Fetal hypoxia

Pregnancy Category C. Reduced uterine blood flow with fetal hypoxia (bradycardia) is a potential risk. Give to a pregnant woman only if clearly needed. 

During the antepartum period, oxytocin induces uterine contractions that transiently reduce placental blood flow to the fetus. The oxytocin challenge test measures the fetal heart rate response to a standardized oxytocin infusion and provides information about placental circulatory reserve. An abnormal response, seen as late decelerations in the fetal heart rate, indicates fetal hypoxia and may warrant immediate cesarean delivery. 

Oxytocin can be used to investigate the presence of reduced uterine blood flow and concurrent fetal hypoxia. Following oxytocin administration to mares in late gestation, the anticipated or negative response is acceleration of the fetal heart rate. The positive or abnormal response is a deceleration of the fetal heart rate. 

Cocaine Causes miscarriages, fetal hypoxia (lack of oxygen), low birth weight, tremors, strokes, congenital heart disease, skull defects, and other malformations... 

Hydrogen ion concentration can also be measured in fetal blood to assess fetal distress during labour. Capillary blotxl samples can be obtained directly from the baby s scalp once the cervix is sufficiently dilated. Fetal hypoxia causes a lactic acidosis and elevated hydrogen ion concentration.. VleasLirement of fetal PO, can be obtained directly using a transcutaneous oxygen electrode. 

Another idea is that prenatal impact on the activity of the neurotransmitter dopamine, including the effects of maternal psychosocial stress, maternal fever, maternal genetics and hormonal status, use of certain medications, and fetal hypoxia, may be involved in the epigenetic etiology of autism.67... 

Fetal Infection, Fetal Hypoxia, and Other Impacts... 

Tabulating the occurrence and degree of fetal hypoxia in past births is usually done by examining hospital records and by interviews—indirect assessment at best. But most studies agree that MRI scans of the brains of adult schizophrenics show greater brain abnormalities for those patients who apparendy experienced fetal hypoxia during gestation, and that fetal hypoxia predicts early onset schizophrenia.35... 

The most common consequence of maternal tobacco smoking during pregnancy is fetal hypoxia. But the metabolites of tobacco smoke also have an impact on fetal development.32 In general, the consequences of maternal tobacco smoking include... 

Van Erp, T. G., Saleh, P. A., Rosso, I. M., Huttunen, M., Lonnqvist, J., Pirkola, T., Salonen, O., Valanne, L., Poutanen, V. P., Standertskjold-Nordenstam, C. G.,Cannon, T. D. (2002). Contributions of genetic risk and fetal hypoxia to hippocampal volume in patients with schizophrenia or schizoaffective disorder, their unaffected siblings, and healthy unrelated volunteers. Am. J. Psychiatry. 159 1514—1520. 

Figure 3 Diagrammatic representation of components of the initial chemoreflex-driven responses to acute isocapnic hypoxaemia in the late-gestation fetal sheep in ntero (30). Hypoxia stimulates both carotid chemoreflex and hormonal responses. Catecholamines are released from the adrenal medulla in response to fetal hypoxia and act to increase carcass (e.g., femoral) vascular resistance and to increase fetal heart rate.

AVP is synthesized in the fetal hypothalamus. In addition to its role in altering gene expression (e.g., POMC), plasma AVP levels also increase in response to fetal hypoxia-ischemia (30,70,71). The release of AVP is not mediated by peripheral chemoreceptor mechanisms and therefore is unlikely to contribute to the rapid cardiovascular changes at the onset of hypoxia (see above) (30). Exogenously administered AVP produces hypertension, peripheral vasoconstriction, and bradycardia (71-73), although the contribution of hypoxia-stimulated increases in AVP to the redistribution of fetal CVO is uncertain (74,75). Endothehal VI receptors mediate an AVP vasodUatory effect, which means that the net effect of AVP on the cardiovascular system is likely to reflect an integrated picture of vasoconstriction from a number of vascular beds, modulated by endothelium-dependent vasodUatory mechanisms (76). 

Abortion in pregnant cattle is frequently reported but exact amounts and mechanism of action is not fully understood. The fetus is particularly susceptible to hypoxia induced by the methemoglobinemia. Fetal death and abortion may occur at any stage of pregnancy because of the decreased fetal oxygen and the limited ability of the fetus to metabolize nitrate (Knight and Walter, 2001). 

Skeletal myoblasts can survive prolonged periods of hypoxia [77]. Like fetal cardiomyocytes, skeletal myoblasts survive and may engraft (although this is controversial) when injected into the border zone of an AMI. 

Clark and colleagues (27) found evidence of maternal toxicity influencing fetal findings in studies with diflunisal in rabbits, in which fetal axial skeletal defects were observed. Diflunisal was found to produce severe maternal hemolytic anemia and greatly decreased erythrocyte ATP levels. The authors were able to demonstrate that the skeletal malformations resulted from maternal hypoxia secondary to anemia, rather than from a direct effect of the drug on the embryo or fetus. In addition, it was demonstrated that diflunisal had no effects on rat erythrocyte ATP levels, and the compound was categorized as not teratogenic in rats or mice. 

PEDF, first purified from human retinal pigment epithelial cultures as a factor that induces neuronal differentiation of cultured retinoblastoma cells (Tombran-Tink et al., 1991 Steele et al., 1993), has been recently shown to regulate normal angiogenesis in the eye (Dawson et al., 1999). PEDF is found both intracellularly and extracellularly in the fetal and early adult eye but is lost at the onset of senescence (Becerra, 1997 Araki et al., 1998). It is down-regulated by hypoxia and induced in the retina as a result of... 

Drugs given to the mother just prior to labour can cause postnatal effects CNS depressants may persist in and affect the baby for days after birth vasoconstrictors can cause fetal distress by reducing uterine blood supply 3-adrenoceptar blockers may impair fetal response to hypoxia sulphonamides displace bilirubin from plasma protein (risk of kernicterus) anticoagulants can cause haemorrhage. 

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