bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ameliorative potentials of Annona muricata against Potassium dichromate‐induced hypertension through antioxidant defence system
Authors: Ola‐Davies Olufunke Eunice , Oyagbemi Ademola Adetokunbo , Omobowale Temidayo Olutayo , Akande Isreal Adetokunbo 
Published: June 2021

Potassium dichromate is an environmental and industrial pollutant. It has already been reported that the accumulation of K2Cr2O7 can alter the activities of some enzymes involved in the free‐radical metabolism and also decrease the activities of some enzymes involved in the antioxidant defense system. This study investigated the antihypertensive effect of Annona muricata extract against K2Cr2O7 induced hypertension. Fifty rats were used for this study and were divided into ten rats per group. Rats in Group A received normal saline, Groups B (Annona muricata extract alone at 250 mg/kg, Group C K2Cr2O7 at 30 mg/kg, Groups D and E were pre‐treated with extract at 250 mg/kg and Gallic acid at 60 mg/kg for fourteen days respectively and thereafter administered with single intra‐peritoneal injection of K2Cr2O7 (30 mg/kg). Administration of K2Cr2O7 significantly increased systolic, diastolic and mean arterial pressure. Further, pre‐treatment with extract at 250 mg/kg and Gallic acid at 60 mg/kg significantly reduced high blood pressure to near normal. Also, K2Cr2O7 led to significant increase in hydrogen peroxide (H2O2) generated, malondialdehyde contents, protein carbonyl together with significant reductions in reduced glutathione (GSH), glutathione‐S‐transferase (GST), glutathione peroxidase (GPx) and superoxide dismutase (SOD). Serum nitric oxide (NO) also reduced significantly whereas serum advanced oxidative protein product (AOPP), myeloperoxidase (MPO) and xanthine oxidase (XO) significantly increased in K2Cr2O7 alone‐administered rats. Immunohistochemistry of renal Kidney injury molecule (Kim−1) and p38 MAPK showed increased expressions following administration of K2Cr2O7 together with down‐regulation of nuclear factor erythroid 2‐related factor 2 (nrf2). Pre‐treatment with extract at 250 mg/kg and Gallic acid at 60 mg/kg also increased the expressions of nrf2 and down‐regulated Kim−1 and p38. Together, pre‐treatment with extract at 250 mg/kg and Gallic acid at 60 mg/kg normalize blood pressure, reduced markers of oxidative stress, improved antioxidant defense system and serum NO bioavailabilityThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Increases of capillary blood pressure in the supine position in persons with cervical spinal cord injuries
Authors: Kouda Ken , Nakamura Takeshi , Umemoto Yasunori , Kamijo Yoshi‐ichiro , Tajima Fumihiro 
Published: June 2021

BackgroundCervical spinal cord injuries (CSCI) subjects have hypotension and most of physicians have believed that capillary pressure in CSCI would be decreased and easily formed pressure ulcers. Systemic blood pressure (BP) decreases are mainly caused by attenuated total peripheral resistance in CSCI. However, BP in capillary was not measured in CSCI. We hypothesized that the measurement of peripheral pressure such as arteriole pressure and capillary pressure could be a simple and efficient means of expecting to occur with lasting tissue damage for CSCI. The purpose of the present study was to investigate capillary BP in CSCI.MethodsEleven male CSCI individuals with a lesion between C6 and C7 (ASIA A, age, 32.5 +/− 2.8 y) and 13 healthy subjects (age, 40.1 +/− 3.5 y) participated in the present study. Measurements were performed in the supine position with the legs at heart level. To measure capillary BP, a pressure transducer with probe of Laser Tissue Blood Flowmeter was attached to the pretibial skin and the probe was gradually and continually compressed for five seconds until the output signal of the flowmetry showed constant values. When the output of the velocimeter showed constant values, the pressure of the probe compression should mean the Capillary BP. Because the termination of capillary blood flow demonstrated constant signals of velocimeter and at the time the compression pressure should be the capillary pressure. Simultaneously, systolic and diastolic BP was non‐invasively measured during the measurement on the contralateral arm of the blood flow measuring leg.ResultsA significant lower MBP was observed in CSCI (76.7 +/−3.9 mm Hg) than in healthy subjects (91.0 +/− 4.0 mm Hg). Capillary BP in CSCI (55.7 +/− 2.0 mm Hg) was significantly greater than in control subjects (45.9 +/− 2.3 mm Hg).ConclusionWe demonstrated here that transection of sympathetic nervous system from medulla to peripheral nerves in CSCI resulted in the increase of capillary pressure. We suggested that the cervical spinal transection diminished tonic impulses of sympathetic nerves to resistant vessels in CSCI.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effects of Phenylephrine and Norepinephrine on the Diameter of the Epineurial Vessels Supplying the Sciatic Nerve
Authors: Cleary Shane R. , Orr Julie I. , Killey Chelsa , Jackson Dwayne N. , Frisbee Jefferson C. , Twynstra Jasna 
Published: June 2021

