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At least 307 records · Page 17
All sourcesNASA NTRSDOE OSTI
DOE OSTI2022

Influence of Cryomilling on Crystallite Size of Aluminum Powder and Spark Plasma Sintered Component

The present investigation aims to develop nanocrystalline (NC) pure aluminum powders using cryomilling technique and manufacture bulk components using spark plasma sintering (SPS). The cryomilling was performed on pure Al powders for 2, 6, and 8 h. The cryomilled powders were then consolidated using SPS to produce bulk components. The particle morphology and crystallite size of the powders and the bulk SPS components were analyzed using scanning electron microscopy (SEM), X-ray diffraction (XRD), and transmission electron microscopy (TEM). The results showed that the crystallite size of pure Al powders decreases with increased cryomilling time. The results also showed that the SPS at elevated temperatures resulted in a slight increase in crystallite size, however, the changes were insignificant. The mechanical properties of the bulk components were determined using a Vickers microhardness tester. The hardness of the cryomilled SPS component was determined to be three times higher than that of the unmilled SPS component. The mechanism for the reduction in crystallite size with increasing cryomilling time is discussed. This fundamental study provides an insight into the development of bulk nanomaterials with superior mechanical properties for automotive, aerospace, marine, and nuclear applications.

36 MATERIALS SCIENCE↗
DOE OSTI2020

Enhanced Corneal Penetration of a Poorly Permeable Drug Using Bioadhesive Multiple Microemulsion Technology

Corneal penetration is a key rate limiting step in the bioavailability of topical ophthalmic formulations that incorporate poorly permeable drugs. Recent advances have greatly aided the ocular delivery of such drugs using colloidal drug delivery systems. Ribavirin, a poorly permeable BCS class-III drug, was incorporated in bioadhesive multiple W/O/W microemulsion (ME) to improve its corneal permeability. The drug-loaded ME was evaluated regarding its physical stability, droplet size, PDI, zeta potential, ultrastructure, viscosity, bioadhesion, in vitro release, transcorneal permeability, cytotoxicity, safety and ocular tolerance. Our ME possessed excellent physical stability, as it successfully passed several cycles of centrifugation and freeze–thaw tests. The formulation has a transparent appearance due to its tiny droplet size (10 nm). TEM confirmed ME droplet size and revealed its multilayered structure. In spite of the high aqueous solubility and the low permeability of ribavirin, this unique formulation was capable of sustaining its release for up to 24 h and improving its corneal permeability by 3-fold. The in vitro safety of our ME was proved by its high percentage cell viability, while its in vivo safety was confirmed by the absence of any sign of toxicity or irritation after either a single dose or 14 days of daily dosing. Our ME could serve as a vehicle for enhanced ocular delivery of drugs with different physicochemical properties, including those with low permeability.

Ibrahim, Mohamed Moustafa↗
NASA NTRS1980

Interactions between surface cooling and LBNP-induced central hypovolemia

The paper describes a study carried out to determine the extent to which whole body surface cooling (WBSC) modifies the effects of the central hypovolemia produced by lower body negative pressure (LBNP) at normal skin temperatures. It is shown that WBSC produces a central displacement of cutaneous venous volume resulting in an increase in stroke volume.

Raven, P. B.↗
NASA NTRS1981

Hemodynamic changes during whole body surface cooling and lower body negative pressure

Six young healthy male subjects were studied to evaluate the use of whole body surface cooling (WBSC) as an antiorthostatic intervention. Previous studies have demonstrated that perfusion of an Apollo cooling garment with 16 C water produced a significant increase in stroke volume and decrease in heart rate at rest and during lower body negative pressure (LBNP). However, optimal perfusion temperatures have not been determined. The present study examined the effects of WBSC using perfusion of water at a temperature of 10 C. This perfusion temperature produced a greater decrease in mean skin temperature than water at 16 C (4 C drop compared to 2 C). The hemodynamic effects were also more prominent with 10 C water as shown by the increase in stroke volume of 11% at rest and of 35% during LBNP at -50 torr compared to control measurements at ambient temperature. Heart rates were lowered significantly (8 beats/min) and systolic arterial blood pressure was higher (8 torr). Cooling with 10 C water produced a slight increase in muscle tone, reflected by a small but significant increase (+84 ml/min) in oxygen uptake. These data suggest that WBSC is an effective nonpharmacologic means of controlling preload and deserves further investigation as an antiorthostatic intervention.

