Chronic hypoxia increases fetoplacental vascular resistance and vasoconstrictor reactivity in the rat

2008 ◽  
Vol 294 (4) ◽  
pp. H1638-H1644 ◽  
Author(s):  
Vít Jakoubek ◽  
Jana Bíbová ◽  
Jan Herget ◽  
Václav Hampl
Keyword(s):  
Vascular Resistance ◽  
Intrauterine Growth Restriction ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Hypoxic Exposure ◽  
High Dose ◽  
Key Factors ◽  
Intrauterine Growth ◽  
The Relationship

An increase in fetoplacental vascular resistance caused by hypoxia is considered one of the key factors of placental hypoperfusion and fetal undernutrition leading to intrauterine growth restriction (IUGR), one of the serious problems in current neonatology. However, although acute hypoxia has been shown to cause fetoplacental vasoconstriction, the effects of more sustained hypoxic exposure are unknown. This study was designed to test the hypothesis that chronic hypoxia elicits elevations in fetoplacental resistance, that this effect is not completely reversible by acute reoxygenation, and that it is accompanied by increased acute vasoconstrictor reactivity of the fetoplacental vasculature. We measured fetoplacental vascular resistance as well as acute vasoconstrictor reactivity in isolated perfused placentae from rats exposed to hypoxia (10% O2) during the last week of a 3-wk pregnancy. We found that chronic hypoxia shifted the relationship between perfusion pressure and flow rate toward higher pressure values (by ∼20%). This increased vascular resistance was refractory to a high dose of sodium nitroprusside, implying the involvement of other factors than increased vascular tone. Chronic hypoxia also increased vasoconstrictor responses to angiotensin II (by ∼75%) and to acute hypoxic challenges (by >150%). We conclude that chronic prenatal hypoxia causes a sustained elevation of fetoplacental vascular resistance and vasoconstrictor reactivity that are likely to produce placental hypoperfusion and fetal undernutrition in vivo.

Store-operated channels in the pulmonary circulation of high- and low-altitude neonatal lambs

2013 ◽  
Vol 304 (8) ◽  
pp. L540-L548 ◽  
Author(s):  
Daniela Parrau ◽  
Germán Ebensperger ◽  
Emilio A. Herrera ◽  
Fernando Moraga ◽  
Raquel A. Riquelme ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Resistance ◽  
Vascular Reactivity ◽  
Chronic Hypoxia ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Arterial Blood ◽  
Low Altitude

We determined whether store-operated channels (SOC) are involved in neonatal pulmonary artery function under conditions of acute and chronic hypoxia, using newborn sheep gestated and born either at high altitude (HA, 3,600 m) or low altitude (LA, 520 m). Cardiopulmonary variables were recorded in vivo, with and without SOC blockade by 2-aminoethyldiphenylborinate (2-APB), during basal or acute hypoxic conditions. 2-APB did not have effects on basal mean pulmonary arterial pressure (mPAP), cardiac output, systemic arterial blood pressure, or systemic vascular resistance in both groups of neonates. During acute hypoxia 2-APB reduced mPAP and pulmonary vascular resistance in LA and HA, but this reduction was greater in HA. In addition, isolated pulmonary arteries mounted in a wire myograph were assessed for vascular reactivity. HA arteries showed a greater relaxation and sensitivity to SOC blockers than LA arteries. The pulmonary expression of two SOC-forming subunits, TRPC4 and STIM1, was upregulated in HA. Taken together, our results show that SOC contribute to hypoxic pulmonary vasoconstriction in newborn sheep and that SOC are upregulated by chronic hypoxia. Therefore, SOC may contribute to the development of neonatal pulmonary hypertension. We propose SOC channels could be potential targets to treat neonatal pulmonary hypertension.