BackgroundPhenylephrine (PE) and norepinephrine (NE) are known vasoconstrictors; however, little is known about their role in blood flow regulation at the sciatic nerve. The purpose of this study was to determine the effects of PE and NE on the epineurial vessels supplying the sciatic nerve.MethodsAdult male Sprague‐Dawley rats (323.1 ± 5.2 g) were anaesthetized using urethane, α‐chloralose, then were tracheotomized, catheterized, and had the sciatic nerve exposed. Alexa Fluor 488 Isolectin GS‐IB4 conjugate [178.6 μm/ml] was used to label the endothelial cells of the vessel wall allowing for visualization of the epineurial vessels using intravital video microscopy. PE (10−5 M) or NE (10−5 M) was topically applied to the sciatic region for 4 minutes, separately. Images were obtained at baseline, immediately prior to drug application, and every minute for 4 minutes during application. Data are expressed at the time point that maximum change in diameter occurred. Data are expressed as mean ± standard error.ResultsApplication of PE (n=11) resulted in a vasoconstriction (baseline: 22.0 ± 2.1 μm, PE: 19.3 ± 2.0 μm; P<0.05). Similarly, topical application of NE (n=8) induced a vasoconstriction (baseline: 31.2 ± 4.5 μm, NE: 26.5 ± 4.6 μm; P<0.05). Mean arteriolar pressure was unaffected during either PE (baseline: 99.1 ± 5.6 mmHg, PE: 97.4 ± 5.4 mmHg) or NE (baseline: 104.0 ± 4.5 mmHg, NE: 107.3 ± 7.7 mmHg) application.ConclusionBoth PE and NE caused vasoconstriction at the sciatic nerve, which is consistent with previous studies in other tissues observing vasoconstriction through activation of α‐1 adrenergic receptors. As PE and NE are both α‐1 receptor agonists, these findings suggest that α‐1 receptors may be involved in blood flow regulation at the peripheral nerves.Support or Funding InformationThis study was supported by the SEED Research Grant from The University of Western Ontario.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effect of aging on Rho‐kinase activity and vascular smooth muscle contractility in skeletal muscle resistance arteries
Authors: Shin Song Yi , Padgham Samuel , Trache Andreea , Woodman Christopher 
Published: June 2021

IntroductionVasoconstrictor responses decline with age in resistance arteries. The mechanism for the decrement in constrictor function is not fully understood but has been proposed to involve signaling through the RhoA pathway.ObjectiveWe tested whether aging affects Rho kinase (ROCK) activity in aged resistance arteries.MethodsSoleus feed arteries (SFA) were isolated from young (4 mo) and old (24 mo) male Fischer 344 rats. Smooth muscle cells isolated from one group of SFA were lysed and ELISA assay was used for assessment of both ROCK isoforms, total ROCK 1 and 2, and their activity, phospho ROCK 1 and 2. A separate group of young and old SFA was cannulated with glass micropipettes for assessment of vasoconstrictor function. To isolate the role of smooth muscle in constrictor responses, endothelial cells were removed from cannulated arteries (denuded) by passing 5 ml of air through the lumen of the artery. Vasoconstrictor responses were assessed using increasing whole log doses of norepinephrine (NE; 10−9–10−4 M), angiotensin II (Ang II; 10−11–10−7 M), and phenylephrine (PE; 10−9–10−4 M).ResultsTotal ROCK 1 and ROCK 2 was similar in cells isolated from young and old SFA, whereas phospho‐ROCK 1 and phospho‐ROCK 2 were higher in cells isolated from old SFA relative to young arteries. Constrictor responses of denuded SFA to PE and Ang II were significantly impaired in old SFA relative to young SFA whereas constrictor responses to NE were preserved. In addition, presence of a ROCK inhibitor, Y 27632, reduced further the constrictor response to agonists.ConclusionThe results of this study indicate that smooth muscle contractile function declines with age in SFA. Contractility regulation involves the ROCK pathway, but upregulation of ROCK activity in old arteries is not able to rescue the reduced contractility state in aging.Support or Funding InformationAHA grant 0765043Y, AHA grant 4150031, and Sydney and J.L. Huffines Institute of Sports Medicine and Human Performance.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Thrombin Cleavage of Endothelial Glycocalyx Syndecan‐4 Ectodomain in Human Lung Vasculature
Authors: Jannaway Melanie , Yang Xiaoyuan (Sherry) , Meegan Jamie E. , Ospina Santiago Rodriguez , Coleman Danielle C. , Yuan Sarah Y. 
Published: June 2021