Raven, P. B.↗
NASA NTRS1984

Physical fitness and cardiovascular response to lower body negative pressure

Klein et al. (1977) have questioned the concept of endurance training as an appropriate means of preparing for prolonged space flights. Their opinion was mainly based on reports of endurance athletes who had a decreased tolerance to orthostatic or gravitational stress induced by lower body negative pressure (LBNP), upright tilt, or whole body water immersion. The present investigation had the objective to determine if the hemodynamic response to LBNP is different between a high and average fit group of subjects. In addition, the discrete aspect of cardiovascular function which had been altered by chronic training was to be identified. On the basis of the results of experiments conducted with 14 young male volunteers, it is concluded that the reflex response to central hypovolemia is altered by endurance exercise training.

Raven, P. B.↗
NASA NTRS1994

Does training-induced orthostatic hypotension result from reduced carotid baroreflex responsiveness?

As manned space travel has steadily increased in duration and sophistication, the answer to a simple, relevant question remains elusive. Does endurance exercise training - high intensity rhythmic activity, performed regularly for extended periods of time - alter the disposition to, or severity of, postflight orthostatic hypotension? Research results continue to provide different views; however, data are difficult to compare because of the following factors that vary between investigations: the type of orthostatic stress imposed (+Gz, lower body negative pressure (LBNP), head-up tilt); pretest perturbations used (exercise, heat exposure, head-down tilting, bed rest, water immersion, hypohydration, pharmacologically-induced diuresis); the length of the training program used in longitudinal investigations (days versus weeks versus months); the criteria used to define fitness; and the criteria used to define orthostatic tolerance. Generally, research results indicate that individuals engaged in aerobic exercise activities for a period of years have been reported to have reduced orthostatic tolerance compared to untrained control subjects, while the results of shorter term longitudinal studies remain equivocal. Such conclusions suggest that chronic athletic training programs reduce orthostatic tolerance, whereas relatively brief (days to weeks) training programs do not affect orthostatic tolerance to any significant degree (increase or decrease). A primary objective was established to identify the alterations in blood pressure control that contribute to training-induced orthostatic hypotension (TIOH). Although any aspect of blood pressure regulation is suspect, current research has been focused on the baroreceptor system. Reductions in carotid baroreflex responsiveness have been documented in exercise-trained rabbits, reportedly due to an inhibitory influence from cardiac afferent, presumably vagal, nerve fibers that is abolished with intrapericardiac denervation. The purpose of this investigation was to attempt to determine if similar relationships existed in men with varied levels of fitness, using maximal aerobic power, VO2 max, as the marker of fitness.

Pawelczyk, James A.↗
NASA NTRS1994

Aortic baroreflex control of heart rate after 15 days of simulated microgravity exposure

To determine the effects of simulated microgravity on aortic baroreflex control of heart rate, we exposed seven male subjects to 15 days of bed rest in the 6 deg head-down position. The sensitivity of the aortic-cardiac baroreflex was determined during a steady-state phenylephrine-induced increase in mean arterial pressure combined with lower body negative pressure to counteract central venous pressure increases and neck pressure to offset the increased carotid sinus transmural pressure. The aortic-cardiac baroreflex gain was assessed by determining the ratio of the change in heart rate to the change in mean arterial pressure between baseline conditions and aortic baroreceptor-isolated conditions (i.e., phenylephrine + lower body negative pressure + neck pressure stage). Fifteen days of head-down tilt increased the gain of the aortic-cardiac baroreflex. Reductions in blood volume and/or maximal aerobic capacity may represent the underlying mechanism(s) responsible for increased aortic baroreflex responsiveness after exposure to a ground-based analogue of microgravity.

