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Showing 881–900 of 2058 publications.
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Hiob, Matti A.; Trane, Andy E.; Wise, Steven G.; Bernatchez, Pascal N.; Weiss, Anthony StevenAims: This study aimed to characterize the role of tropoelastin in eliciting a nitric oxide response in endothelial cells. Materials and methods: Nitric oxide production in cells was quantified following the addition of known nitric oxide synthase pathway inhibitors such as LNAME and 1400W. The effect of eNOS siRNA knockdowns was studied using western blotting and assessed in the presence of PI3K-inhibitor, wortmannin. Results: Tropoelastin-induced nitric oxide production was LNAME and wortmannin sensitive, while being unaffected by treatment with 1400W. Conclusion: Tropoelastin acts through a PI3K-specific pathway that leads to the phosphorylation of eNOS to enhance nitric oxide production in endothelial cells. This result points to the benefit of the use of tropoelastin in vascular applications, where NO production is a characteristic marker of vascular health. 2016 Future Medicine Ltd.
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Thompson, Peter Lindsay; McQuillan, Brendan M.Despite being more likely to present with NSTEMI than STEMI, women have worse outcomes after an ACS than men, due in part to older age at ACS occurrence and having more comorbidities. Women generally have longer delays from symptom onset to treatment and are more likely not to report chest pain and less likely to have diagnostic ECG changes and elevated troponin levels. MedicineToday 2016.
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Santos, Miguel; Filipe, Elysse C.; Michael, Praveesuda Lorwattanapongsa; Hung, Juichien; Wise, Steven G.; Bilek, Marcela M.M.The long-term performance of many medical implants is limited by the use of inherently incompatible and bioinert materials. Metallic alloys, ceramics, and polymers commonly used in cardiovascular devices encourage clot formation and fail to promote the appropriate molecular signaling required for complete implant integration. Surface coating strategies have been proposed for these materials, but coronary stents are particularly problematic as the large surface deformations they experience in deployment require a mechanically robust coating interface. Here, we demonstrate a single-step ion-assisted plasma deposition process to tailor plasma-activated interfaces to meet current clinical demands for vascular implants. Using a process control-feedback strategy which predicts crucial coating growth mechanisms by adopting a suitable macroscopic plasma description in combination with noninvasive plasma diagnostics, we describe the optimal conditions to generate highly reproducible, industry-scalable stent coatings. These interfaces are mechanically robust, resisting delamination even upon plastic deformation of the underlying material, and were developed in consideration of the need for hemocompatibility and the capacity for biomolecule immobilization. Our optimized coating conditions combine the best mechanical properties with strong covalent attachment capacity and excellent blood compatibility in initial testing with plasma and whole blood, demonstrating the potential for improved vascular stent coatings. 2016 American Chemical Society.
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Jongberg, Sisse; Lund, Marianne Nissen; Pattison, David I.; Skibsted And, Leif H.; Davies, Michael J.Competitive kinetics were applied as a tool to determine apparent rate constants for the reduction of hypervalent haem pigment ferrylmyoglobin (MbFe(IV)=O) by proteins and phenols in aqueous solution of pH 7.4 and I = 1.0 at 25 C. Reduction of MbFe(IV)=O by a myofibrillar protein isolate (MPI) from pork resulted in k<inf>MPI</inf> = 2.2 0.1 104 M-1 s-1. Blocking of the protein thiol groups on the MPI by N-ethylmaleimide (NEM) markedly reduced this rate constant to k<inf>MPI-NEM</inf> = 1.3 0.4 103 M-1 s-1 consistent with a key role for the Cys residues on MPI as targets for haem protein-mediated oxidation. This approach allows determination of apparent rate constants for the oxidation of proteins by haem proteins of relevance to food oxidation and should be applicable to other systems. A similar approach has provided approximate apparent rate constants for the reduction of MbFe(IV)=O by catechin and green tea extracts, though possible confounding reactions need to be considered. These kinetic data suggest that small molar excesses of some plant extracts relative to the MPI thiol concentration should afford significant protection against MbFe(IV)=O-mediated oxidation. 2015 Published by Elsevier Ltd.
