bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effects of Resistance Exercise on Intracranial Pressure
Authors: Fischman Jessica Jayne , Cowen Robin , Petersen Lonnie , Healey Robert , Hargens Alan 
Published: June 2021

IntroductionOne of the primary health concerns faced by NASA astronauts on board the International Space Station is a decline in visual acuity. It is believed that increases in intracranial pressure (ICP) due to resistive exercise performed on the station's Advanced Resistive Exercise Device (ARED) may contribute to Spaceflight Associated Neuro‐Ocular Syndrome (SANS), also referred to as the Visual Impairment and Intracranial Pressure (VIIP) syndrome. In a manner similar to low level Valsalva exertion, it is hypothesized that ICP would increase during low level resistance exercise.MethodsSix healthy subjects (4 male, 2 female, age: 27 ± 10 years, weight: 77 ± 15 kg) were recruited to perform low‐level resistance exercises in both the seated and supine positions. A Cerebral Cochlear Fluid Pressure analyzer (CCFP) was used to noninvasively measure ICP by assessing tympanic membrane displacement (Vm) in the inner ear following an auditory stimulus. Increased values of Vm correspond to a decrease in ICP. After a 10‐minute acclimation period, a baseline measurement was taken with the subject at rest in the seated position. ICP was then measured during randomized, isometric, overhead shoulder holds with weights of 0lbs, 2lbs, and 5lbs (per hand). This procedure was then repeated in the supine position. ICP was also measured in the 15‐degree head down tilt (HDT) position following a 10‐minute acclimation period. Significant differences between groups were determined at p<0.05 using a Student's T‐test.ResultsThe relative changes in Vm with increased loading by position are shown in Figure 1. Vm decreased by 40% ± 15% (p=0.001) in the HDT position as compared to the supine baseline, showing a predicted, reliable increase in ICP for positional changes. In the seated position, displacement increased slightly from baseline (12% ± 63%, p=0.412) for all subjects across all weight levels, indicating a statistically nonsignificant decrease in ICP. Measurements in the supine position were more consistent, with decreasing Vm (3% ± 3%, p=0.563) for all subjects across all weight levels, indicating a nonsignificant increase in ICP.DiscussionContrary to our hypothesis, measured data showed no significant change in ICP during low level resistance exercise in either the seated or supine positions. Based on these results, resistance exercise may not be the primary contributing factor to the development of SANS in astronauts. This study will form the basis of future investigation into the effects of exercise and ICP in different such as gender, age, and clinical populations. Sensitivity of the CCFP to motion and pulse artifacts will also be addressed to reduce variability between subjects.Support or Funding InformationSupported by NASA grant NNX13AJ12GThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Individual Differences in Response to Cold‐Pressor Test: Are the Corresponding Blood Pressure, Sympathetic, and Pain Perception Responses Associated to a Family Risk of Hypertension?
Authors: Huang Mu , Yoo Jeung‐Ki , Stickford Abigail S.L. , Hendrix Joseph M. , Moore Jonathon P. , Crandall Craig G. , Fu Qi 
Published: June 2021

There is a considerable amount of inter‐individual variability in the perception of pain to a given stimulus. Given that pain, and its management, is a major public health problem, expanding an understanding of the underlying causes of these individual differences is important. Recent studies have demonstrated divergent muscle sympathetic nerve activity (MSNA) responses to physical and mental stressors. Perhaps there is similar variability in the sympathetic responses related to the perception of pain. Therefore, the purpose of this investigation was to test the hypothesis that during a cold‐pressor stimulus in healthy individuals, the sympathetic neural responses correspond with perceived levels of pain. Heart rate (HR), blood pressure (BP), and MSNA were measured at baseline and during a 2‐minute cold‐pressor test (CPT) with subjects in the supine position. Immediately following the CPT, pain was rated on a numeric scale (range 0–10), with two groups being established: subjects who rated their pain ≥7 (HP: high pain, n=10) and those that rated their pain ≤6 (LP: low pain, n=8). The HP group (age: 37±12, 5 females) exhibited greater increases in MSNA during the first 30 seconds (HP: 9±8 vs. LP: −1±3 bursts/min change from baseline, P=0.04) and peak MSNA responses (HP: 25±11 vs. LP: 10±6 bursts/min change from baseline, P=0.0009) compared to the LP group (age: 31±6, 5 females). Likewise, peak changes in mean BP (HP: 16±7 vs. LP: 9±7 mmHg, P=0.02) were greater in the HP group. HR responses were similar between the two groups. Interestingly, a greater proportion of the LP group reported a parental history of hypertension (HP: 20% vs. LP: 87.5%, x2: P=0.007). In summary, sympathetic neural and BP responses to an acute painful stimulus correspond to the magnitude of pain perception in healthy humans. Moreover, this data provides additional intrique to better understand the associative model between a family risk of hypertension and hypoalgesia.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Muscle Metaboreflex Control of Left Ventricular Filling Pressure
Authors: Senador Danielle , Gross Matthew , McNitt Megan , Kaur Jasdeep , Coutsos Matthew , Krishnan Abhinav C. , Mannozzi Joseph T. , Aung Kimberly , Alvarez Alberto , Hanna Hanna W. , Lovelace Abe T. , Levanovich Peter , Dombrowski Maryetta , Lessanework Beruk , O'Leary Donal S. 