Methylprednisolone on circulating eicosanoids and vasomotor tone after endotoxin

1986 ◽  
Vol 61 (1) ◽  
pp. 185-191 ◽  
Author(s):  
C. A. Hales ◽  
R. D. Brandstetter ◽  
C. F. Neely ◽  
M. B. Peterson ◽  
D. Kong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Physiological Effect ◽  
High Dose ◽  
Systemic Blood ◽  
Eicosanoid Production ◽  
Circulating Levels

Acute pulmonary and systemic vasomotor changes induced by endotoxin in dogs have been related, at least in part, to the production of eicosanoids such as the vasoconstrictor thromboxane and the vasodilator prostacyclin. Steroids in high doses, in vitro, inhibit activation of phospholipase A2 and prevent fatty acid release from cell membranes to enter the arachidonic acid cascade. We, therefore, administered methylprednisolone (40 mg/kg) to dogs to see if eicosanoid production and the ensuing vasomotor changes could be prevented after administration of 150 micrograms/kg of endotoxin. The stable metabolites of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay. Methylprednisolone by itself did not alter circulating eicosanoids but when given 2.5 h before endotoxin not only failed to inhibit endotoxin-induced eicosanoid production but actually resulted in higher circulating levels of 6-keto-PGF1 alpha (P less than 0.05) compared with animals receiving endotoxin alone. Indomethacin prevented the steroid-enhanced concentrations of 6-keto-PGF1 alpha after endotoxin and prevented the greater fall (P less than 0.05) in systemic blood pressure and systemic vascular resistance with steroid plus endotoxin than occurred with endotoxin alone. Administration of methylprednisolone immediately before endotoxin resulted in enhanced levels (P less than 0.05) of both TxB2 and 6-keto-PGF1 alpha but with a fall in systemic blood pressure and vascular resistance similar to the animals pretreated by 2.5 h. In contrast to the early steroid group in which all of the hypotensive effect was due to eicosanoids, in the latter group steroids had an additional nonspecific effect. Thus, in vivo, high-dose steroids did not prevent endotoxin-induced increases in eicosanoids but actually increased circulating levels of TxB2 and 6-keto-PGF1 alpha with a physiological effect favoring vasodilation.

Melatonin-MT1 signal is essential for endometrial decidualization

Reproduction ◽  
2021 ◽  
Author(s):  
Liyuan Cui ◽  
Feng Xu ◽  
Songcun Wang ◽  
Zhuxuan Jiang ◽  
Lu Liu ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Endometrial Stromal Cells ◽  
Reproductive Process ◽  
Intrauterine Growth ◽  
In Vivo Experiments ◽  
Adverse Pregnancy

Deficient decidualization of endometrial stromal cells (ESCs) can cause adverse pregnancy outcomes including miscarriage, intrauterine growth restriction and pre-eclampsia. Decidualization is regulated by multiple factors such as hormones and circadian genes. Melatonin, a circadian-controlled hormone, is reported to be important for various reproductive process, including oocyte maturation and placenta development. Its receptor, MT1, is considered to be related to intrauterine growth restriction and pre-eclampsia. However, the role of melatonin-MT1 signal in decidualization remains unknown. Here, we reported that decidual stromal cells from miscarriages displayed deficient decidualization with decreased MT1 expression. The expression level of MT1 is gradually increased with the process of decidualization induction in vitro. MT1 knockdown suppressed decidualization level, while overexpression of MT1 promoted the decidualization process. Moreover, changing MT1 level could regulate the expression of decidualization-related transcription factor FOXO1. Melatonin promoted decidualization and reversed the decidualization deficiency due to MT1 knockdown. Using in vitro and in vivo experiments, we further identified that lipopolysaccharide (LPS) could induce inflammation and decidualization resistance with downregulated MT1 expression, and melatonin could reverse the inflammation and decidualization resistance induced by LPS. These results suggested melatonin-MT1 signal might be essential for decidualization and might provide a novel therapeutic target for decidualization deficiency-associated pregnancy complications.

scholarly journals The interplay between thyroid hormones and the placenta: a comprehensive review†

