Hypoxia In Women Research Articles

Реакція на дозовану гіпоксію у жінок, що перебували у стані хронічного стресу, зумовленого війною

Military stress has a traumatic effect on mental and physical health, and disrupts the adaptive capabilities of the body, in particular, its ability to adequately respond to hypoxia. However, the specifics of the reaction of the cardiorespiratory system to dosed hypoxia in individuals who experiencing warrelated chronic stress (WRCS) have not yet been elucidated. The peculiarities of the reaction of the cardiorespiratory system to dosed hypoxia in women experiencing WRCS were clarified. It was shown that during breathing of atmospheric air, the blood saturation level, lung ventilation indicators, and hemodynamics did not differ significantly between women exposed to WRCS and those not exposed to it. However, during a controlled hypoxic test (breathing a gas mixture with 12% oxygen for 20 min), women experiencing WRCS experienced a more significant decrease in blood saturation, indicating a lower tolerance to hypoxia. This is also evidenced by a reduced lung ventilation response to controlled hypoxia in the WRCS group, where the increase in ventilation primarily occurred due to an elevation in breathing rate rather than tidal volume. At the same time, the hemodynamic response to hypoxia in women with WRCS was characterized by a more substantial increase in heart rate and systolic arterial pressure. Thus, it was established that in women who were in the state of HCV, the body’s resistance to the effects of hypoxia decreases. At the same time, in conditions of hypoxia, the nature of their breathing changes, and the compensatory growth of pulmonary ventilation decreases, but the growth of hemodynamic indicators increases.

Hypoxia briefly increases diuresis but reduces plasma volume by fluid redistribution in women.

We have recently reported that hypobaric hypoxia (HH) reduces plasma volume (PV) in men by decreasing total circulating plasma protein (TCPP). Here, we investigated whether this applies to women and whether an inflammatory response and/or endothelial glycocalyx shedding could facilitate the TCCP reduction. We further investigated whether acute HH induces a short-lived diuretic response that was overlooked in our recent study, where only 24-h urine volumes were evaluated. In a strictly controlled crossover protocol, 12 women underwent two 4-day sojourns in a hypobaric chamber: one in normoxia (NX) and one in HH equivalent to 3,500-m altitude. PV, urine output, TCPP, and markers for inflammation and glycocalyx shedding were repeatedly measured. Total body water (TBW) was determined pre- and postsojourns by deuterium dilution. PV was reduced after 12 h of HH and thereafter remained 230-330 mL lower than in NX (P < 0.0001). Urine flow was 45% higher in HH than in NX throughout the first 6 h (P = 0.01) but lower during the second half of the first day (P < 0.001). Twenty-four-hour urine volumes (P ≥ 0.37) and TBW (P ≥ 0.14) were not different between the sojourns. TCPP was lower in HH than in NX at the same time points as PV (P < 0.001), but inflammatory or glycocalyx shedding markers were not consistently increased. As in men, and despite initially increased diuresis, HH-induced PV contraction in women is driven by a loss of TCPP and ensuing fluid redistribution, rather than by fluid loss. The mechanism underlying the TCPP reduction remains unclear but does not seem to involve inflammation or glycocalyx shedding.NEW & NOTEWORTHY This study is the first to investigate the mechanisms underlying plasma volume (PV) contraction in response to hypoxia in women while strictly controlling for confounders. PV contraction in women has a similar time course and magnitude as in men and is driven by the same mechanism, namely, oncotically driven redistribution rather than loss of fluid. We further report that hypoxia facilitates an increase in diuresis, that is, however, short-lived and of little relevance for PV regulation.