Published: June 2021

When oxygen delivery to active skeletal muscle is limited, afferent signals from the muscle elicit reflex increases in cardiac output (CO) and mean arterial pressure (MAP) in order to increase perfusion to the ischemic muscle ‐ termed the muscle metaboreflex (MMR). Previous studies have shown that in normal subjects, CO is increased predominantly through increases in heart rate (HR) while maintaining stroke volume (SV) essentially constant. However, increases in HR alone have limited ability to raise CO because as HR increases, SV falls due to decreased filling time. Increases in ventricular contractility can limit the falls in SV, however with sustained increases in CO, blood is translocated from the venous to the arterial circulation and ventricular filling pressure falls which limits the ability to maintain elevated CO. To sustain increases in CO, central blood volume mobilization must also occur to maintain ventricular filling pressure. We previously showed that MMR activation does increase central venous pressure (Sheriff, Augustyniak and O'Leary, Am. J. Physiol., 1998), but whether this translates into increases in left ventricular end‐diastolic pressure (LVEDP) is unknown. MMR was activated via reductions in hindlimb blood flow during mild treadmill exercise in chronically instrumented canines before and after induction of heart failure (HF, rapid ventricular pacing, 220–240 bpm, ~30 days). In normal animals, MMR activation induced a rise in LVEDP from 14.4 ± 1.8 to 18.2 ± 1.8 mmHg (p<0.05) despite substantial increases in HR (Δ 26 ± 4 bpm), CO (Δ 1.45 ± 0.16 l/min) and MAP (Δ 42.3 ± 2.6 mmHg). After induction of HF, MMA activation increased LVEDP from 28.6 ± 2.5 to 38.7 ± 2.6 mmHg (p<0.05) which was a significantly larger rise than observed in normal animals. In HF, the attenuated rise in CO (Δ 0.20 ± 0.08 l/min) with MMR activation likely contributes to the exaggerated increase in LVEDP. We conclude that MMR activation elicits significant blood volume mobilization which increases cardiac filling pressure which thereby likely helps sustain SV despite shortened filling time. In HF, the limited ability to raise CO is not due to reduced filling pressures.Support or Funding InformationNIH RO1 Grants HL055473 and HL126706This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Intrarenal High Salt Administration Causes Tonic Inhibition of Renal Sympathetic Nerve Activity (RSNA)
Authors: Hindermann Martin , Rodionova Kristina , Dietz Amelie , Ditting Tilmann , Ott Christian , Schmieder Roland , Amann Kerstin , Veelken Roland 
Published: June 2021

Afferent renal nerve fibers from the kidney likely counterregulate salt sensitive blood pressure increases by decreasing renal sympathetic nerve activity. We recently reported on a long‐lasting tonic sympatho‐inhibition due to intrarenal afferent renal nerve stimulation eliciting a TRPV1 dependent neuro‐humoral pathway. We wanted to test the hypothesis that sodium influences this afferent sympatho‐depressory mechanism.Groups of anesthetized SD rats (n=8) were equipped with femoral catheters (blood pressure (BP) & heart rate (HR) recording, drug application), a renal arterial catheter for intrarenal administration (IRA) of high salt (10 % NaCl, 10 μl) or Capsaicin (CAP 3.3, 6.6, 10, 33*10–7 M, 10 μl) and a bipolar electrode for RSNA recordings; eventually an intravenous (iv) bolus of the NK1‐receptor blocker RP67580 (10*10–3M, 15 μl) was given. Cultured dorsal root ganglion neurons (Th11‐L2) of rats with renal afferents were investigated in current clamp mode to assess action potential generation or in voltage clamp mode to investigate inward currents during 10 sec exposure to 4.5 % NaCl or equi‐osmotic 20% mannitol. Results are given in mean±SEM.IRA high salt and IRA CAP decreased RSNA from baseline 4.1±0.6 