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Kapoor, Komal; Bhandare, Amol M.; Farnham, M. M. J.; Pilowsky, Paul M.Microglia, commonly known as the tissue resident macrophages of the central nervous system (CNS), are ubiquitously expressed in the CNS. Microglia, in their resting, or surveilling, stage, play a critical role in the maintenance of normal neuronal physiology and homeostasis. On activation, microglia can acquire either a neurotoxic (M1) or a neuroprotective (M2) phenotype. Prior to development of the M1 or M2 phenotype, little was known about changes in microglial activity, when subjected to stimuli. It is postulated, that an inability of microglia to maintain neuronal physiology within a normal working range can contribute to the development of cardiovascular disorders (CVDs) such as hypertension, but clear evidence supporting this hypothesis is missing. Even though our understanding of microglial function in a state of CNS injury/inflammation is extensive, the literature concerning role of microglia in the healthy CNS, is limited. Involvement of microglia in the pathophysiology of CVDs, in a neuroprotective/neurotoxic manner, is a key area that requires further investigation. 2015.
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Wang, Xiaolu; Guo, Ruichen; Zhao, Wenjing; Pilowsky, Paul M.The laryngeal adductor reflex (LAR) is a laryngeal protective reflex. Vagal afferent polymodal sensory fibres that have cell bodies in the nodose ganglion, originate in the sub-glottal area of the larynx and upper trachea. These polymodal sensory fibres respond to mechanical or chemical stimuli. The central axons of these sensory vagal neurons terminate in the dorsolateral subnuclei of the tractus solitarius in the medulla oblongata. The LAR is a critical, reflex in the pathways that play a protective role in the process of ventilation, and the sychronisation of ventilation with other activities that are undertaken by the oropharyngeal systems including: eating, speaking and singing. Failure of the LAR to operate properly at any time after birth can lead to SIDS, pneumonia or death. Despite the critical nature of this reflex, very little is known about the central pathways and neurotransmitters involved in the management of the LAR and any disorders associated with its failure to act properly.Here, we review current knowledge concerning the medullary nuclei and neurochemicals involved in the LAR and propose a potential neural pathway that may facilitate future SIDS research. 2016 Elsevier B.V.
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Bhandare, Amol M.; Kapoor, Komal; Farnham, M. M. J.; Pilowsky, Paul M.Seizure-induced cardiorespiratory autonomic dysfunction is a major cause of sudden unexpected death in epilepsy (SUDEP), and the underlying mechanism is unclear. Seizures lead to increased synthesis, and release of glutamate, pituitary adenylate cyclase activating polypeptide (PACAP), and other neurotransmitters, and cause extensive activation of microglia at multiple regions in the brain including central autonomic cardiorespiratory brainstem nuclei. Glutamate contributes to neurodegeneration, and inflammation in epilepsy. PACAP has neuroprotective, and anti-inflammatory properties, whereas microglia are key players in inflammatory responses in CNS. Seizure-induced increase in PACAP is neuroprotective. PACAP produces neuroprotective effects acting on microglial PAC1 and VPAC1 receptors. Microglia also express glutamate transporters, and their expression can be increased by PACAP in response to harmful or stressful situations such as seizures. Here we discuss the mechanism of autonomic cardiorespiratory dysfunction in seizure, and the role of PACAP, glutamate and microglia in regulating cardiorespiratory brainstem neurons in their physiological state that could provide future therapeutic options for SUDEP. 2016 Elsevier B.V.
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Sheriff, Mohammed Javed; Mouline, Omar; Hsu, Chijen; Grieve, Stuart M.; Wilson, Michael Keith; Bannon, Paul Gerard; Vallely, Michael P.; Puranik, RajeshBackground: The euroSCORE II is a widely used pre-coronary artery bypass graft surgery (CAGS) risk score, but its predictive power lacks the specificity to predict outcomes in high-risk patients (<LVEF 40%) due to changes in cardiac surgery case mix, revascularisation techniques and related outcomes in recent years. We investigated the utility of Cardiac Magnetic Resonance Imaging (CMRI) in predicting immediate and six-week outcomes after CAGS. Methods: Fifty-two consecutive patients with high euroSCORE II (>16) and left ventricular (LV) dysfunction (<40%) based on 2D-echocardiography who underwent CAGS and in whom CMRI (1.5T) was performed preoperatively were retrospectively studied. Cardiac magnetic resonance imaging parameters were assessed in patients who either had complications immediately post-surgery (n=35), six weeks post-surgery (n=20) or were uncomplicated. Results: The average age of patients recruited was 695 years with high euroSCORE II (224) and low 2D-echocardiography LV ejection fraction (38%2%). Cardiac magnetic resonance imaging results demonstrated that those with immediate complications had higher LV scar/infarct burden as a proportion of LV mass (173% vs 103%; p=0.04) with lower circumferential relaxation index (2.50.46 vs 2.80.56; p=0.05) compared to those with no complications. Early mortality from surgery was 17% (n=9) and was associated with lower RV stroke volume (5512 vs 6818; p=0.03) and higher LV infarct scar/burden (182% vs 102%, p=0.04). Cardiac magnetic resonance imaging showed patients with complications at six weeks post-surgery had higher LV scar/infarct burden (14.52% vs 6.82%, p=0.03) compared to those without complications. Conclusion: Cardiac magnetic resonance imaging preoperative LV and RV parameters are valuable in assessing the likelihood of successful outcomes from CAGS in high-risk patients with LV dysfunction. 2016.
