scholarly journals The effects of experimental acute decrease of uterine perfusion and maternal hypoxia on the fetus

1973 ◽  
Vol 1 (1) ◽  
pp. 36-52 ◽  
Author(s):  
D. Berg ◽  
J. Schulz ◽  
K. Wernicke ◽  
R. Muschaweck
Keyword(s):  
Uterine Perfusion ◽  
Maternal Hypoxia

scholarly journals Characterisation of cardiac health in the reduced uterine perfusion pressure model and a 3D cardiac spheroid model, of preeclampsia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Claire Richards ◽  
Kimberly Sesperez ◽  
Michael Chhor ◽  
Sahar Ghorbanpour ◽  
Claire Rennie ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Late Onset ◽  
Cardiac Fibroblasts ◽  
Immunofluorescent Staining ◽  
Collagen Deposition ◽  
Human Coronary Artery ◽  
Pregnant Rats ◽  
Cardiac Health ◽  
Increased Risk ◽  
Uterine Perfusion

Abstract Background Preeclampsia is a dangerous cardiovascular disorder of pregnancy that leads to an increased risk of future cardiovascular and metabolic disorders. Much of the pathogenesis and mechanisms involved in cardiac health in preeclampsia are unknown. A novel anti-angiogenic protein, FKBPL, is emerging as having a potential role in both preeclampsia and cardiovascular disease (CVD). Therefore, in this study we aimed to characterise cardiac health and FKBPL regulation in the rat reduced uterine perfusion pressure (RUPP) and a 3D cardiac spheroid model of preeclampsia. Methods The RUPP model was induced in pregnant rats and histological analysis performed on the heart, kidney, liver and placenta (n ≥ 6). Picrosirius red staining was performed to quantify collagen I and III deposition in rat hearts, placentae and livers as an indicator of fibrosis. RT-qPCR was used to determine changes in Fkbpl, Icam1, Vcam1, Flt1 and Vegfa mRNA in hearts and/or placentae and ELISA to evaluate cardiac brain natriuretic peptide (BNP45) and FKBPL secretion. Immunofluorescent staining was also conducted to analyse the expression of cardiac FKBPL. Cardiac spheroids were generated using human cardiac fibroblasts and human coronary artery endothelial cells and treated with patient plasma from normotensive controls, early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE); n = 3. FKBPL and CD31 expression was quantified by immunofluorescent labelling. Results The RUPP procedure induced significant increases in blood pressure (p < 0.001), collagen deposition (p < 0.001) and cardiac BNP45 (p < 0.05). It also induced a significant increase in cardiac FKBPL mRNA (p < 0.05) and protein  expression  (p < 0.01). RUPP placentae also exhibited increased collagen deposition and decreased Flt1 mRNA expression (p < 0.05). RUPP kidneys revealed an increase in average glomerular size (p < 0.05). Cardiac spheroids showed a significant increase in FKBPL expression when treated with LOPE plasma (p < 0.05) and a trend towards increased FKBPL expression following treatment with EOPE plasma (p = 0.06). Conclusions The rat RUPP model induced cardiac, renal and placental features reflective of preeclampsia. FKBPL was increased in the hearts of RUPP rats and cardiac spheroids treated with plasma from women with preeclampsia, perhaps reflective of restricted angiogenesis and inflammation in this disorder. Elucidation of these novel FKBPL mechanisms in cardiac health in preeclampsia could be key in preventing future CVD.

Reduced uterine perfusion pressure does not influence the endocannabinoid system (ECBS) transcripts in the rat model

Placenta ◽  
2013 ◽  
Vol 34 (9) ◽  
pp. A27
Author(s):  
Mauro Schenone ◽  
Zorica Janjetovic ◽  
Ramona Phinehas ◽  
Brian Brocato ◽  
Giancarlo Mari ◽  
...  
Keyword(s):  
Rat Model ◽  
Perfusion Pressure ◽  
Endocannabinoid System ◽  
Uterine Perfusion

Vertebral malformation in the mouse foetus caused by X-radiation of the mother during pregnancy

Development ◽  
1964 ◽  
Vol 12 (4) ◽  
pp. 841-850
Author(s):  
Ujihiro Murakami ◽  
Yoshiro Kameyama
Keyword(s):  
Early Pregnancy ◽  
Vertebral Column ◽  
Strain Differences ◽  
In Utero ◽  
Oxygen Deprivation ◽  
Experimental Animals ◽  
Vertebral Malformation ◽  
Pregnant Mice ◽  
Maternal Hypoxia ◽  
In Pregnancy