μV*sec to 2.2±0.8 μV*sec (10% NaCl, p<0.05) and 3.9±0.5 μV*sec to 0.9±0.2 μV*sec (CAP, p<0.01). Suppressed RSNA in high salt groups and CAP could be unmasked by systemic (i.v.) administration of the NK1‐blocker (2.7±1.8 μV*sec to 5.8±2.2 μV*sec; p<0.05 (10% NaCl); 1.0±0.2 μV*sec to 6.1±1.5 μV*sec; p<0.01 (CAP)). Cultured renal neurons exhibited production of action potentials (3.5±0.8*, from baseline, p<0.05) and increased sustained inward currents from baseline during exposure to NaCl 4.5 % (−10708.8±3546.5 pA*, from baseline, p<0.05). No responses to mannitol 20%.Increased intrarenal sodium concentrations might induce long‐lasting sympatho‐depression via a neuro‐humoral TRPV1 dependent and tachykinin mediated afferent nerve pathway from the kidney. Impairment of this sympatho‐depressory mechanism could be involved in salt sensitive hypertension.Support or Funding InformationDFG Deutsche Forschungsgemeinschaft VE 104/4‐1This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hypertonic saline infusion affects glycemic responses following glucose load in healthy men
Authors: Jansen Lisa Tjorven , Suh Hyun‐Gyu , Sprong Cameron , Adams J.D. , Butts Cory , Seal Adam , Scott Dylan , Melander Olle , Lemetais Guillaime , Dolci Alberto , Vanhaecke Tiphaine , Perrier Erica , Kirkland Tracie , Kavouras Stavros 
Published: June 2021

Low water intake and plasma hypertonicity have been independently associated with hyperglycemia and incidence of diabetes mellitus in epidemiological studies. Recent data also suggest that reducing water intake deteriorates glucose regulation in patients with type 2 diabetes. To date, it is unclear whether plasma hypertonicity would also impact glycemic control in subjects with normal glycemic and insulinemic function.OBJECTIVETo assess the effect of hypertonic saline infusion on glycemic responses to an oral glucose tolerance test (OGTT) in healthy adult men.METHODS30 healthy, non‐smoking adult men (36.6±7.0 y, 83.9±12.8 kg, body mass index 27.0±3.4 kg·m−2, HbA1c 5.2±0.3%, HOMA‐IR 1.59±0.97) were recruited for this study. Each subject underwent two experimental trials, consisting of a 2‐h intravenous infusion of saline (ISO: 0.9% NaCl and HYPER: 3.0% NaCl) at an infusion rate of 0.1 ml·kg·min−1, followed by a 4‐h oral OGTT. Blood samples were taken at 30 min intervals throughout the infusion period and during the OGTT. Plasma osmolality (POsm), glucose (Glu), angiotensin II (AngII), renin, and aldosterone (Ald) were measured and plasma volume (PV) was calculated using hematocrit and hemoglobin based on the Dill & Costill equation.RESULTSPOsm at baseline was similar between conditions (287±3 and 286±3 mmol·kg−1 in HYPER and ISO, respectively). Following the 2‐h infusion, POsm was significantly higher in the HYPER condition than the ISO condition (305‐±3 vs. 288±3 mmol·kg−1; P < 0.0001), with greater PV expansion (20.1±6.9 vs. 10.9±3.2%, P < 0.0001). In the HYPER condition, POsm remained above baseline throughout the OGTT (296±3 mmol·kg−1 at OGTT4‐h; P < 0.0001). During the OGTT, Glu in the HYPER trial was higher than in the ISO trial at 60 min (HYPER: 157±24; ISO: 145±29 mg·dL−1; P < 0.018) and 90 min (HYPER: 139±33; ISO 128±29 mg·dL−1; P < 0.038). The renin‐angiotensin‐aldosterone system was suppressed as indicated by decreased plasma values of AngII, renin, and Ald, probably due to PV expansion in both trials.CONCLUSIONPlasma hypertonicity induced by hypertonic saline infusion unfavorably affected glycemic response to an OGTT in healthy adult men.Support or Funding InformationThis research was supported by Danone ResearchThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Neurons in the Organum Vasculosum of the Lamina Terminalis Sense Both Angiotensin II and NaCl to Regulate Thirst
Authors: Kinsman Brian J. , Browning Kirsteen N. , Stocker Sean D. 