2019 ◽  
Author(s):  
Enoch Appiah Adu-Gyamfi ◽  
Ying-Xiong Wang ◽  
Yu-Bin Ding
Keyword(s):  
Thyroid Hormones ◽  
Pregnancy Complications ◽  
Intrauterine Growth Restriction ◽  
Growth And Development ◽  
Molecular Mechanisms ◽  
Trophoblast Invasion ◽  
Trophoblast Differentiation ◽  
Comprehensive Review ◽  
Intrauterine Growth ◽  
The Relationship

Abstract Thyroid hormones (THs) regulate a number of metabolic processes during pregnancy. After implantation, the placenta forms and enhances embryonic growth and development. Dysregulated maternal THs signaling has been observed in malplacentation-mediated pregnancy complications such as preeclampsia, miscarriage, and intrauterine growth restriction (IUGR), but the molecular mechanisms involved in this association have not been fully characterized. In this review, we have discussed THs signaling and its roles in trophoblast proliferation, trophoblast differentiation, trophoblast invasion of the decidua, and decidual angiogenesis. We have also explored the relationship between specific pregnancy complications and placental THs transporters, deiodinases, and THs receptors. In addition, we have examined the effects of specific endocrine disruptors on placental THs signaling. The available evidence indicates that THs signaling is involved in the formation and functioning of the placenta and serves as the basis for understanding the pathogenesis and pathophysiology of dysthyroidism-associated pregnancy complications such as preeclampsia, miscarriage, and IUGR.

The Relationship of Intrauterine Growth Restriction with Placental Pathologic Changes in Newborns

2020 ◽  
Author(s):  
Hossein Dalili ◽  
Fatemeh Sadat Nayeri ◽  
Seyed Reza Mirjalili ◽  
Seyyed Nasrollah Hossein ◽  
Alireza Abdollahi ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Pathological Examination ◽  
Histological Changes ◽  
Intrauterine Growth ◽  
Study Population ◽  
The Mean ◽  
Relationship Of ◽  
The Relationship ◽  
Restriction Group

Introduction: Intrauterine growth restriction is a multifaceted problem and is associated with a significant increase in the level of morbidity and perinatal mortality. According to some studies, failure of the placenta is responsible for the most cases of intrauterine growth restriction. The aim of this study was to evaluate the placental pathologic changes in the intrauterine growth restriction (IUGR) samples and compare them with normal cases.   Methods: A study population consisted of 60 intrauterine growth restriction neonates and 60 normalized neonates born at Tehran Imam Khomeini Hospital between June 2016 and July 2017. The placenta was weighed, immediately after delivery, and the umbilical cord was separated, then stored in 10% formalin and sent for pathological examination as soon as possible. Data collection was performed according to the following items: the pathologist's report, the results of the infants' examination, and the data in the neonatal cases.   Results: The intrauterine growth restriction group showed a high frequency of placenta infarction (P < 0.001), inflammation of the villous (P < 0.001), villous fibrosis (P = 0.044), villous vascularization disorder (P = 0.001), prevalence of chorioamnionitis (P = 0.027), prevalence of Syncytiotrophoblastic knots (P < 0.001) and placental necrosis (P = 0.048) than normal group. However, the mean weight of the placenta (P < 0.001), the length and width of the macroscopic placenta changes was less (P < 0.001).   Conclusion: The results of the current study showed that a major part of the macroscopic and histological changes are detectable in the intrauterine growth restriction samples, which are considerably more common than normal, although they are not pathognomonic, but in the future, more accurate results can be obtained from more extensive studies.

scholarly journals Upregulation of vascular calcium channels in neonatal piglets with hypoxia-induced pulmonary hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. L915-L924 ◽  
Author(s):  
Dinesh K. Hirenallur-S. ◽  
Steven T. Haworth ◽  
Jeaninne T. Leming ◽  
James Chang ◽  
Guillermo Hernandez ◽  
...  
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Chronic Hypoxia ◽  
Pulmonary Arteries ◽  
Fold Increase ◽  
Symptomatic Improvement ◽  
Channel Blockers ◽  
Neonatal Piglets ◽  
Isolated Lungs