The association between uterine contraction frequency and fetal scalp pH in women with suspicious or pathological fetal heart rate tracings: A retrospective study

ObjectiveCurrent guidelines provide little supporting literature for the definition of uterine tachysystole during labour and no distinction is made for optimal contraction frequency depending on the clinical situation. We hypothesize that fetal hypoxia is frequently caused by uterine tachysystole and that high uterine contraction frequencies are especially harmful when fetal heart rate (FHR) abnormalities are present. We studied the association between contraction frequency and fetal scalp pH values in women with an indication for fetal blood sampling (FBS) based on FHR abnormalities. Study designA retrospective study including 762 women was performed in a tertiary teaching hospital in the Netherlands from January 2015 until January 2020. Women with a singleton pregnancy with a gestational age ≥ 34+0 weeks were included when FBS was performed because of suspicious or pathological FHR tracings. Exclusion criteria were maternal age < 18 years, failed fetal scalp pH values, lack of thirty minute registration by tocodynamometry prior to FBS, poor quality of uterine monitoring, intrauterine resuscitation in the thirty minutes prior to FBS, maternal body mass index ≥ 30 kg/m2 and neonatal birth weight < 10th percentile.Uterine contractions in the thirty minutes prior to FBS were manually annotated by a researcher who was blinded to FBS values, FHR and other obstetrical data. Linear and logistic analysis were used to explore the association between uterine contraction frequency and FBS results. ResultsLow fetal scalp pH values were significantly associated with contraction frequency prior to FBS. Fetuses of women with four to five contractions per ten minutes prior to FBS were 2.4 times more likely to have hypoxia as compared to fetuses of women with two to three contractions per ten minutes (aOR 2.4, 95% CI 1.1–5.4). With increasing contraction frequency, the risk of fetal hypoxia further increased. ConclusionsContraction frequency above four per ten minutes prior to FBS is significantly associated with fetal hypoxia in women with FHR abnormalities. We suggest to aim for a maximum contraction frequency of four per ten minutes in these women.

245 Sleep and cortical thickness are influenced by surgical menopause

Abstract Introduction Early loss of 17β-estradiol (E2), as experienced by women with bilateral salpingo-oophorectomy (BSO; removal of ovaries and fallopian tubes), is associated with increased prevalence of sleep disorders and greater Alzheimer’s disease (AD) risk. In older adults, poor sleep heightens AD risk; hypoxia increases markers for incipient AD, including circulating Aβ, and is linked to prefrontal cortical thinning. Thus, we wondered: 1) if this at-risk population of middle-aged women with BSO had sleep hypoxia, measured by oxygen desaturation, and 2) whether this related to decreased prefrontal cortical thickness in women taking and not taking estradiol therapy (ET). Methods Sleep and percent oxygen desaturation (SPO2%) were measured via at-home polysomnography (TEMEC). Prefrontal cortical thickness was obtained from T1-weighted structural scans using the CIVET pipeline. We recruited middle-age women with BSO, some of whom were taking ET (BSO+ET; n=15), and some not (BSO; n=15). We compared their sleep and cortical thickness with that of age and education-matched premenopausal controls (AMC; n=18). Results Women with BSO (BSO, BSO+ET) had lower minimum SPO2% values than AMC, and thinner right medial orbitofrontal (rmOF) cortices. There was a trend for women with BSO to have lower average SPO2% than AMC. Analyses separating groups based on ET therapy status (BSO vs BSO+ET vs AMC) revealed only trending differences between groups, such that women with BSO tended to have lower minimum SPO2% and thinner rmOF cortices than AMC. Conclusion These preliminary results suggest early loss of E2 due to BSO may drive greater drops in SPO2% in middle-age women, and may be related to reduced prefrontal cortical thickness. This study is the first to show hypoxia in women with BSO. Support (if any) Ontario Graduate Scholarship Award (to LG), Alzheimer’s Association Research Fellowship (co-sponsored by Brain Canada Foundation; AARF-17-504715 to NJG), Alzheimer’s Society Canada Postdoctoral Fellowship (to AA), Canadian Institutes of Health Research (CIHR) Masters Award (to LG, AB, and RR), Wilfred and Joyce Posluns Chair in Women’s Brain Health and Aging (from the Posluns Family Foundation, CIHR, Ontario Brain Institute, and Alzheimer Society of Canada; WJP-150643 to GE)