The endothelial glycocalyx (eGCX) is a protective barrier on the luminal surface of endothelial cells. The syndecan family of proteoglycans constitute integral components of the eGCX and can act as receptors for many cell signaling pathways. Under inflammatory conditions, the eGCX can be cleaved and shed by proteases such as matrix metalloproteinases and thrombin. We analyzed the ability of thrombin to cleave syndecan core proteins from the eGCX of microvessels in human lung samples using transmission electron microscopy (TEM) and immunogold staining for syndecan‐4 ectodomain (SDC4ecto). The concentration of SDC4ecto in supernatant from human lung slices treated with thrombin was assessed via enzyme‐linked immunosorbent assay and western blotting. The effect of thrombin‐cleaved recombinant SDC4ecto fragments on endothelial barrier resistance was investigated using electric cell‐substrate impedance sensing assay. TEM immunogold staining of human lung demonstrated decreased expression of SDC4ecto within the eGCX following thrombin treatment. Similarly, the concentration of SDC4ecto in human lung slice supernatant was reduced following thrombin treatment, consistent with western blot analysis showing thrombin‐induced cleavage of both recombinant and endogenous full‐length SDC4ecto. In human umbilical vein endothelial cell monolayers, recombinant SDC4ecto treated with thrombin generated a significant decrease in barrier resistance, and this effect was sensitive to a pharmacological inhibitor of Rho kinase, suggesting the involvement of the RhoA pathway in SDC4ecto signaling. In conclusion, these findings suggest that thrombin causes endothelial barrier injury by cleaving SDC4ecto from the eGCX in human lung vessels. Furthermore, an autocrine mechanism may exist whereby thrombin‐cleaved SDC4ecto can act as a signaling molecule to promote endothelial hyperpermeability.Support or Funding InformationNIH Grant HL070752 & GM097270This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Evidence for modulation of heat induced changes in erythrocytes by cytochalasin D: potential role for oxygen nanobubbles in aggregation
Authors: Weber‐Fishkin Samantha D. , Blasco Joey F. , Gallegos Eva M. , Frame Mary D. 
Published: June 2021

