bluuebunny/crossref_metadata_2025_split huggingface dataset:
Maternal Heart Rate and Heart Rate Variability During Pregnancy and Exercise Training
Authors: Paynter Christopher , Meacham Crystal , Ramar Cassandra , Gustafson Kathleen M , Suminski Richard R , May Linda E 
Published: June 2021

Exercise in non‐pregnant women increases parasympathetic control resulting in lower resting heart rates (HR) and increased heart rate variability (HRV). This is important given the relationships between pregnancy complications (hypertension, pre‐eclampsia and gestational diabetes) and altered autonomic control. This study tested the hypothesis that maternal exercise throughout gestation alters maternal cardiac autonomic control as indicated by changes in HR and HRV. We used magnetocardiography to record maternal HR between 28 and 32 wks GA from 20 women who exercised regularly (>30 min aerobic activity, 3 times per week) and 19 women who did not exercise during pregnancy. R‐R intervals were used to determine HR and HRV. HR (82.9 + 9.1 vs 90.4 + 9.9 bpm; F=6.2(1,37);p<0.05) was lower, pNN50 was greater (16.3 + 19.4 vs. 6.1 + 6.0; F= 4.7(1,37);p<0.05), and there was a trend of higher SDNN (p=0.05) indicating increased parasympathetic control in the exercise relative to the non‐exercise group. LF/HF, an index of sympathovagal balance, was lower (0.55 + 0.36 vs. 0.82 + 0.53; F=4.3(1,37), p<0.05) in the exercise group. Indices of parasympathetic control are altered in women who exercise regularly throughout their pregnancy. Therefore, exercise can be used as an intervention to decrease the risk of pregnancy complications associated with increased sympathetic input.Research supported by: KCUMB and Hoglund Brain Imaging Center funds
The influence of the intensity of a single bout of aerobic exercise on endothelial function in obese post‐menopausal women
Authors: Cheek Dennis Jefferson , Boyd Kara , Mitchell Joel 
Published: June 2021

Endothelial dysfunction increases the risk of cardiovascular disease, and regular exercise has been shown to increase endothelial function (EF); however, single bouts of exercise may also produce beneficial effects lasting at least 24 h.PurposeThe purpose of this study was to observe the effects of two intensities of a single bout of aerobic exercise on endothelial function (EF) in obese, post‐menopausal women.MethodsEleven obese (% fat = 37.23 ± 2.75; BMI = 30.57 ± 2.14) women between the ages of 54 and 70 yrs completed two, one‐hour sessions of treadmill exercise at 50 and 70% of HRmax, and a resting control trial. EF was assessed via flow‐mediated dilation (FMD) of the brachial artery and via blood levels of nitrate/nitrite (N/N) before and after exercise and at two, 24, 48, and 72 hours post exercise. FMD was measured by ultrasound images of the brachial artery before and for 5 min after 5 min of occlusion. A 3 × 6 repeated measures ANOVA was used to examine differences between condition and time for FMD and blood measures.ResultsData at 24 h post exercise are shown below (mean ± SD).

Condition
FMD Max (mm)
Δ Dilation (%)
AUC
N/N (μM)

Control
3.75±0.58
0.14±4.87
8.09±5.68
9.09±4.13

50 % HRmax
3.82±0.62
5.64±9.18
10.28±5.89
7.01±2.99

70% HRmax
3.91±0.70
4.28±10.40
8.86±5.89
7.57±4.75

None of the responses were significantly different from each other; however, there was a tendency for a greater Δ dilation in the 50% condition (p=0.075).ConclusionIn elderly, obese females, one hour of exercise did not impact subsequent FMD responses, nor the blood markers of EF at any time points, regardless of the exercise intensity.
Short‐term AMPK activation improves vascular endothelial function in old mice by a different mechanism than habitual aerobic exercise
Authors: Lawson Brooke R , Seals Douglas R , Magerko Katherine A , Durrant Jessica R , Zigler Melanie L , Donato Anthony J , Lesniewski Lisa A 
Published: June 2021