Перебіг вагітності, пологів та стан новонароджених у жінок з рубцем на матці після попереднього кесарева розтину

The objective: Analysis of pregnancy, delivery and the condition of newborns in women with uterus scar after previous Cesarean section. Materials and methods. Observations and retrospective analysis of individual maps of pregnant women, birth record and condition of newborns in 180 women with uterus scar after previous Cesarean section from 2014-2019. Results. It was found that women in I group had no history of miscarriage, and in II group this indicator was 6.7%. We were determined that the threat of early pregnancy was observed twice often in II group as in I group. Failure uterus scar during pregnancy was diagnosing in 21.1% of women of I group against 18.9% of women of II group, as well as during childbirth in 10% of women of II group against none of women of I group. In addition, 76.7% of women of I group were born by vaginal delivery against 24.4% of women of II group. In addition, 10% of newborns in women of I group on the Apgar scale were rated 6-7 points against 65.5% in a state of varying degrees of hypoxia in women of II group. Conclusion. Pregnancy and childbirth in women with uterus scar after previous Cesarean section were accompanying by complications of fetal and neonatal disorders. More pronounced changes were observing during pregnancy, delivery and changes in the condition of newborns in women of II group against with women of I group, which can be explaining by better pre-pregnancy preparation of women of I group and better monitoring during pregnancy. Keywords: сesarean section, pre-pregnancy preparation of women, the condition of newborns.

Submicroscopic infection of placenta by Plasmodium produces Th1/Th2 cytokine imbalance, inflammation and hypoxia in women from north-west Colombia

BackgroundA large-scale study was set up in order to study the epidemiology, clinical aspects, and immunopathology of gestational and placental malaria in north-west Colombia. In this region, recent reports using a qPCR technique, confirmed frequencies of infection, by Plasmodium falciparum or Plasmodium vivax, up to 45%. Given the high rates of infection observed both in mother and placenta, a first exploratory study was proposed in order to characterize the effect on the inflammation status, tissue damage and hypoxia in Plasmodium spp. infected placentas.MethodsA descriptive, prospective, cross-sectional design was applied to pregnant women with (PM+) and without (PM-) placental malaria. Messenger RNA expression of Fas, FasL; COX-1, COX-2, HIF, VEGF, and the cytokines IL-2, IL-4, IL-10, IFN-γ and TNF, were measured in peripheral and placental blood using a quantitative PCR. The percentage of apoptotic cells was determined with a TUNEL assay.ResultsIn total 50 placentas were studied: 25 were positive for submicroscopic infection and 25 were negative for Plasmodium infection. Expression of IL-4 and IL-10 was observed high in placental tissue of PM+, while IL-2 was high in peripheral blood of the same group. Expression of TNF and IFNγ in peripheral blood of the PM + group was high. Similarly, the apoptotic index and Fas expression were significantly high in PM+. However, FasL expression was observed low in PM + compared to PM-. Inflammation markers (HIF, VEGF) and hypoxia markers (COX-1, COX-2) were high in the PM + group.ConclusionDuring placental malaria expression of some pro-inflammatory cytokines is up-regulated and markers of hypoxia and tissue damage are increased in cases of submicroscopic infection.

Determinant factors of the decrease in aerobic performance in moderate acute hypoxia in women endurance athletes

The purpose of this study was to evaluate the limiting factors of maximal aerobic performance in endurance trained (TW) and sedentary (UW) women. Subjects performed four incremental tests on a cycle ergometer at sea level and in normobaric hypoxia corresponding to 1000, 2500 and 4500 m. Maximal oxygen uptake decrement (Delta VO2 max) was larger in TW at each altitude. Maximal heart rate and ventilation decreased at 4500 m in TW. Maximal cardiac output remained unchanged. In both groups, arterialized oxygen saturation (Sa'O2 max) decreased at and above 2500 m and maximal O2 transport (QaO2 max) decreased from 1000 m. At 4500 m, there was no more difference in QaO2 max between TW and UW. Mixed venous O2 pressure (PvO2 max) was lower and O2 extraction (O2ERmax) greater in TW at each altitude. The primary determinant factor of VO2 max decrement in moderate acute hypoxia in trained and untrained women is a reduced maximal O2 transport that cannot be compensate by tissue O2 extraction.