Crandall, Craig G.↗
NASA NTRS1994

Altered thermoregulatory responses after 15 days of head-down tilt

To determine whether extended exposure to a simulation of microgravity alters thermoregulatory reflex control of skin blood flow, six adult males were exposed to 15 days of 6 deg head-down tilt (HDT). On an ambulatory control day before HDT exposure and on HDT day 15 the core temperature of each subject was increased by 0.5 - 1.0 C by whole body heating with a water-perfused suit. Mean skin temperature, oral temperature (T (sub or)), mean arterial pressure, and forearm blood flow were measured throughout the protocol. Forearm vascular conductance (FVC) was calculated from the ratio of forearm blood flow to mean arterial pressure. After HDT exposure, the T(sub or) threshold at which reflex thermally induced increases in FVC began was elevated, whereas the slope of the T(sub or)-FVC relationship after this threshold was reduced. Moreover, normothermic FVC and FVC at the highest common T(sub or) between pre- and post-HDT trials were reduced after HDT. These data suggest that HDT exposure reduces thermoregulatory responses to heat stress. The mechanisms resulting in such an impaired thermoregulatory response are unknown but are likely related to the relative dehydration that accompanies this exposure.

Crandall, Craig G.↗
NASA NTRS1996

Tissue-Engineered Skeletal Muscle Organoids for Reversible Gene Therapy

Genetically modified murine skeletal myoblasts were tissue engineered in vitro into organ-like structures (organoids) containing only postmitotic myoribers secreting pharmacological levels of recombinant human growth hormone (rhGH). Subcutaneous organoid implantation under tension led to the rapid and stable appearance of physiological sera levels of rhGH for up to 12 weeks, whereas surgical removal led to its rapid disappearance. Reversible delivery of bioactive compounds from postmitotic cells in tissue engineered organs has several advantages over other forms of muscle gene therapy.

Vandenburgh, Herman↗
NASA NTRS1996

Tissue-Engineered Skeletal Muscle Organoids for Reversible Gene Therapy

Genetically modified murine skeletal myoblasts were tissue engineered in vitro into organ-like structures (organoids) containing only postmitotic myofibers secreting pharmacological levels of recombinant human growth hormone (rhGH). Subcutaneous organoid Implantation under tension led to the rapid and stable appearance of physiological sera levels of rhGH for up to 12 weeks, whereas surgical removal led to its rapid disappearance. Reversible delivery of bioactive compounds from postimtotic cells in tissue engineered organs has several advantages over other forms of muscle gene therapy.

Vandenburgh, Herman↗
NASA NTRS1999

Cardiovascular Session Summary

It was apparent that the bed-rest and spaceflight data indicated that decreases in plasma volume and cardiac atrophy along with cardiac remodeling were fundamental changes which predisposed many astronauts to post flight orthostatic intolerance. Despite the recently acquired in-flight and post-flight muscle sympathetic nerve activity findings suggesting that the sympathetic nerve responses were appropriate there remains significant contrary data from bed-rest studies, post- flight stand tests and hind-limb unweighted rat studies that suggest that the vasoconstrictive responses were compromised at least insufficient in susceptible individuals. The key issues raised is whether a diminished increase in sympathetic activity from baseline without changes in 254 First Biennial Space Biomedical Investigators'Workshop Cardiovascular peak response or receptor adaptations is an abnormal response or is an individual variance of response to the accentuated decrease in stroke volume. Data relating autonomic neural control of heart rate were presented to suggest that the vagal and sympathetic control of heart rate was attenuated. Also, bed-rest and space flight induced attenuated baroreflex control of heart rate was shown to be restored to pre-bedrest function by one bout of maximal dynamic exercise. However, these data were confounded by relying on the use of R-R interval as a measure of efferent responses of the baroreflex during a condition in which the baseline heart rate was changed. Clearly the idea that the autonomic control of heart rate may be changed by microgravity needs further investigation. This direction is suggested despite the fact that in the triple product (HR x SV x TPR = MAP) assessment of the regulation of arterial blood pressure during orthostasis the role of the HR reflex may be less influential than that associated. with cardiac atrophy (SV changes) and aberrant sympathetic vasoconstriction (resistance) changes. Although sympathetic nerve activity responses in-flight and post-flight on neurolab appeared appropriate, enough bed-rest and post-flight stand test data, along with animal model data suggest that vasoconstriction was compromised. The mechanism of this compromised vasoconstriction needs to be delineated. Other major findings concerning microgravity and physiological regulatory systems are that: I . Thermoregulatory adaptation appear to suggest some decrements in the control of cutaneous vasodilation and sweating; 2. Calcium resorption and dietary calcium need to be defined for differing durations of spaceflight, especially as the effects of excess calcium on vasomotor function appears to be detrimental; 3. Neurohumoral mechanisms of microgravity induced changes in neural function and the regulation of plasma volume and total body water, bone resorption and autonomic neural control of the circulation need further delineation; 4. As performance of work tasks become prolonged, the mechanisms of blood pressure regulation in microgravity needs to be used in the recovery period from prolonged work tasks.