Maternal hypoxia in early pregnancy can result in malformations of the vertebrae of mouse foetuses, and there is a tendency for more posterior vertebrae to be affected the later in pregnancy the oxygen deprivation occurs (Murakami & Kameyama, 1963). Ingalls et al. (1957) and Degenhardt (1954, 1959) had earlier obtained similar results. We have also exposed pregnant mice to X-radiation and studied the consequent malformations. The effects on the extremities have already been described (Murakami, Kameyama & Nogami, 1963), and in the present paper we shall describe the effects on the vertebral column. Vertebral malformations in animals irradiated in utero have been described by Job, Leibold & Fitzmaurice (1935), Warkany and Schraffenberger (1947), Russell. (1950, 1954), and Russell & Russell (1954). In order to obtain results comparable with those of our experiments with hypoxia, no less than to detect inter-strain differences, we used mice of the ddN and CF1 strains originally supplied by the Central Laboratories for Experimental Animals, Tokyo (Zikkendobutsu Chuo Kenkyujo).

Impact of hyperleptinemia during placental ischemia-induced hypertension in pregnant rats

2021 ◽  
Author(s):  
Ana C. Palei ◽  
Hunter L. Martin ◽  
Barbara A. Wilson ◽  
Christopher D. Anderson ◽  
Joey P. Granger ◽  
...  
Keyword(s):  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
No Donor ◽  
Induced Hypertension ◽  
Cgmp Signaling ◽  
Uterine Perfusion ◽  
Plasma Leptin ◽  
Placental Ischemia

The prevalence of preeclampsia and obesity have increased. While obesity is a major risk factor for preeclampsia, the mechanisms linking these morbidities are poorly understood. Circulating leptin levels increase in proportion to fat mass. Infusion of this adipokine elicits hypertension in non-pregnant rats, but less is known about how hyperleptinemia impacts blood pressure during placental ischemia, an initiating event in the pathophysiology of hypertension in preeclampsia. We tested the hypothesis that hyperleptinemia during reduced uterine perfusion pressure (RUPP) exaggerates placental ischemia-induced hypertension. On gestational day (GD) 14, Sprague-Dawley rats were implanted with osmotic mini-pumps delivering recombinant rat leptin (1 mg/kg per min, i.v.) or vehicle concurrently with the RUPP procedure to induce placental ischemia or Sham. On GD 19, plasma leptin was elevated in Sham+Leptin and RUPP+Leptin. Leptin infusion did not significantly impact mean arterial pressure (MAP) in Sham. MAP was increased in RUPP+Vehicle vs. Sham+Vehicle. In contrast to our hypothesis, placental ischemia-induced hypertension was attenuated by leptin infusion. To examine potential mechanisms for attenuation of RUPP-induced hypertension during hyperleptinemia, endothelial-dependent vasorelaxation to acetylcholine was similar between Sham and RUPP; however, endothelial-independent vasorelaxation to the nitric oxide (NO)-donor, sodium nitroprusside, was increased in Sham and RUPP. These findings suggest that NO/cyclic guanosine monophosphate (cGMP) signaling was increased in the presence of hyperleptinemia. Plasma cGMP was elevated in Sham and RUPP hyperleptinemic groups compared to vehicle groups but plasma and vascular NO metabolites were reduced. These data suggest that hyperleptinemia during placental ischemia attenuates hypertension by compensatory increases in NO/cGMP signaling.

Abstract 052: Placental Growth Factor (PlGF) Reduces Blood Pressure and Improves Endothelin Type B Receptor (ETBR)-Mediated Microvascular Dilation in Hypertensive Pregnant Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Marc Q Mazzuca ◽  
Zongli Ren ◽  
Chen Lin ◽  
Jose S Possomato-Vieira ◽  
Minglin Zhu ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Mesenteric Arteries ◽  
Hypertensive Disorder ◽  
Type B ◽  
Pregnant Rats ◽  
Western Blots ◽  
New Approach ◽  
Nitrite Production ◽  
Uterine Perfusion ◽  
Mesenteric Microvessels

