Local Cold Stress to the Soles Induces Retroplacental Hemorrhage in Rats

Abstract

The aim of this study was to investigate the effect of local cold stress to the soles on placental histology in rats. Pregnant rats were subjected to a cold provocation (0 degrees C, 12 degrees C) and room temperature (23 degrees C) for 15 and 30 minutes. During cold stimulation and at the control temperature, uterine blood flow and uterine contraction were measured simultaneously. Histological studies of the placentas of these rats were also performed. Cold stress at 0 degrees C and 12 degrees C significantly decreased uterine blood flow (P < .005, P < .02) compared with controls (23 degrees C). The decrease in uterine blood flow was greater at 0 degrees C than at 12 degrees C stress. Cold-induced stress (0 degrees C) also evoked an isometric tension with increased frequency and amplitude in the rat uterus (P < .003, P < .0002) compared with controls (23 degrees C). Stimulation at 12 degrees C did not induce any uterine contractions. Placental histology of rats stressed at 0 degreesC revealed hemorrhages into the decidua basalis. These findings suggest that local cold stress decreases uterine blood flow and increases uterine contraction, resulting in retroplacental hemorrhage in rats. This model may account for human abruptio placentae.

Loss of a close family member the year before or during pregnancy and the risk of placental abruption: a cohort study from Denmark and Sweden

“…Our results corroborate those of the only case-control study on this topic, reporting a two-fold higher risk of placental abruption in women with frequent stress symptoms during pregnancy compared with their less exposed counterparts (de Paz et al 2011). Our findings are also consistent with an animal model showing that retroplacental hematomas were substantially more frequent among pregnant rodents exposed to cold stress to the soles than among nonexposed (Khatun et al 2001). Our results complement and extend findings regarding the link between mood disorders -also related to the dysregulation of Year of offspring 's birth 1973-1977 10.1 12.0 1978-1982 11.1 12.5 1983-1987 14.0 15.4 1988-1992 17.9 18.5 1993-1997 16.6 16.3 1998-2002 15 the hypothalamic-pituitary-adrenal (HPA) axis -and the risk of placental abruption (Jablensky et al 2005;de Paz et al 2011).…”

“…In light of the vasoconstrictive (Khatun et al 2001) and prothrombotic (von Känel et al 2001) effects of stress, the similarity in pathophysiology Brosens et al 2011) and in some risk factors (Ananth & Vintzileos, 2011) amongst fetal growth restriction, pre-eclampsia and placental abruption, it is possible that maternal stress during pregnancy is associated with increased placental abruption risk.…”

Effect of cold stress on ovarian & uterine microcirculation in rats and the role of endothelin system

“…Parborell et al pointed out that by inhibiting angiopoietin activity, the number of atretic follicles mediated by ovarian apoptosis increased [40]. Cold can also cause a reduction in uterine blood flow and increase in uterine contraction, leading to post -placental hemorrhaging and endometrial morphological changes in rats [32,41]. In addition, Meirow's experiment explained that the change in ovarian resistance index in endometriosis is related to interstitial fibrosis and microvascular damage [42].…”

The relationship between prenatal psychological stress and placental abruption in Japan, The Japan Environment and Children’s Study (JECS)

“…A possible mechanism to explain the effect of stressful life events on PA occurrence is that stress exposure promotes the secretion of stress hormones, which is followed by vasoconstriction, rises in blood pressure [23], and pro-inflammatory [24, 25] and pro-thrombotic [26] changes that result in uteroplacental ischemia [27]. This stress-induced pathology may cause IUGR [6, 7] or pre-eclampsia [8], thereby leading to the occurrence of PA [9, 10].…”