Raven, Peter↗
NASA NTRS1999

Carotid Baroreflex Function During Prolonged Exercise

Astronauts are often required to work (exercise) at moderate to high intensities for extended periods while performing extra-vehicular activities (EVA). Although the physiologic responses associated with prolonged exercise have been documented, the mechanisms involved in blood pressure regulation under these conditions have not yet been fully elucidated. An understanding of this issue is pertinent to the ability of humans to perform work in microgravity and complies with the emphasis of NASA's Space Physiology and Countermeasures Program. Prolonged exercise at a constant workload is know to result in a progressive decrease in mean arterial pressure (MAP) concomitant with a decrease in stroke volume and a compensatory increase in heart rate. The continuous decrease in MAP during the exercise, which is related to the thermoregulatory redistribution of circulating blood volume to the cutaneous circulation, raises the question as to whether there is a loss of baroreflex regulation of arterial blood pressure. We propose that with prolongation of the exercise to 60 minutes, progressive increases on central command reflect a progressive upward resetting of the carotid baroreflex (CBR) such that the operating point of the CBR is shifted to a pressure below the threshold of the reflex rendering it ineffectual in correcting the downward drift in MAP. In order to test this hypothesis, experiments have been designed to uncouple the global hemodynamic response to prolonged exercise from the central command mediated response via: (1) continuous maintenance of cardiac filling volume by intravenous infusion of a dextran solution; and (2) whole body surface cooling to counteract thermoregulatory cutaneous vasodialation. As the type of work (exercise) performed by astronauts is inherently arm and upper body dependent, we will also examine the physiologic responses to prolonged leg cycling and arm ergometry exercise in the supine positions with and without level lower body negative pressure (-10 torr) to mimic spaceflight- related decreases in cardiac filling volumes.

Raven, P. B.↗
NASA NTRS2003

New insights into differential baroreflex control of heart rate in humans

Recent data indicate that bilateral carotid sinus denervation in patients results in a chronic impairment in the rapid reflex control of blood pressure during orthostasis. These findings are inconsistent with previous human experimental investigations indicating a minimal role for the carotid baroreceptor-cardiac reflex in blood pressure control. Therefore, we reexamined arterial baroreflex [carotid (CBR) and aortic baroreflex (ABR)] control of heart rate (HR) using newly developed methodologies. In 10 healthy men, 27 +/- 1 yr old, an abrupt decrease in mean arterial pressure (MAP) was induced nonpharmacologically by releasing a unilateral arterial thigh cuff (300 Torr) after 9 min of resting leg ischemia under two conditions: 1) ABR and CBR deactivation (control) and 2) ABR deactivation. Under control conditions, cuff release decreased MAP by 13 +/- 1 mmHg, whereas HR increased 11 +/- 2 beats/min. During ABR deactivation, neck suction was gradually applied to maintain carotid sinus transmural pressure during the initial 20 s after cuff release (suction). This attenuated the increase in HR (6 +/- 1 beats/min) and caused a greater decrease in MAP (18 +/- 2 mmHg, P < 0.05). Furthermore, estimated cardiac baroreflex responsiveness (DeltaHR/DeltaMAP) was significantly reduced during suction compared with control conditions. These findings suggest that the carotid baroreceptors contribute more importantly to the reflex control of HR than previously reported in healthy individuals.