Preeclampsia is a pregnancy-related hypertensive disorder (HTN-Preg) with an imbalance between anti-angiogenic soluble fms-like tyrosine kinase-1 (sFlt-1) and angiogenic PlGF, but the vascular targets involved are unclear. We have shown downregulation of endothelial ET B R in Preg rats with reduced uterine perfusion pressure (RUPP), and studies have shown increased plasma sFlt-1 in RUPP rats. We tested if raising PIGF/sFlt-1 ratio by infusing PIGF (10 μg/kg/day) in RUPP rats would improve BP and microvascular ET B R signaling, and vice versa, if lowering PIGF/sFlt-1 ratio by infusing sFlt-1 (10 μg/kg/day) in Preg rats increases BP and reduces ET B R signaling. On day 19, BP was recorded and mesenteric microvessels were isolated for measurement of diameter and [Ca 2+ ] i (fura-2 340/380 ratio). BP was in PlGF-RUPP 105±2 < RUPP 126±1 and in sFlt-Preg 125±4 > Norm-Preg 97±5 mmHg. ET-1 vasoconstriction was in PlGF-RUPP 62.6±3.0 < RUPP 83.4±5.3 and in sFlt-Preg 76.1±4.7 > Norm-Preg 52.1±3.2%. ET-1 caused parallel increases in microvascular [Ca 2+ ] i that was in PlGF-RUPP 0.87±0.02 < RUPP 0.92±0.01 and in sFlt-Preg 0.93±0.02 > Norm-Preg 0.85±0.01. Endothelium removal or microvessel treatment with ET B R antagonist BQ-788 enhanced ET-1 vasoconstriction and [Ca 2+ ] i in Norm-Preg and PlGF-RUPP, but not RUPP or sFlt-Preg. The ET B R agonists sarafotoxin 6c (S6c) and IRL-1620 caused relaxation that was in PlGF-RUPP 42.9±10.8, 38.0±11.2% > RUPP 4.7±3.4, 7.5±2.3% and in sFlt-Preg 3.1±1.0, 5.4±1.6% < Norm-Preg 29.9±7.8, 28.0±9.1%. L-NAME partially reduced ACh- and ET B R-induced relaxation in Norm-Preg, PlGF-RUPP, but not RUPP or sFlt-Preg, suggesting that PlGF improves the decreased NO-dependent and ET B R-mediated vasorelaxation in HTN-Preg. Basal, ACh-, S6c-, and IRL-1620-induced nitrate/nitrite production was enhanced in mesenteric arteries of PIGF-RUPP and Norm-Preg vs. RUPP rats. Western blots and immunohistochemistry revealed greater levels of endothelial ET B R in PlGF-RUPP and Norm-Preg vs. RUPP and sFlt-Preg. Thus improving PlGF/sFlt-1 balance reduces BP and ET-1 vasoconstriction, and enhances ET B R-mediated NO-dependent vasodilation in RUPP rats, and could be a new approach in the management of HTN-Preg.

scholarly journals Maternal hypoxia and caffeine exposure depress fetal cardiovascular function during primary organogenesis

2012 ◽  
Vol 38 (12) ◽  
pp. 1343-1351 ◽  
Author(s):  
Nobuo Momoi ◽  
Joseph P. Tinney ◽  
Bradley B. Keller ◽  
Kimimasa Tobita
Keyword(s):  
Cardiovascular Function ◽  
Maternal Hypoxia ◽  
Caffeine Exposure

scholarly journals Hemodynamic gestational adaptation in bitches

2017 ◽  
Vol 47 (7) ◽  
Author(s):  
Vívian Tavares de Almeida ◽  
Ricardo Andres Ramirez Uscategui ◽  
Priscila Del Aguila da Silva ◽  
Michele Lopes Avante ◽  
Ana Paula Rodrigues Simões ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Cardiovascular System ◽  
Vascular Resistance ◽  
Diagnostic Tool ◽  
Fetal Development ◽  
Vascular System ◽  
Literature Analysis ◽  
Vasoactive Peptides ◽  
Uterine Perfusion ◽  
Available Information

ABSTRACT: Throughout pregnancy, maternal hemodynamic adaptation is needed to ensure proper uterine perfusion and fetal development. When the uteroplacental vascular system is formed, starting with reduced resistance to uterine arterial flow, this results in decreased total vascular resistance, an activation of neuroendocrine vasoactive peptides, an increase in circulating blood and changes in the cardiovascular system morphophysiology to respond to the increasing demands of uterine perfusion. There has been considerable study of hemodynamic adaptation in pregnant women and this assessment has become a diagnostic tool for fatal obstetric disorders. However, in bitches the available information in this regard is limited; therefore a parallel was drawn between other species of animals and women, in order to subsidize the paucity of information about this process and facilitate the understanding of maternal-fetal hemodynamic adaptation in pregnant bitches. This review and literature analysis aimed\ to discuss morphophysiological cardiovascular adaptations during pregnancy and the possible disorders that can affect this process in pregnant female dogs.

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