Thermal burn injury is associated with an increase in erythrocyte (RBC) aggregation (rouleaux) prior to fibrin clot formation; unresolved rouleaux occlude vessels and contribute to thermal burn injury progression (Clark, 2013). RBC aggregation is reversible, yet the mechanism is unknown. Current models do not include all biophysical phenomena, including the role of the cytoskeleton, and sudden oxygen release from hemoglobin. We previously proposed that thermally induced membrane deformation creates nucleation sites for excess oxygen to coalesce, i.e., form nanobubbles, which may contribute to surface tension induced aggregation. To begin to address the role of the cytoskeleton in membrane deformation through changes in the band 3‐ankyrin/adducin bridge and spectrin‐actin interactions, we have disrupted actin polymerization with cytochalasin D (cytoD). We hypothesized that disrupting the cytoskeleton would alter the apparent presence of oxygen nanobubbles on singlet RBCs. Our experimental model examines both size and greyscale appearance of RBCs with sudden changes in temperature. Temperatures of 41–49 C cause shifts in brighter greyscale and larger apparent RBC size, consistent with light diffraction through concentrated gas bubbles that dissipates with time or return to 37 C (Blasco, 2017). Washed murine RBCs (obtained through a tissue sharing program) were suspended in saline (PBS) containing 1% EtOH, 0.5 uM CytoD (in 0.1% EtOH) or control, and incubated at 37°C prior to use. RBCs settled to a monolayer within an enclosed microchannel at 37°C (heated stage). The stage temperature rapidly heated from 37°C to test temperature (37, 39, 41, 43, 45, 47, or 49°C) and we imaged at 2 Hz for 70 seconds (60X, SWI). Singlet RBCs were followed over time, measuring greyscale and apparent size of the cell (outer rim) and core (central biconcave) (ImageJ). The initial changes were seen during the temperature shift and included increased core greyscale and apparent size of 20–40% between 41–47°C, with corresponding changes in cell size. Over the next several seconds there was temperature dependent fluctuations in size and greyscale of up to 50%. Cells in EtOH were similar overall to controls. CytoD prevented changes in greyscale and in size, and suppressed further fluctuations until higher temperatures where those treated cells had formed echinocytes. The data are consistent with gas bubbles forming at the RBC membrane, causing diffraction of the light, in a temperature dependent fashion. As destabilization of the cytoskeleton prevented these changes, we conclude that the cytoskeleton contributes to membrane shape change necessary for oxygen nanobubble formation with heat.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
IGF‐1 deficiency promotes pathological remodeling of cerebral arteries: a potential mechanism contributing to the pathogenesis of intracerebral hemorrhages in aging
Authors: Fulop Gabor A. , Ramirez‐Perez Francisco I. , Kiss Tamas , Tarantini Stefano , Toth Peter , Yabluchanskiy Andriy , Conley Shannon M. , Ballabh Praveen , Martinez‐Lemus Luis A. , Ungvari Zoltan , Csiszar Anna 
Published: June 2021

Clinical and experimental studies show that age‐related decline in circulating IGF‐1 levels promotes the pathogenesis of intracerebral hemorrhages, which critically contribute to the development of vascular cognitive impairment and disability in older adults. Yet, the mechanisms by which IGF‐1 deficiency compromises structural integrity of the cerebral vasculature are not completely understood. To determine the role of IGF‐1 deficiency in pathological remodeling of middle cerebral arteries (MCAs), we compared alterations in vascular mechanics, morphology and remodeling‐related gene expression profile in mice with liver‐specific knockdown of IGF‐1 (Igf1f/f + TBG‐Cre‐AAV8) and control mice with or without hypertension induced by angiotensin‐II treatment. We found that IGF‐1 deficiency resulted in thinning of the media and decreased wall‐to‐lumen ratio in MCAs. MCAs of control mice exhibited structural adaptation to hypertension, manifested as a significant increase in wall thickness, vascular smooth muscle cell hypertrophy, decreased internal diameter and up‐regulation of extracellular matrix (ECM)‐related genes. IGF‐1 deficiency impaired hypertension‐induced adaptive media hypertrophy and dysregulated extracellular matrix remodeling, decreasing elastin content and attenuating adaptive changes in ECM‐related gene expression. Thus, circulating IGF‐1 plays a critical role in maintenance of the structural integrity of cerebral arteries. Alterations of VSMC phenotype and pathological remodeling of the arterial wall associated with age‐related IGF‐1 deficiency have important translational relevance for the pathogenesis of ICHs and vascular cognitive impairment in elderly hypertensive patients.Support or Funding InformationThis work was supported by grants from the American Heart Association, the National Center for Complementary and Alternative Medicine, and the National Institute on AgingThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Selective Brain Cooling with Transnasal Flow of Ambient Air for Pediatric Resuscitation
Authors: Koehler Raymond C. , Reyes Michael , Armstrong Jillian S. , Hopkins C Danielle , Kulikowicz Ewa , Tandri Harikrishna 
Published: June 2021