Habitual exercise improves endothelium‐dependent dilation (EDD) in old rodents by increasing nitric oxide (NO) bioavailability. Acute exercise activates adenosine monophosphate protein kinase (AMPK), activating endothelial NO synthase and increasing NO production. We determined if pharmacological AMPK activation by aminoimidazole carboxamide ribonucleotide (AICAR, 0.25 mg/kg/day for 14 days, sq) mimics habitual exercise‐induced improvements in EDD and NO bioavailability. Acetylcholine‐mediated EDD was assessed in carotid arteries of young (Y: 4–6 mo), old (O: 29–31 mo), O voluntary wheel running (O‐VR, 10–14 weeks) and O AICAR treated B6D2F1 mice. AMPK phosphorylation was lower in O vs. Y (0.2±0.1 vs. 1.0±0.2 AUs, P=0.01) and was increased after VR (1.4±0.4 AUs, P<0.05) and AICAR treatment (0.5±0.1 AUs, P<0.05) in old mice. Age‐associated decreases in maximal EDD (Y: 97±1 vs. O: 63±11%, P<0.05) and NO bioavailability (Y: 52±6 vs. O: 27±6%, P<0.005) were restored by VR (Max EDD: 96±2%, P<0.05; NO: 48±8%, P<0.05). Short‐term treatment with AICAR improved EDD (91±4%, P<0.05), but not NO bioavailability (28±4%, P=0.47). Sensitivity (IC50) to the NO donor sodium nitroprusside was not significantly different among Y, O and O‐VR groups (SNP; Y: 5.8E‐9±2.4E‐9; O: 5.3E‐9±2.0E‐9; OVR: 8.9E‐9±2.4E‐9 log M, all P>0.05), but AICAR treatment markedly increased sensitivity to SNP (5.6E‐10±1.5E‐10 log M, P<0.05) in old mice. Unlike habitual exercise, short‐term pharmacological activation of AMPK by AICAR improves EDD in old mice by increasing smooth muscle sensitivity to NO.NIH AG013038, AG033755, AG029337
Impact of dietary fish oil on the atrial endothelin system and inositol triphosphate signaling: relevance to post‐operative atrial fibrillation
Authors: Mayyas Fadia , Sakurai Seiichiro , Niebauer Mark , Chung Mina K , Van Wagoner David R 
Published: June 2021

BackgroundEndothelin‐1 (ET‐1) modulates inositol triphosphate (IP3) signaling and may be involved in the etiology of atrial fibrillation (AF). We hypothesized that ET‐1 is also involved in post‐operative AF (POAF), and that ET‐1 signaling may be modulated by fish oil, FO. In a cardiac surgery model we studied the impact of dietary fish oil (FO) on inducibility of POAF and atrial ET system/IP3 receptors.MethodsAdult dogs received control chow (n=10), or chow supplemented with FO (EPA/DHA, 0.6g/Kg/day, n=9) for 3 weeks. Surgery was performed to excise left atrial appendage (LAA, internal CTL). Atrial burst pacing (30s) was used daily to assess AF inducibility. Left and right atria (LA, RA) and pulmonary veins (PV) were obtained on terminal postoperative day (POD) 2 or 4.ResultsPOAF was induced in 4/6 CTL but none of FO treated dogs. Plasma ET‐1 did not change after surgery, but was reduced by FO prior to surgery and at POD 1–4. Relative to baseline LAA, LA ET‐1 level was increased after surgery in both groups. ET‐1 content in the PV and RA was 2× higher than LA and was lowered by FO on the PV and LAA. After surgery, ETBR and ETAR expression was decreased in CTL LA, while IP3R‐I,II was increased. In FO group, ETAR expression was unchanged (POD2) or increased (POD4), but IP3R‐II was unchanged.ConclusionsOur study links the atrial ET system and IP3Rs with POAF. Peri‐operative FO may in part suppress POAF by modulating IP3 signaling.
Effects Of Isoflurane Anesthesia On Murine Glucose Metabolism
Authors: Constantinides Christakis , Mean Richard , Janssen Ben JA , Hedlund Laurence W 
Published: June 2021