Published: June 2021

Angiotensin II (AngII) and NaCl are sensed by hypothalamic circumventricular organs to subsequently regulate body fluid homeostasis and blood pressure. AngII predominantly acts within the subfornical organ (SFO), whereas NaCl is sensed by neurons in the organum vasculosum of the lamina terminalis (OVLT). However, OVLT neurons also abundantly express AngII‐type I receptors. Therefore, we performed a series of in vitro and in vivo experiments in adult male Sprague‐Dawley rats to determine whether OVLT neurons sense both AngII and NaCl to impact body fluid homeostasis. First, in vitro whole‐cell recordings were performed on OVLT neurons in the presence of kynurenic acid (1mM) and bicuculline (20μM) to assess discharge responses to +7.5 mM NaCl (3 min) versus 100pM AngII (90s) in a randomized order. The majority of OVLT neurons (66%, 23/35) demonstrated an increase in discharge frequency to both AngII (1.31±0.25Hz to 2.19±0.31Hz; p<0.001) and hypertonic NaCl (1.11±0.18Hz to 2.16±0.27 Hz; p<0.001). Smaller proportions of OVLT neurons were either excited by NaCl alone (3/35), AngII alone (4/35), neither stimulus (3/35), or were inhibited by NaCl (2/35). In a second set of experiments, in vivo single‐unit recordings of OVLT neurons were performed to assess discharge responses to intracarotid injection (50uL over 15 s) of hypertonic NaCl (0.5M NaCl) or AngII (200ng). Half of OVLT neurons (50%, 6/12) displayed an increase in discharge to intracarotid injection of AngII (3.2±0.7 to 9.2±1.9 Hz, P<0.01) and 0.5M NaCl (3.6±0.6 to 9.0±1.6 Hz, P<0.01). The remainder of OVLT neurons showed an increase in discharge to hypertonic NaCl only (n=1) or AngII only (5/12). In a final set of experiments, we employed an optogenetic approach to determine the extent by which inhibition of OVLT neurons would attenuate thirst stimulated by NaCl versus AngII. rAAV2‐CamKII‐eNPHR3.0‐mCherry (5×1012 particles/mL, 50nL) was injected into the OVLT, and an optical ferrule (200um OD) was implanted 300um dorsal to the injection site. Approximately 4 weeks later, optogenetic inhibition of OVLT neurons (561nm, 10mW) significantly reduced water intake in response to intravenous infusion (1.25 mL per 30 min) of 2M NaCl (control: 5.1±0.9 mL vs laser: 1.6±0.9 mL; n=4, P<0.01). In addition, optogenetic inhibition of OVLT neurons also attenuated hypotension‐induced thirst produced by intravenous injection of 25 mg/kg diazoxide (control: 4.5±0.8 mL vs laser: 1.3±0.7 mL; n=4, P<0.01). These findings suggest that individual OVLT neurons can sense both NaCl and AngII to functionally regulate thirst to both stimuli.Support or Funding InformationNIH R01 HL113270 and AHA Established Investigator AwardThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Role of the Superior Cervical Ganglion in Response to Hypoxia in Juvenile Rats
Authors: Coffee Gregory A. , Getsy Paulina M. , Lewis Stephen J. 