Discharge rates and neurologic outcome from out‐of‐hospital pediatric cardiac arrest remains poor. The recent THAPCA trial for out‐of‐hospital pediatric cardiac arrest reported only a small, non‐significant favorable outcome with hypothermic treatment. A major limitation of this study was the median 5.9‐hour delay in inducing hypothermia, as studies in animals show loss of efficacy with this delay in initiation of hypothermia. To minimize this delay, we developed a simple yet innovative technique of transnasal cooling. Air at ambient temperature is passed through standard nasal cannula and out of the mouth to produce evaporative cooling of the nasal passages and a countercurrent heat exchange with cephalic arterial blood. We determined whether an age‐dependent effect exists in the ability to cool the brain because of potential differences in air humidification capacity during development. We studied piglets at 2–5 days of age (1.8 kg; 40 g brain weight), 2 weeks of age (4 kg; 45 g brain weight) and 6 weeks of age (16 kg; 75 g brain weight; adult brain = 110 g). The corresponding nasal turbinate surface area was estimated to be 3176±243, 4847±417, and 8651±1234 mm2. In anesthetized 1.8‐kg piglets with mechanical ventilation and an open mouth to permit airflow exit, institution of nasal airflow of 4 L/min through nasal cannula decreased brain temperature from 38.0±0.4°C to 36.4±0.9, 35.6±1.2, and 34.4±1.7°C at 30, 60, and 120 min, respectively. In 4‐kg piglets, nasal airflow of 32 L/min decreased brain temperature from 38.3±0.3°C to 35.0±0.6, 33.8±0.6, and 31.9±0.6°C at 30, 60, and 120 min, respectively. In 16‐kg piglets, nasal airflow of 32 L/min decreased brain temperature from 38.5±0.4°C to 35.1±1.6, 34.1±1.8, and 32.9±1.6°C at 30, 60, and 120 min, respectively. No further benefit was seen by increasing airflow to 48 L/min. No substantial spatial temperature gradients were seen among the sensory cortex, putamen, thalamus, cerebellum and olfactory bulb in any age group, suggesting that heat transfer is via blood convection rather than direct conduction from the airway wall. Decreases in rectal temperature lagged brain temperature by 30–60 min at all three ages. The rapid and selective brain cooling indicates that a high humidifying capacity of the nasal turbinates is present early in life. Because of its simplicity, portability, and low cost, transnasal cooling potentially could be deployed in the field by emergency medical technicians, in both community hospital emergency rooms, and in low resource areas for early initiation of brain cooling prior to maintenance with standard surface cooling after pediatric cardiac arrest.Support or Funding InformationSupported by NIH NS095036This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Single Session Mindfulness Meditation Reduces Aortic Pulsatile Load and Anxiety in Mild to Moderately Anxious Adults
Authors: Durocher John J. , Marti Hannah , Morin Brigitte , Wakeham Travis R. 
Published: June 2021

Mindfulness meditation has been shown to have numerous health benefits when used over the course of days or weeks, but the effect of a single session on aortic pulsatility and anxiety is unclear. Therefore we sought to determine if a single session of mindfulness meditation could effectively reduce aortic pulsatile load and anxiety. Fourteen adults (24±8 years) with mild to moderate anxiety (≥8 Beck Anxiety Inventory (BAI)) participated in a 60 minute guided mindfulness meditation session. Baseline aortic pulsatile load (aortic pulse pressure × heart rate) and BAI were assessed approximately one week prior to the mindfulness meditation session during a study orientation. Aortic pulsatile load was assessed before, immediately after, and 60 minutes after the mindfulness meditation session. Anxiety was also assessed 60 minutes following meditation. The single mindfulness session reduced aortic pulsatile load from 2008±108 to 1730±85 a.u. immediately after meditation (p<0.01). The reduction in aortic pulsatile load was maintained 60 minutes post‐meditation (1729±99 a.u.; p<0.02). The BAI score was also significantly reduced 60 minutes post‐meditation compared to baseline (15±1 vs. 11±2; p<0.02). Our findings demonstrate that even a single session of mindfulness meditation can have cardiovascular and psychological benefits for adults with mild to moderate anxiety. Reductions in pulsatile load may help to reduce damage to end organs such as the brain and kidneys, while reduced anxiety could help to prevent vascular dysfunction.Support or Funding InformationSupported by the Portage Health Foundation.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.