Maintaining optimal blood glucose (Glu) and insulin (Ins) levels is essential for physiological studies in anesthetized mice. This study examined the temporal effects of varying levels of isoflurane (ISO) anesthesia on blood Glu and Ins levels in mice for 90 min. post‐induction. Male C57BL/6 mice were allowed to breath freely ISO at 1 (n=5), 1.5 (n=7), and 2.0% (n=8) in 100% O2 while body temperature was maintained at 37.1±0.4°C. ECG and respiratory flowrate were monitored. A 0.6μl tail vein blood aliquot was extracted at 5 min. intervals for Glu measurements. Ins was measured from 1ml arterial blood at 1 and 2% ISO in 20 mice euthanized at t=0, 20, 40, 60 and 80 min. Mean heart rates (±SD) were 532±39, 488±39, and 449±23 bpm at 1, 1.5, and 2% ISO respectively (p<0.0001). Glu concentrations (mg/dl) ranged between 155±28–196±76 [1% ISO], 162±43–239±38 [1.5% ISO], and 159±52–205±49 [2.0% ISO]. Ins values ranged between 3.5±0.3–4.2±0.6ng/dl [2% ISO], and 3.4±0.5–4.2±0.9ng/dl at 1% ISO. Glu values were significantly higher in the ISO=1.5 and 2% groups compared to the 1% group (p<0.0001). No significant temporal change was noted in Glu values at the 3 ISO doses. Ins concentrations did not differ significantly between groups. The results confirm that ISO levels ≥1.5% produce a mild hyperglycemic effect, prominent at later time periods post‐induction.Research supported by the Hellenic Bank and the Research Promotion Foundation.
Expression of c‐Fos protein in the nucleus of tractus solitary (NTS) and paraventricular nucleus of the hypothalamus (PVN) elicited by electrical stimulation of the aortic depressor nerve in conscious L‐NAME‐induced hypertensive rats
Authors: Pereira Ricardo M , Durand Marina T , Castania Jaci A , Oliveira Mauro , Salgado Maria Cristina O , Fazan Rubens , Salgado Helio C 
Published: June 2021

To detect possible alterations of the baroreflex arch, we assessed the expression of c‐Fos in the NTS and PVN of L‐NAME‐induced hypertensive rats submitted to electrical stimulation of the aortic depressor nerve (ADN) in conscious state. Rats were treated for 14 days with L‐NAME (n=7), D‐NAME (n=5) or tap water (CONTROL; n=6). The animals were equipped with catheters in the femoral artery and vein, and a pair of electrodes for intermittent (5s on/10s off) electrical stimulation (1mA, 2ms and 60Hz) during 20 min. L‐NAME treated rats showed higher arterial pressure and heart rate than D‐NAME and CONTROL rats. The hypotensive response and bradycardia due to electrical stimulation did not differ among groups. The density of c‐Fos in the intermediate and commissural caudal NTS, and magnocelular and parvocelular portions of the PVN was higher in L‐NAME treated rats. In conclusion, electrical stimulation of the ADN activated more effectively neurons in the NTS and PVN of L‐NAME induced hypertensive rats. These findings suggest a greater buffering effect of the NTS upon the PVN in this hypertensive model.Supported by CAPES, CNPq and FAPESP.
Role of epinephrine in 5HT1A receptor agonist‐mediated increase in venous tone during hypovolemic shock
Authors: Tiniakov Ruslan L , Scrogin Karie E 
Published: June 2021