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Makris, Angela; Yeung, Kristen R.; Lim, Shirlene M.; Sunderland, Neroli; Heffernan, Scott J.; Thompson, John F.; Iliopoulos, Jim N.; Killingsworth, Murray C.; Yong, James L.C.; Xu, Bei; Ogle, Robert F.; Thadhani, Ravi Ishwar; Karumanchi, Subbian Ananth; Hennessy, AnnemarieAn imbalance in the angiogenesis axis during pregnancy manifests as clinical preeclampsia because of endothelial dysfunction. Circulating soluble fms-like tyrosine kinase 1 (sFLT-1) increases and placental growth factor (PlGF) reduces before and during disease. We investigated the clinical and biochemical effects of replenishing the reduced circulating PlGF with recombinant human PlGF (rhPlGF) and thus restoring the angiogenic balance. Hypertensive proteinuria was induced in a nonhuman primate (Papio hamadryas) by uterine artery ligation at 136 days gestation (of a 182-day pregnancy). Two weeks after uteroplacental ischemia, rhPlGF (rhPlGF, n=3) or normal saline (control, n=4) was administered by subcutaneous injection (100 ?g/kg per day) for 5 days. Blood pressure was monitored by intra-arterial radiotelemetry and sFLT-1 and PlGF by ELISA. Uteroplacental ischemia resulted in experimental preeclampsia evidenced by increased blood pressure, proteinuria, and endotheliosis on renal biopsy and elevated sFLT-1. PlGF significantly reduced after uteroplacental ischemia. rhPlGF reduced systolic blood pressure in the treated group (-5.20.8 mm Hg; from 132.66.6 mm Hg to 124.17.6 mm Hg) compared with an increase in systolic blood pressure in controls (6.53 mm Hg; from 131.31.5 mm Hg to 138.61.5 mm Hg). Proteinuria reduced in the treated group (-72.755.7 mg/mmol) but increased in the control group. Circulating levels of total sFLT-1 were not affected by the administration of PlGF; however, a reduction in placental sFLT-1 mRNA expression was demonstrated. There was no significant difference between the weights or lengths of the neonates in the rhPlGF or control group; however, this study was not designed to assess fetal safety or outcomes. Increasing circulating PlGF by the administration of rhPlGF improves clinical parameters in a primate animal model of experimental preeclampsia. 2016 American Heart Association, Inc.
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Kim, Seung Jae; Kim, Yeon-jae; Kakall, Zohra Mohtat; Farnham, M. M. J.; Pilowsky, Paul M.Intermittent hypoxia induces plasticity in neural networks controlling breathing and cardiovascular function. Studies demonstrate that mechanisms causing cardiorespiratory plasticity rely on intracellular signalling pathways that are activated by specific neurotransmitters. Peptides such as serotonin, PACAP and orexin are well-known for their physiological significance in regulating the cardiorespiratory system. Their receptor counterparts are present in cardiorespiratory centres of the brainstem medulla and spinal cord. Microglial cells are also important players in inducing plasticity. The phenotype and function of microglial cells can change based on the physiological state of the central nervous system. Here, we propose that in the autonomic nuclei of the ventral brainstem the relationship between neurotransmitters and neurokines, neurons and microglia determines the overall neural function of the central cardiorespiratory system. 2016 Elsevier B.V.
