi, Shigeharu; Park, Soung-Day

doi:10.1016/s0002-9378(98)70156-5

Cited by 52 publications

(46 citation statements)

References 13 publications

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“…Fetal heart rate variability (SD-RR) was already significantly decreased at 3 d post-UCO and gradually decreased further during the remainder of the study. This observation is in agreement with that of Ikeda et al, who showed that decreased long-term fetal heart rate variability at 24-72 h of recovery after UCO is an indicator of the severity of histological damage in term fetal brain (29). To our knowledge, our study is the first to describe this change in fetal heart rate variability in preterm asphyxiated fetal lambs.…”

Section: Long-term Effects Of Hypoxia-ischemiasupporting

confidence: 93%

Heart rate–mediated blood pressure control in preterm fetal sheep under normal and hypoxic–ischemic conditions

et al. 2013

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Background:The understanding of hypoxemia-induced changes in baroreflex function is limited and may be studied in a fetal sheep experiment before, during, and after standardized hypoxic conditions. Methods: Preterm fetal lambs were instrumented at 102 d gestation (term: 146 d). At 106 d, intrauterine hypoxia-ischemia was induced by 25 min of umbilical cord occlusion (UCO). Baroreflex-related fluctuations were calculated at 30-min intervals during the first week after UCO by transfer function (crossspectral) analysis between systolic blood pressure (SBP) and R-R interval fluctuations, estimated in the low-frequency (LF, 0.04-0.15 Hz) band. LF transfer gain (baroreflex sensitivity) and delay (s) reflect the baroreflex function. results: Baseline did not differ in LF transfer gain and delay between controls and the UCO group. In controls, LF gain showed postnatal increase. By contrast, LF gain gradually decreased in the UCO group, resulting in significantly lower values 4-7 d after UCO. In the UCO group, LF delay increased and differed significantly from controls. conclusion: Our results show that intrauterine hypoxiaischemia results in reduced baroreflex sensitivity over a period of 7 d, indicating limited efficacy to buffer BP changes by adapting heart rate. Cardiovascular dysregulation may augment already present cerebral damage after systemic hypoxiaischemia in the reperfusion period.P reterm infants have a higher incidence of neurological morbidity and mortality as compared with term infants (1). Neurological sequelae in preterm infants may be the consequence of hypoxia-ischemia during fetal and early postnatal life (2). Hemodynamic factors during hypoxia-ischemia and the posthypoxia-ischemia reperfusion phase contribute considerably to these neurological disorders (3). To ensure adequate blood flow to organs throughout the body, including the brain, blood pressure (BP) is controlled by baroreflex and chemoreflex mechanisms. Under normoxemia, the baroreflex stabilizes perfusion pressure in the face of disturbances of circulatory homeostasis by adapting heart rate, myocardial contraction, and vascular resistance. A poorly developed baroreflex function could contribute to BP instabilities, which may lead to impaired cerebral perfusion or hemorrhage (4). A better understanding of the dynamics underlying the control mechanisms regulating BP may be useful to improve diagnosis of these disorders.Low-frequency (LF) fluctuations in arterial BP with a wavelength of approximately 10 s (also called Mayer waves) have historically been attributed to baroreflex activity (5). The oscillations are assumed to be caused by a feedback control and mediated through the sympathetic and parasympathetic innervations of the baroreflex (6). Assessment of the baroreflex function (i.e., heart rate-mediated BP control) can be performed through quantification of baroreceptor sensitivity. Baroreceptor sensitivity (ms/mm Hg) may simply be defined as the change in heart rate (or R-R interval) in response to changes in arterial BP and may be e...

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Section: Long-term Effects Of Hypoxia-ischemiasupporting

confidence: 93%

Heart rate–mediated blood pressure control in preterm fetal sheep under normal and hypoxic–ischemic conditions

et al. 2013

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“…Aceita-se que existam várias e complexas interações no metabolis-mo fetal que regulem o pH e o consumo das bases tampões em face do sofrimento fetal 19 . A evolução do padrão cardiotocográfico do feto normalmente oxigenado para o observado na hipoxemia, principalmente nas hipoxemias com magnitude suficiente para produzir o dano neurológico, não é bem compreendida 20,21 . Do mesmo modo, característi-cas individuais do organismo fetal devem influenciar os mecanismos de lesão celular decorrente da hipoxia e acidose tecidual.…”

Section: Discussionunclassified

Modelo Matemático para Predição da Acidose Metabólica no Nascimento em Gestações com Diástole Zero ou Reversa

Nomura¹,

Francisco²,

Miyadahira³

et al. 2002

Rev. Bras. Ginecol. Obstet.

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IntroduçãoO principal objetivo da avaliação da vitalidade fetal é a detecção precoce da hipoxemia fetal 1 , evitando-se, assim, as seqüelas neurológicas pós-natais desencadeadas pela anoxia tecidual antenatal. A insuficiência placentária constitui importante fator de risco para a hipoxemia, e, nessa situação, é imprescindível assistência pré-natal especializada, oferecendo à gestante toda a propedêutica obstétrica para o diagnóstico precoce do comprometimento fetal [2][3][4] . Apesar dos avanços na área da neonatologia e da terapia intensiva neonatal, persistem, ainda, os riscos relacionados à prematuridade. O diagnóstico preciso da condição fetal permite ao perinatologista planejar o momento mais oportuno para a resolução destas gestações, confrontando sempre os riscos da prematuridade com as seqüelas neurológicas da hipoxia fetal 5 . Entre os métodos que compõem a semiologia obstétrica, tem destaque a dopplervelocimetria,

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“…[93] This underscores the pitfall of determining an injury in the presence of an acute hypoxic/ischemic event. Fetal lamb experiments involving the interruption of the vagus nerve [94], or the direct injection of atropine into the human fetus [95], uncover the CTG patterns of (vagal) denervation (or injury) matching the "conversion pattern" seen in injured human fetuses [40].…”

Section: Ctg and The Prediction Of Fetal Neurological Injurymentioning

confidence: 99%