The 5‐HT1A receptor agonist, 8‐OH‐DPAT, improves hemodynamic parameters and tissue oxygenation during hypovolemic shock via splanchnic sympathetic nerve‐dependent increases in venous tone. To determine if endogenous epinephrine contributes to this response, effects of 8‐OH‐DPAT (30 nmol/kg, iv) and saline on arterial pressure (AP) and mean circulatory filling pressure (MCFP, an index of venous tone) were measured in adrenal‐demedullated (ADMX) and sham‐operated rats during fixed‐pressure (FPH) and fixed‐volume (FVH) hemorrhagic shock. ADMX rats had lower baseline MCFP (5.4 ± 0.1 vs. 7.5 ±0.2 mmHg; P< 0.01) and reached an AP of 50 mmHg with less blood loss (31.3 ± 0.9 vs. 35.0 ± 0.4 ml/kg; P<0.01) than sham‐operated rats. In both hemorrhage models, 8‐OH‐DPAT produced a rapid and persistent pressor effect in sham‐ and ADMX rats (FPH: +29 ± 5 and +28 ± 3 mmHg, P<0.01; FVH: +34 ± 4 mmHg and +36 ± 4 mmHg, P<0.01). This was paralleled by a persistent increase in MCFP in sham‐operated rats (+1.6 ± 0.4 and +1.9 ± 0.4 mmHg, 5 and 35 min after injection, FVH; P<0.01), but only a transient increase in ADMX rats (+1.1 ± 0.4 mmHg, P<0.05, and +0.4 ± 0.4 mmHg, 5 and 35 min post injection, FVH). Saline had no effect on AP or MCFP in either hemorrhage model. Blood volume before FVH (50 ± 1 vs. 53 ± 2 ml/kg) and after treatment with 8‐OH‐DPAT (31 ± 2 vs. 31 ± 5 ml/kg) did not differ between sham‐ and ADMX rats. The data indicate that persistent elevation of MCFP induced by 8‐OH‐DPAT in hypovolemic rats, but not the rise in AP, is mediated, in part, by endogenous epinephrine.Supported by HL 076162.
Central Ang‐(1–7) enhances baroreflex gain in rabbits with chronic heart failure
Authors: Kar Sumit , Curry Pamela L , Zucker Irving H 
Published: June 2021

In chronic heart failure (CHF), arterial baroreflex function is impaired in part by activation of the central renin‐angiotensin system. A metabolite of Angiotensin II (Ang II), Ang‐(1–7), has been shown to exhibit cardiovascular effects that are in opposition to that of Ang II. However, the action of Ang‐(1–7) on sympathetic outflow and baroreflex function is not well understood, especially in CHF. This study aimed to determine the effect of intracerebroventricular infusion of Ang‐(1–7) on baroreflex control of heart rate (HR) in rabbits with CHF. We hypothesized that central Ang‐(1–7) would improve baroreflex function in CHF. Ang‐(1–7) (2 nmol/μl/hour) or artificial cerebrospinal fluid (1 μl/hour) was infused by an osmotic mini‐pump for 4 days in sham and pacing‐induced CHF rabbits (n=5–6/group). CHF rabbits showed depressed baroreflex gain in the conscious state. Ang‐(1–7) treatment increased baroreflex gain (7.4±1.5 bpm/mm Hg vs. 2.5±0.4 bpm/mm Hg, P<.05). Central Ang‐(1–7) improved baroreflex control in CHF by lowering minimum HR and increasing maximum gain. This suggests that modulation of baroreflex function by Ang‐(1–7) may be due to increased vagal tone.Source of support: PO1 HL‐62222
Nitric Oxide and Vasopressin Expression during Sepsis
Authors: Oliveira‐Pelegrin Gabriela Ravanelli , Athayde Letícia Antunes , Azevedo Sergio Vicente , Yao Song , Murphy David , Rocha Maria José Alves 
Published: June 2021

We investigated the role of centrally produced NO on hypothalamic arginine vasopressin (AVP) expression and release and on cardiovascular response during experimental sepsis. Male Wistar rats were i.c.v injected with the non‐selective NO synthase (NOS) inhibitor L‐NAME, or aminoguanidine (AG), a selective inhibitor of the inducible isoform (iNOS). After 30min sepsis was induced by cecal ligation and puncture (CLP) causing increases in NO plasma levels and heart rate (HR) and a reduction in arterial pressure (MAP) and AVP expression ratio (AVPR) in the supraoptic (SON) and paraventricular (PVN) nuclei. AVP plasma levels (AVPp) increased, but only in the early phase. L‐NAME pretreatment, reduced NO production and increased MAP and did not change HR. AVPp further increased in the early phase but decreased in the late phase while AVPR decreased in both phases. AG i.c.v injected did not change substantially the increase of NO plasma levels but increased MAP in the initial phase of sepsis. AVPR increased only in the SON, and AVPp remained all time elevated. These results show that increased central NO production differentially inhibits AVPR in SON and PVN, contributing to basal AVPp and hypotension in the late phase of sepsis.Financial support: FAPESP
High Egg Cholesterol Consumption May Not Affect Blood Serum Cholesterol Levels in Elite Athletes in Training
Authors: Bui Steve , Oliver Jonathan , Mardock Michelle , Beihl Adam , Riechman Steven E. 
Published: June 2021