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Ju, Lining Arnold; Chen, Yunfeng; Xue, Lingzhou; Du, Xiaoping; Zhu, ChengHow cells sense their mechanical environment and transduce forces into biochemical signals is a crucial yet unresolved question in mechanobiology. Platelets use receptor glycoprotein Ib (GPIb), specifically its ? subunit (GPIb?), to signal as they tether and translocate on von Willebrand factor (VWF) of injured arterial surfaces against blood flow. Force elicits catch bonds to slow VWFGPIb? dissociation and unfolds the GPIb? leucine-rich repeat domain (LRRD) and juxtamembrane mechanosensitive domain (MSD). How these mechanical processes trigger biochemical signals remains unknown. Here we analyze these extracellular events and the resulting intracellular Ca2+ on a single platelet in real time, revealing that LRRD unfolding intensifies Ca2+ signal whereas MSD unfolding affects the type of Ca2+ signal. Therefore, LRRD and MSD are analog and digital force transducers, respectively. The >30 nm macroglycopeptide separating the two domains transmits force on the VWFGPIb? bond (whose lifetime is prolonged by LRRD unfolding) to the MSD to enhance its unfolding, resulting in unfolding cooperativity at an optimal force. These elements may provide design principles for a generic mechanosensory protein machine. Ju et al.
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Talib, Jihan; Davies, Michael J.Smokers have an elevated risk of cardiovascular disease, but the origin(s) of this increased risk are incompletely defined. Evidence supports an accumulation of the oxidant-generating enzyme myeloperoxidase (MPO) in the inflamed artery wall, and smokers have high levels of SCN?, a preferred MPO substrate, with this resulting in HOSCN formation. We hypothesised that HOSCN, a thiol-specific oxidant may target the iron-sulphur cluster of aconitase (both isolated, and within primary human coronary artery endothelial cells; HCAEC) resulting in enzyme dysfunction, release of iron, and conversion of the cytosolic isoform to iron response protein-1, which regulates intracellular iron levels. We show that exposure of isolated aconitase to increasing concentrations of HOSCN releases iron from the aconitase [Fe-S]<inf>4</inf> cluster, and decreases enzyme activity. This is associated with protein thiol loss and modification of specific Cys residues in, and around, the [Fe-S]<inf>4</inf> cluster. Exposure of HCAEC to HOSCN resulted in increased intracellular levels of chelatable iron, loss of aconitase activity and increased iron response protein-1 (IRP-1) activity. These data indicate HOSCN, an oxidant associated with oxidative stress in smokers, can induce aconitase dysfunction in human endothelial cells via Cys oxidation, damage to the [Fe-S]<inf>4</inf> cluster, iron release and generation of IRP-1 activity, which modulates ferritin protein levels and results in dysregulation of iron metabolism. These data may rationalise, in part, the presence of increased levels of iron in human atherosclerotic lesions and contribute to increased oxidative damage and endothelial cell dysfunction in smokers. Similar reactions may occur at other sites of inflammation. 2016, SBIC.
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Freedman, Ben Ben; Martinez, Carlos; Katholing, Anja; Rietbrock, Stephan[No abstract available]
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Kapoor, Komal; Bhandare, Amol M.; Mohammed, Suja; Farnham, M. M. J.; Pilowsky, Paul M.Microglia are ubiquitously distributed throughout the central nervous system (CNS) and play a critical role in the maintenance of neuronal homeostasis. Recent advances have shown that microglia, never resting cells of the CNS, continuously monitor and influence neuronal/synaptic activity levels, by communicating with neurons with the aid of their dynamic processes. The brainstem contains many catecholaminergic nuclei that are key to many aspects of brain function. This includes C1 neurons of the ventrolateral medulla that are thought to play a critical role in control of the circulation. Despite the role of catecholaminergic brainstem neurons in normal physiology, the presence of microglia that surrounds them is poorly understood. Here, we investigate the spatial distribution and morphology of microglia in catecholaminergic nuclei of the brainstem in 3 strains of rat: Sprague-Dawley (SD), Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Our data reveal that microglia are heterogeneously distributed within and across different strains of rats. Interestingly, intra-strain comparison of tyrosine hydroxylase-immunoreactive (TH-ir) neuronal and microglial number reveals that microglial number varies with the TH-ir neuronal number in the brainstem. Even though microglial spatial distribution varies across brainstem nuclei, microglial morphology (% area covered, number of end point processes and branch length) does not differ significantly. This work provides the first evidence that even though microglia, in their surveilling state, do not vary appreciably in their morphology across brainstem areas, they do have a heterogeneous pattern of distribution that may be influenced by their local environment. 2016