Published: June 2021

The superior cervical ganglion (SCG) sends sympathetic input to the carotid body (CB) via the ganglioglomerular nerve (GGN) in order to modulate carotid sinus nerve (CSN) chemosensory afferent discharge via controlling vascular tone. This chemoafferent discharge is then relayed to the nucleus tractus solitarius (NTS) where the information is processed resulting in a compensatory increase in respiration. Hypoxic gas challenge stimulates the GGN. However, little is known as to the effects of superior cervical ganglionecomy (SCGx) on carotid body chemosensory afferent response to hypoxia (HX).Our objective was to determine the effect of unilateral SCGx on the ventilatory responses elicited by HX (10% O2, 90% N2) gas challenge (5 episodes of 5 min in duration separated by 15 min) in freely‐moving juvenile (P25) Sprague‐Dawley rats.Male rats postnatal (P) 21 were subjected to sham or unilateral (right) SCGx and were allowed 4 days to recover. On the day of the experiment, P25 rats were placed in whole‐body plethysmography chambers and subjected to the hypoxic gas exposure. Ventilatory parameters included frequency of breathing, tidal volume, minute ventilation (= frequency x tidal volume), inspiratory and expiatory times, end inspiratory and expiratory pauses, peak inspiratory and expiratory flows, EF50 (expiratory flow at 50% expired tidal volume) and central inspiratory drive (tidal volume/inspiratory time).The HX challenge elicited robust ventilatory responses in sham‐operated rats compared to unilateral (right) SCGx. Frequency (breathes/min), minute ventilation (ml/min), peak inspiratory flow (msec), and peak expiratory flow (msec) were diminished in unilateral (right) SCGx rats compared to sham. End expiratory pause (msec) showed a faster return to baseline following hypoxic challenge in unilateral (right) SCGx compared to sham. These findings demonstrate a role for CB sympathetic input from the SCG in modulating the ventilatory response to hypoxia.Support or Funding InformationNIH‐SPARC 1OT2OD023860‐02 SJLewisThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Superior Cervical Ganglionectomy alters Glomus Cell Potassium‐Channel Properties in Response to Hypoxia
Authors: Getsy Paulina M. , Coffee Gregory A. , Lewis Stephen J. 
Published: June 2021

The carotid body (CB) chemosensory glomus (type I) cells respond to changes in blood PO2, PCO2, and pH by releasing neurotransmitters that increase action potential discharge of chemosensory afferent fibers within the carotid sinus nerve (CSN). The CSN then signals to the nucleus tractus solitarius (NTS) within the dorsal brainstem, which leads to a compensatory increase in ventilation in order to restore blood gas levels and pH. Along with the CSN, the ganglioglomerular nerve (GGN) also innervates the carotid body. The GGN consists of post‐ganglionic sympathetic fibers, which originate from the superior cervical ganglion (SCG). Stimulation of the GGN causes an increase in CB chemosensory afferent discharge. However, it is unknown whether loss of sympathetic input to the CB directly alters the chemosensitivity of glomus cells. Our objective was to characterize electrophysiological properties of CB glomus cell potassium (K+) channels in response to acute hypoxia following superior cervical ganglionectomy (SCGx). Sprague Dawley (SD) male rats postnatal (P) 21 were subjected to unilateral (right) SCGx. The left SCG was identified, but not removed. Four days post surgery at P25 the right and left carotid bodies were removed, and primary glomus cells were isolated and plated on coverslips. Glomus cell K+ channel properties were then recorded using the whole‐cell perforated patch‐clamp technique. Our preliminary results reveal that following unilateral (right) SCGx, glomus cells respond to hypoxia with significant reductions (P<0.05 to P<0.01) in outward K+ current amplitudes over the test potential range +10 to +60 mV. The mean maximal effect, a reduction in K+ amplitude of 64.9 ± 18.5% (mean ± SD, n = 3 cells), occurred at a Vtest of +30 mV. In contrast, wild‐type control CB glomus cells respond to hypoxia with a significant reduction (P<0.05) in outward K+ current amplitude at only a Vtest of +60 mV (n = 4 cells). In addition, glomus cells from SCGx rats appear to respond to hypoxia via a different population of K+ channels that do not appear to be presently active in wild‐type glomus cells when exposed to hypoxia. These findings demonstrate that loss of sympathetic input from the SCG increases CB glomus cell sensitivity to hypoxia, and modulates the O2‐sensing capabilities of glomus cell K+ channels.Support or Funding InformationNIH‐SPARC 1OT2OD023860‐02 SJLewisThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.