Ventilatory sensitivity to carbon dioxide before and after episodic hypoxia in women treated with testosterone

We hypothesized that the ventilatory threshold and sensitivity to carbon dioxide in the presence of hypoxia and hyperoxia during wakefulness would be increased following testosterone administration in premenopausal women. Additionally, we hypothesized that the sensitivity to carbon dioxide increases following episodic hypoxia and that this increase is enhanced after testosterone administration. Eleven women completed four modified carbon dioxide rebreathing trials before and after episodic hypoxia. Two rebreathing trials before and after episodic hypoxia were completed with oxygen levels sustained at 150 Torr, the remaining trials were repeated while oxygen was maintained at 50 Torr. The protocol was completed following 8-10 days of treatment with testosterone or placebo skin patches. Resting minute ventilation was greater following treatment with testosterone compared with placebo (testosterone 11.38 +/- 0.43 vs. placebo 10.07 +/- 0.36 l/min; P < 0.01). This increase was accompanied by an increase in the ventilatory sensitivity to carbon dioxide in the presence of sustained hyperoxia (VSco(2)(hyperoxia)) compared with placebo (3.6 +/- 0.5 vs. 2.9 +/- 0.3; P < 0.03). No change in the ventilatory sensitivity to carbon dioxide in the presence of sustained hypoxia (VSco(2 hypoxia)) following treatment with testosterone was observed. However, the VSco(2 hypoxia) was increased after episodic hypoxia. This increase was similar following treatment with placebo or testosterone patches. We conclude that treatment with testosterone leads to increases in the VSco(2)(hyperoxia), indicative of increased central chemoreflex responsiveness. We also conclude that exposure to episodic hypoxia enhances the VSco(2 hypoxia), but that this enhancement is unaffected by treatment with testosterone.

Ventilation and arousal responses to hypercapnia in normal sleeping humans.

We measured arousal and ventilatory responses to rebreathing from a small bag, initially approximately 7% CO2 in 40% O2, via a nose mask in 13 normal human adults. With deepening non-rapid-eye-movement sleep (NREM), males aroused at increasing alveolar PCO2 (mean +/- SE: stage II 58.6 +/- 1.7, stage III 61.2 +/- 1.0, stage IV 63.8 +/- 0.8 Torr), whereas in rapid-eye-movement sleep (REM), arousal alveolar PCO2 was 57.7 +/- 0.7 Torr, i.e., much lower than in stage III and IV NREM. Females showed no significant change in arousal alveolar PCO2, (II 57.6 +/- 0.9, III 57.3 +/- 1.3, IV 59.4 +/- 0.9, REM 56.3 +/- 1.0 Torr). Male ventilatory response was 2.5 +/- 0.1 (SE) 1 X min-1 X Torr-1 and fell by 49% in NREM (1.29 +/- 0.13) and by 69% in REM (0.78 +/- 0.18). Female response was little affected by state, being similar to male NREM response (wake 1.39 +/- 0.14, NREM 1.40 +/- 0.13, REM 1.11 +/- 0.26 1 X min-1 X Torr-1). In NREM tests, there was no change in sleep state until arousal, whereas in REM, subjects awoke abruptly with the onset of rebreathing (11 cases), showed a transient arousal with onset but continued in REM until final arousal (21 cases), or changed to NREM at onset (2 cases). These arousal results contrast sharply with findings in tracheostomized dogs and in obstructive sleep apnea syndrome, where asphyxic arousal is later in REM than in NREM, suggesting that the events at test onset in REM in the present study may be related to upper airway sensitivity to CO2 specific to REM.