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Harith, Hanis H.; Di Bartolo, Belinda Ann; Cartland, Si; Genner, Scott W.; Kavurma, Mary M.Background: Insulin regulates glucose homeostasis but can also promote vascular smooth muscle (VSMC) proliferation, important in atherogenesis. Recently, we showed that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) stimulates intimal thickening via accelerated growth of VSMCs. The aim of the present study was to determine whether insulin-induced effects on VSMCs occur via TRAIL. Methods: Expression of TRAIL and TRAIL receptor in response to insulin and glucose was determined by polymerase chain reaction. Transcriptional activity was assessed using wild-type and site-specific mutations of the TRAIL promoter. Chromatin immunoprecipitation studies were performed. VSMC proliferation and apoptosis was measured. Results: Insulin and glucose exposure to VSMC for 24 h stimulated TRAIL mRNA expression. This was also evident at the transcriptional level. Both insulin- and glucose-inducible TRAIL transcriptional activity was blocked by dominant-negative specificity protein-1 (Sp1) overexpression. There are five functional Sp1-binding elements (Sp1-1, Sp1-2, Sp-5/6 and Sp1-7) on the TRAIL promoter. Insulin required the Sp1-1 and Sp1-2 sites, but glucose needed all Sp1-binding sites to induce transcription. Furthermore, insulin (but not glucose) was able to promote VSMC proliferation over time, associated with increased decoy receptor-2 (DcR2) expression. In contrast, chronic 5-day exposure of VSMC to 1 g/mL insulin repressed TRAIL and DcR2 expression, and reduced Sp1 enrichment on the TRAIL promoter. This was associated with increased cell death. Conclusions: The findings of the present study provide a new mechanistic insight into how TRAIL is regulated by insulin. This may have significant implications at different stages of diabetes-associated cardiovascular disease. Thus, TRAIL may offer a novel therapeutic solution to combat insulin-induced vascular pathologies. 2015 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
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Skilton, Michael R.; Nakhla, Shirley; Ayer, Julian Ganesh J.; Harmer, Jason A.; Toelle, Brett G.; Leeder, Stephen Ross; Jones, Graham J.; Marks, Guy B.; Celermajer, David S.Background Reduced telomere length is a measure of biological aging that is predictive of cardiac events in adults, and has been mechanistically implicated in the onset and progression of atherosclerosis. We sought to describe the early life factors associated with leukocyte telomere length in early childhood, and to determine whether telomere length measured during early childhood is associated with arterial wall thickening later in childhood. Design A longitudinal birth cohort recruited antenatally in Sydney from 1997 to 1999. Methods Leukocyte telomere length was measured in 331 children at age 3.6 years (SD 1.0); of whom 268 children without diabetes had carotid intima-media thickness assessed by ultrasound at age 8 years. Results Male sex, younger paternal age and higher maternal body mass index were associated with shorter telomere length in early childhood, which in turn was associated with greater carotid intima-media thickness at age 8 years (standardised ? = '0.159, P = 0.01). There was a graded association across quartiles of telomere length (P<inf>trend</inf> = 0.001) with the highest odds of elevated intima-media thickness (>75th percentile) being in children with the shortest telomeres (odds ratio 4.00 (95% confidence interval 1.58 to 10.14) relative to those with the longest telomeres, P = 0.003). This association remained after adjustment for early life risk factors (P<inf>trend</inf> = 0.001). Conclusions Reduced telomere length in early childhood is independently associated with arterial wall thickness in later childhood, suggesting that reduced telomere length during early childhood may be a marker of vascular disease risk. European Society of Cardiology.