BackgroundDue to its high cholesterol content, limiting the intake of egg yolks is a common recommendation; however, recent studies have shown that blood cholesterol levels may be more dependent on other factors such as physical activity levels and genetic predispositions, than on actual cholesterol intake. Therefore, we hypothesized that very high cholesterol consumption in the form of egg yolks will not increase blood cholesterol levels in elite collegiate power lifters during training.MethodsSeven individuals were recruited for this study (age: 23±3.6; height: 66.7±4.7 in; body fat: 17.6±9.3%; weight: 83.2±17.8 kg). Subjects were assigned to one of two supplement groups paired by sum of 1RMs to lean body weight. High cholesterol supplement group was supplemented with 20 mg•kg−1•lean body mass−1 •day−1 of cholesterol via egg yolks (HC, N=4) while the lower cholesterol group was supplemented with equivalent egg control (LC, N=3) to meet 8 mg•kg‐1•lean body mass‐1•day‐1. Blood measurements were taken prior to supplementation and after nine weeks of training/supplementation.ResultsTotal cholesterol decreased in HC (−11.8±18.4 mg•dl−1) but increased in LC (21.7±9.5 mg•dl−1) after nine weeks (P<0.05). HDL followed a similar pattern (−11.3±6.8 HC and 4.7±6.4 LC mg•dl−1, P<0.05), while LDL levels did not change (5.3±.11. HC and 8.0±.14.4 LC mg•dl−1, P>0.05).ConclusionIt is unclear what may have caused a decrease in total cholesterol and HDLs while maintaining LDL levels. The relationship of dietary cholesterol to blood parameters is not straightforward as generally perceived and exercise training at the elite level may alter this relation.
Expression of Angiotensin II Subtype 1a Receptor (AT1a) During Pregnancy in Mouse
Authors: Chen Kai , Rose James C 
Published: June 2021

ObjectiveThe AT1a receptor plays an important role in blood pressure regulation during pregnancy but its expression in gestation is not well defined. There is also significant interaction between AT1a and angiotensin II subtype 2 receptors (AT2). Therefore, we examined AT1a expression in wild type(WT) and AT2 knockout mice (AT2(−/−)) throughout pregnancy to determine the pattern of expression and if the AT2 receptor influences any pregnancy‐related changes.MethodsSix mice from each group were sacrificed in early‐, mid‐ and late gestation. Tissues such as kidney and placenta were collected. Western blot was used to examine the expression of the receptor. ANOVA followed with Newman‐Keuls test was used to analyze data from kidney, t test was used to analyze data from placenta.ResultsIn placenta, compared to mid gestation, AT1a decreased in late gestation in WT mice (0.63±0.13 vs. 0.27±0.07*) but not in AT2(−/−) mice (0.77±0.17 vs. 0.75±0.07). Similarly, in kidney, compared to early gestation, AT1a was lower in mid‐ and late gestation in WT mice (1.16±0.03, 0.91± 0.12*, 0.81±0.05*) but not in AT2(−/−) mice (0.79±0.05, 0.66±0.05, 0.78±0.12).ConclusionExpression of the AT1a decreases during pregnancy in placenta and kidney in normal but not in AT2(−/−) mice. AT2 receptors might play an important role in AT1 expression variation during pregnancy in mice.
High muscle mass in Oregon women is associated with decreased antioxidant expression in the term placenta
Authors: O'Tierney Perrie Faye , Cedar Anna , Morris Cynthia , Thornburg Kent L 
Published: June 2021