Inhibition of voltage-gated, L-type Ca2+ (CaL) channels by clinical calcium channel blockers provides symptomatic improvement to some pediatric patients with pulmonary arterial hypertension (PAH). The present study investigated whether abnormalities of vascular CaL channels contribute to the pathogenesis of neonatal PAH using a newborn piglet model of hypoxia-induced PAH. Neonatal piglets exposed to chronic hypoxia (CH) developed PAH by 21 days, which was evident as a 2.1-fold increase in pulmonary vascular resistance in vivo compared with piglets raised in normoxia (N). Transpulmonary pressures (ΔPtp) in the corresponding isolated perfused lungs were 20.5 ± 2.1 mmHg (CH) and 11.6 ± 0.8 mmHg (N). Nifedipine reduced the elevated ΔPtp in isolated lungs of CH piglets by 6.4 ± 1.3 mmHg but only reduced ΔPtp in lungs of N piglets by 1.9 ± 0.2 mmHg. Small pulmonary arteries from CH piglets also demonstrated accentuated Ca2+-dependent contraction, and Ca2+ channel current was 3.94-fold higher in the resident vascular muscle cells. Finally, although the level of mRNA encoding the pore-forming α1C-subunit of the CaL channel was similar between small pulmonary arteries from N and CH piglets, a profound and persistent upregulation of the vascular α1C protein was detected by 10 days in CH piglets at a time when pulmonary vascular resistance was only mildly elevated. Thus chronic hypoxia in the neonate is associated with the anomalous upregulation of CaL channels in small pulmonary arteries in vivo and the resulting abnormal Ca2+-dependent resistance may contribute to the pathogenesis of PAH.

Index of contractility: quantitative analysis of hepatic venous distensibility

1991 ◽  
Vol 260 (2) ◽  
pp. G325-G332
Author(s):  
W. W. Lautt ◽  
C. V. Greenway ◽  
D. J. Legare
Keyword(s):  
Vascular Resistance ◽  
Control Level ◽  
Perfused Liver ◽  
Vascular Bed ◽  
Resistance Vessels ◽  
Venous Distensibility ◽  
Blood Pressures ◽  
Pressure Resistance ◽  
The Relationship

The low-pressure resistance vessels of the splanchnic circulation are passively distensible, and changes in regional blood pressures can lead to large changes in vascular resistance. The relationship between distending blood pressure (Pd) and vascular resistance (R) is described as a constant, the index of contractility (IC) where IC = R x Pd3. IC was derived in an isolated blood-perfused liver and was confirmed in vivo for both pre- and postsinusoidal resistance sites. IC does not change passively in response to wide changes in blood flow or hepatic outflow pressure. IC is dramatically altered in response to active vasoconstriction. In vivo, the presinusoidal IC rose from a control level of 12.2 +/- 4.2 to 92.7 +/- 20.6 IC units (mmHg4.ml-1.min.kg body wt) in response to 1.25 micrograms.kg-1.min-1 norepinephrine intraportal; the postsinusoidal IC rose from 20.4 +/- 2.3 to 59.6 +/- 14.2 IC units. IC reflects resistance changes secondary to active contractile responses independent of the passive consequences of the distensible nature of the resistance sites. We suggest that these concepts can be applied to any vascular bed with distensible resistance vessels.

The relationship between cadmium and lead with selenium, copper and zinc in normal and intrauterine growth restriction pregnancy

2007 ◽  
Vol 172 ◽  
pp. S178-S179
Author(s):  
Suzana Cavar ◽  
Tomislav Klapec ◽  
Zoran Kasac ◽  
Silvija Rucevic ◽  
Ana Popinjac ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Copper And Zinc ◽  
Cadmium And Lead ◽  
The Relationship
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