Non-NASA Center↗
NASA NTRS2002

Role of central command in carotid baroreflex resetting in humans during static exercise

The purpose of the experiments was to examine the role of central command in the exercise-induced resetting of the carotid baroreflex. Eight subjects performed 30 % maximal voluntary contraction (MVC) static knee extension and flexion with manipulation of central command (CC) by patellar tendon vibration (PTV). The same subjects also performed static knee extension and flexion exercise without PTV at a force development that elicited the same ratings of perceived exertion (RPE) as those observed during exercise with PTV in order to assess involvement of the exercise pressor reflex. Carotid baroreflex (CBR) function curves were modelled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid changes in neck pressure and suction during steady state static exercise. Knee extension exercise with PTV (decreased CC activation) reset the CBR-HR and CBR-MAP to a lower operating pressure (P < 0.05) and knee flexion exercise with PTV (increased CC activation) reset the CBR-HR and CBR-MAP to a higher operating pressure (P < 0.05). Comparison between knee extension and flexion exercise at the same RPE with and without PTV found no difference in the resetting of the CBR-HR function curves (P > 0.05) suggesting the response was determined primarily by CC activation. However, the CBR-MAP function curves were reset to operating pressures determined by both exercise pressor reflex (EPR) and central command activation. Thus the physiological response to exercise requires CC activation to reset the carotid-cardiac reflex but requires either CC or EPR to reset the carotid-vasomotor reflex.

Non-NASA Center↗
NASA NTRS2002

Haemodynamic changes during neck pressure and suction in seated and supine positions

We sought to quantify the contribution of cardiac output (Q) and total vascular conductance (TVC) to carotid baroreflex-mediated changes in mean arterial pressure (MAP) in the upright seated and supine positions. Acute changes in carotid sinus transmural pressure were evoked using brief 5 s pulses of neck pressure and neck suction (NP/NS) via a simplified paired neck chamber that was developed to enable beat-to-beat measurements of stroke volume using pulse-doppler ultrasound. Percentage contributions of Q and TVC were achieved by calculating the predicted change in MAP during carotid baroreflex stimulation if only the individual changes in Q or TVC occurred and all other parameters remained at control values. All NP and NS stimuli from +40 to -80 Torr (+5.33 to -10.67 kPa) induced significant changes in Q and TVC in both the upright seated and supine positions (P < 0.001). Cardiopulmonary baroreceptor loading with the supine position appeared to cause a greater reliance on carotid baroreflex-mediated changes in Q. Nevertheless, in both the seated and supine positions the changes in MAP were primarily mediated by alterations in TVC (percentage contribution of TVC at the time-of-peak MAP, seated 95 +/- 13, supine 76 +/- 17 %). These data indicate that alterations in vasomotor activity are the primary means by which the carotid baroreflex regulates blood pressure during acute changes in carotid sinus transmural pressure.

Clinical Trial↗
NASA NTRS2002

The influence of central command on baroreflex resetting during exercise

The arterial baroreflex functions as a negative feedback system regulating blood pressure around an established operating point. Paradoxically, a parallel increase in heart rate and blood pressure manifests during exercise. Experimental evidence suggests these events are caused, in part, by a rapid resetting of the baroreflex by central command.

Non-NASA Center↗
NASA NTRS2001

Increases in intramuscular pressure raise arterial blood pressure during dynamic exercise

This investigation was designed to determine the role of intramuscular pressure-sensitive mechanoreceptors and chemically sensitive metaboreceptors in affecting the blood pressure response to dynamic exercise in humans. Sixteen subjects performed incremental (20 W/min) cycle exercise to fatigue under four conditions: control, exercise with thigh cuff occlusion of 90 Torr (Cuff occlusion), exercise with lower body positive pressure (LBPP) of 45 Torr, and a combination of thigh cuff occlusion and LBPP (combination). Indexes of central command (heart rate, oxygen uptake, ratings of perceived exertion, and electromyographic activity), cardiac output, stroke volume, and total peripheral resistance were not significantly different between the four conditions. Mechanical stimulation during LBPP and combination conditions resulted in significant elevations in intramuscular pressure and mean arterial pressure from control at rest and throughout the incremental exercise protocol (P < 0.05). Conversely, there existed no significant changes in mean arterial pressure when the metaboreflex was stimulated by cuff occlusion. These findings suggest that under normal conditions the mechanoreflex is tonically active and is the primary mediator of exercise pressor reflex-induced alterations in arterial blood pressure during submaximal dynamic exercise in humans.

Non-NASA Center↗