ObjectivePlacental oxidative stress is an imbalance between antioxidants and reactive oxygen species and is known to compromise fetal growth. We hypothesized that high maternal muscle mass and body mass index (BMI) in early pregnancy will lead to suppressed expression of placental antioxidant systems.MethodsWomen were categorized into groups based upon arm muscle area (AMA) [low: 20.1 ± 3.4 and high: 71.3 ± 16.2 cm2] and BMI [low: 19.3 ± 1.4 and high: 38.4 ± 2.5 kg/m2]. Term placental antioxidant gene expression, specifically catalase, superoxide dismutase (SOD) 1 and 2, and glutathione peroxidase (GPX) 1 and 4, was quantified by QPCR. 8‐isoprostane, a marker of oxidized lipid, was measured in maternal and fetal plasma.ResultsSOD2 protein and GPX1 mRNA levels were decreased (P<0.05) in women with high AMA. Antioxidant levels were not changed in placentas of women with high BMI. 8‐isoprostane increased with maternal BMI (R= 0.51, P<0.05) but not AMA (R=0.36), while fetal levels showed no association with maternal body type.Conclusionsa) Antioxidant expression was depressed in high AMA mothers as hypothesized without increased 8‐isoprostane. b) Contrary to the hypothesis, high BMI women had a different response. Placental antioxidant levels were unchanged while oxidative stress was increased in these mothers. Supported by the Collins Medical Trust, Northwest Health Foundation, Holtzman Foundation.
Lifelong sedentary behavior aggravates detrimental age associated effects on bone structure of C57BL/6 mice
Authors: Fonseca Helder Martins , Gonçalves Daniel Moreira , Figueiredo Pedro Carvalho , Mota Paula Gonçalves , Duarte José Alberto 
Published: June 2021

The aim of this study was to compare the femoral bone structure of lifelong sedentary vs active C57BL/6 mice. Thirty male C57BL/6 mice, aged 2 months, were either: i) sacrificed after arrival (young group; Y; n=10); ii) kept in cages equipped with running wheels, where they could perform voluntary running (aged active group; AA; n=10); iii) kept in cages without running wheel (aged sedentary group; AS; n=10). After 23 months of differential housing AS and AA animals were also sacrificed. In all animals the right femur was collected and processed for histomorphometryc analysis of both epiphyses and mid diaphysis. Right hind limb muscles were collected for citrate synthase (CS) activity determination to confirm physically active and sedentary behaviors.Differences in trabecular microarchitecture and cortical bone geometry were identified between AA and AS groups. AA mice showed significantly increased trabecular perimeter (Tb.Pm) and trabecular number (Tb.N) and decreased trabecular separation (Tb.Sp) at both epiphyses when compared to AS mice. Differences in osteocyte density (Oc.N/mm2) were identified between AS and Y mice but not between AA and Y mice. Our results evidence that skeletal changes usually indentified as a result of ageing, are at least in some extent, due to sedentary behavior. Maintenance of a physically active lifestyle is therefore essential for delaying changes in bone quality throughout life.Grant Funding Source: FCT grant SFRH/BD/38110/2007
Transgenic Labeling of Chondrocyte and Osteoblast Lineages in Xenopus laevis Tadpoles
Authors: Kerney Ryan 
Published: June 2021

The extent to which tadpole cells contribute to adult tissues and organs is a long‐standing question in amphibian metamorphosis. These contributions are particularly interesting in skeletal metamorphosis, where the cartilaginous tadpole skeleton is largely replaced by de novo cartilage and bone formation in the adult. Three basic pathways of cellular differentiation are possible. First, larval cells may persist in a single differentiated state to give rise to an adult structure of the same tissue type (e.g. cartilage). Second, larval cells may transdifferentiate from one differentiated state to another during metamorphosis (e.g. cartilage to bone). Third, cellular progenitors to adult structures may persist as mesenchyme in the tadpole, and only achieve terminal differentiation during metamorphosis (e.g. mesenchyme to cartilage and/or bone). This project explores all three of these differentiation pathways during skeletal metamorphosis through novel transgenic labeling of cell populations and cellular lineages in Xenopus laevis. Wnt1, sox10, col2a1 and osterix reporter constructs were used to drive green fluorescent protein (GFP) expression in the neural tube, neural crest, chondrocytes, and osteoblasts respectively. These live labels allow the visualization of skeletogenesis in vivo. In conjunction with cre‐recombinase‐dependent lineage labeling, these reporters reveal both the extent to which differentiated larval chondrocytes contribute to the adult skeleton, and the location of putative skeletogenic precursors that are developmentally quiescent during tadpole stages. These pathways of cellular differentiation have implications for both the mechanisms of skeletal development and the evolution of anuran metamorphosis.Grant Funding Source: NSERC