Disease relevance of Fetal Mortality

• Disseminated gonococcal infection (DGI) and pelvic inflammatory disease (PID) strains in the presence of C1q but not in the presence of bovine serum albumin (BSA) were able to spread from the pregnant rat to the fetus and resulted in fetal mortality [1].
• Administration of aspirin to vitamin E-deficient rats had no protective effect on fetal mortality, incisor depigmentation, body weight gain or red blood cell peroxidative hemolysis [2].
• N omega-nitro-L-arginine methyl ester, but not aminoguanidine, increased fetal mortality and decreased fetal weight [3].
• No other significant protective effects against arsenite toxicity were seen due to BAL; however, concurrent BAL treatment on Day 9 appeared to result in decreased fetal mortality and a decline in skeletal malformations [4].
• These data indicate that, in the sheep, magnesium sulfate increases fetal mortality and inhibits the compensatory increase in fetal cerebral blood flow during maternal hemorrhage-induced fetal hypoxemia [5].

Psychiatry related information on Fetal Mortality

• In order to establish whether vitamin C was embryotoxic or altered CP-induced toxicity, mice were sacrificed on day 18 after copulation to record fetal weights, gross morphological abnormalities, and fetal mortality [6].

High impact information on Fetal Mortality

• Inhibition of nitric oxide production with NG-nitro-L-arginine methyl ester (L-NAME) increases blood pressure and fetal mortality in pregnant rats [7].
• Infusion of pregnant rats with calcitonin gene-related peptide (CGRP)(8-37), a CGRP receptor antagonist, increases blood pressure and fetal mortality and decreases fetal growth [8].
• Pregnant rats were intracervically injected with lipopolysaccharide (LPS) at 15 days of gestation (E15) and a dose of LPS that caused low fetal mortality was determined [9].
• Neither atosiban nor ICI-118.551 infusions alone changed fetal mortality [10].
• However, the duration of parturition, fetal mortality, and the mortality incidence were increased in rats treated with the high dose of the OT antagonist compared to controls [11].

Chemical compound and disease context of Fetal Mortality

• Independently of X-irradiation, ethanol-treatment resulted in increased fetal mortality and LP, and decreased body weight [12].
• To reduce the high maternal and fetal mortality in pheochromocytoma of pregnancy, therapy is advocated with phenoxybenzamine and propranolol to obtain adequate alpha- and beta-adrenergic receptor blockade [13].
• Maternal exposure to 2000 ppm toluene caused significant toxic effects such as body weight suppression of dams and offspring, high fetal mortality and embryonic growth retardation, but no external, internal or skeletal anomalies were observed in the fetuses of any treated group [14].

Biological context of Fetal Mortality

• Naproxen sodium at both dosage levels prolonged gestation by 24 h or longer, doubled the duration of parturition, and markedly increased fetal mortality and mortality incidence [11].
• Pre-treatment with ascorbic acid significantly attenuated LPS-induced lipid peroxidation, decreased fetal mortality, and reversed LPS-induced fetal growth and skeletal development retardation [15].
• Relationship of high nitrate community water supply to infant and fetal mortality [16].
• CONCLUSIONS: Perinatal mortality and neonatal morbidity-mortality according to gestational age before and after the 32nd week were similar in HELLP syndrome compared with severe preeclampsia-eclampsia without HELLP but overall fetal mortality was higher in HELLP syndrome with no regular prenatal care [17].

Anatomical context of Fetal Mortality

• We suggest that immune complex deposition on the trophoblast basement membrane in patients with active systemic lupus erythematosus may play a part in the increased fetal mortality in this disease [18].
• Vasa previa, which is associated with high fetal mortality, is present when fetal vessels cross the internal cervical os as a velamentous insertion of the umbilical cord with or without a succenturiate lobe or bilobate placenta [19].
• Ten mummified fetuses were tested for the deficiency of uridine monophosphate synthase (DUMPS), which is known to contribute to the embryonic and fetal mortality in cattle [20].
• The effects on fetal mortality and on the patency of the ductus arteriosus of several doses of indomethacin administered at different frequencies to pregnant rabbits were studied [21].
• The fetal mortality associated with fetal blood sampling was 6.3 per cent [22].

Associations of Fetal Mortality with chemical compounds

• Polybrominated biphenyls and fetal mortality in Michigan [23].
• It is suggested that a possible cause of these differences is sex-differential fetal mortality caused by interaction of the ABO genes, and some of the sex-determining genes, with oestrogen and progesterone [24].
• In contrast to effects of ethanol and Trenimon treatments, THC, given alone, or in combination with ethanol and/or Trenimon, had no effect on either preimplantational loss, fetal mortality or the resulting mutation index [25].
• Indomethacin treatment did not terminate pregnancy: the proportion of animals pregnant on Days 5, 7, 10 and 16 was not affected, although fetal mortality was slightly greater in these animals [26].
• Results showed that pretreatment with NAC significantly alleviated LPS-induced fetal mortality and reversed LPS-induced growth and skeletal development retardation [27].

Gene context of Fetal Mortality

• Furthermore, pentoxifylline, an inhibitor of TNF-alpha synthesis, significantly inhibited TNF-alpha production, reduced fetal mortality, and reversed LPS-induced fetal intra-uterine growth restriction and skeletal development retardation [28].
• On the basis of these data, which are derived from families of several different backgrounds of European ancestry, it is generalized that, as we proceed from CL sibships to CLP sibships, there is a doubling effect on fetal mortality [29].
• It exhibits high antiretroviral activity against HIV and exhibits immunosuppressive activity in a multiple sclerosis model and reduces embryo and fetal mortality by stimulation of IL-10 production [30].
• Analysis of 418 sibships of oral cleft probands from Indiana, and 288 sibships from Montreal indicate that the incidence of fetal mortality is significantly greater in sibships of probands with cleft lip and cleft palate (CLP) as compared to that in sibships of probands with cleft lip (CL) alone [31].
• Fetal mortality in the uterine arterial catheterized group was 76%, and there was no significant difference in fetal or placental weight or IGF-1 levels between infused and noninfused survivors [32].

Analytical, diagnostic and therapeutic context of Fetal Mortality

• Pregnancy test and evaluation of embryonic and fetal mortality based on progesterone concentrations fore-milk [33].
• In regard to fetal mortality, embryo transfer procedures influenced it in SWV dams and the effect of triamcinolone could not be detected after embryo transfer [34].
• Transamniotic administration of rhIGF-1 significantly increases serum IGF-1 levels and placental weight of fetal runts, while uterine vessel catheterization results in prohibitive fetal mortality and does not increase fetal or placental growth or IGF-1 levels [32].
• Plasma profiles of progesterone and conceptus proteins in cows with spontaneous embryonic/fetal mortality as diagnosed by ultrasonography [35].

References