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Yeung, Kristen R.; Chiu, Christine L.; Pears, Suzanne; Heffernan, Scott J.; Makris, Angela; Hennessy, Annemarie; Lind, Joanne MareeBackground: Ageing is associated with changes at the molecular and cellular level that can alter cardiovascular function and ultimately lead to disease. The baboon is an ideal model for studying ageing due to the similarities in genetic, anatomical, physiological and biochemical characteristics with humans. The aim of this cross-sectional study was to investigate the changes in cardiovascular profile of baboons over the course of their lifespan. Methods: Data were collected from 109 healthy baboons (Papio hamadryas) at the Australian National Baboon Colony. A linear regression model, adjusting for sex, was used to analyse the association between age and markers of ageing with P < 0.01 considered significant. Results: Male (n = 49, 1.5-28.5 years) and female (n = 60, 1.8-24.6 years) baboons were included in the study. Age was significantly correlated with systolic (R2 = 0.23, P < 0.001) and diastolic blood pressure (R2 = 0.44, P < 0.001), with blood pressure increasing with age. Age was also highly correlated with core augmentation index (R2 = 0.17, P < 0.001) and core pulse pressure (R2 = 0.30, P < 0.001). Creatinine and urea were significantly higher in older animals compared to young animals (P < 0.001 for both). Older animals (>12 years) had significantly shorter telomeres when compared to younger (<3 years) baboons (P = 0.001). Conclusion: This study is the first to demonstrate that cardiovascular function alters with age in the baboon. This research identifies similarities within cardiovascular parameters between humans and baboon even though the length of life differs between the two species. 2016 Yeung et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Cao, Lei; Graham, Stuart L.; Pilowsky, Paul M.The role of vagal function in cardiovascular risk in older women remains unclear. Autonomic modulation following carbohydrate ingestion (CI) and postural stress (PS) were investigated in 14 healthy men and 21 age-matched postmenopausal women (age: 65.0 2.1 vs. 64.1 1.6 years), with normal and comparable insulin sensitivity. Continuous noninvasive finger arterial pressure and ECG were recorded in the lying and the standing positions before and after ingestion of a carbohydrate-rich meal (600 kcal, carbohydrate 78%, protein 13%, and fat 8%). Low-frequency (LF, 0.040.15 Hz) and high-frequency (HF, 0.15 0.4 Hz) components (ms2) of heart rate variability (HRV), low-frequency power (mmHg2) of systolic blood pressure variability (SBP LF power), and the sequence method for spontaneous baroreflex sensitivity (BRS, ms/mmHg) were used to quantify autonomic modulation. In response to CI and PS, mean arterial pressure maintained stable, and heart rate increased in women and men in the lying and standing positions. Following CI (60, 90, and 120 min postprandially) in the standing position, SBP LF power increased by 40% in men (P = 0.02), with unchanged HRV parameters; in contrast, in women, HRV HF power halved (P = 0.02), with unaltered SBP LF power. During PS before and after CI, similar magnitude of SBP LF power, HRV, and BRS changes was observed in men and women. In conclusion, CI induces sex-specific vascular sympathetic activation in healthy older men, and cardiac vagal inhibition in healthy older women; this CI-mediated efferent vagal inhibition may suggest differential cardiovascular risk factors in women, irrespective of insulin resistance, and impairment of autonomic control. 2016 the American Physiological Society.
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Freedman, Ben Ben[No abstract available]
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Shanmugalingam, Renuka; Reza Pour, Nina; Chuah, Siang Chye; Vo, Thi Mong; Beran, Roy G.; Hennessy, Annemarie; Makris, AngelaBackground: Arterial dissection is a rare complication of pregnancy and puerperium. There have been reports of aortic, coronary and cervical artery dissection in association with preeclampsia, however, vertebral artery dissection is rarely reported particularly in the antenatal setting in the presence of a Hypertensive Disorder of Pregnancy (HDP).The general annual incidence of symptomatic spontaneous cervicocephalic arterial dissection is 0.0026 % and a data registry reported that 2.4 % of these occurred in the post-partum period. The actual incidence of vertebral artery dissection in HDP is unknown as the current literature consists of case series and reports only with most documenting adverse outcomes. Given the presence of collateral circulation, unilateral vertebral artery dissections may go unrecognised and may be more common than suspected. Case presentation: We present a case series of four patients with vertebral artery dissection in association with HDP, two of which occurred in the antenatal setting and two in the post-partum setting. All our patients had favourable outcome with no maternal neurological deficit and live infants. Our discussion covers the proposed pathophysiology of vertebral artery dissection in HDP and the management of it. Conclusion: Our case series highlights the need to consider VAD an important differential diagnosis when assessing pregnant women with headache and neck pain particularly in the context of HDP. 2016 The Author(s).
