Search NASA⌕ Search

SEARCH · Search NASA

Results for “Hemodynamics”

Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS1999

Hypertrophic response to hemodynamic overload: role of load vs. renin-angiotensin system activation

Myocardial hypertrophy is one of the basic mechanisms by which the heart compensates for hemodynamic overload. The mechanisms by which hemodynamic overload is transduced by the cardiac muscle cell and translated into cardiac hypertrophy are not completely understood. Candidates include activation of the renin-angiotensin system (RAS) and angiotensin II receptor (AT1) stimulation. In this study, we tested the hypothesis that load, independent of the RAS, is sufficient to stimulate cardiac growth. Four groups of cats were studied: 14 normal controls, 20 pulmonary artery-banded (PAB) cats, 7 PAB cats in whom the AT1 was concomitantly and continuously blocked with losartan, and 8 PAB cats in whom the angiotensin-converting enzyme (ACE) was concomitantly and continuously blocked with captopril. Losartan cats had at least a one-log order increase in the ED50 of the blood pressure response to angiotensin II infusion. Right ventricular (RV) hypertrophy was assessed using the RV mass-to-body weight ratio and ventricular cardiocyte size. RV hemodynamic overload was assessed by measuring RV systolic and diastolic pressures. Neither the extent of RV pressure overload nor RV hypertrophy that resulted from PAB was affected by AT1 blockade with losartan or ACE inhibition with captopril. RV systolic pressure was increased from 21 +/- 3 mmHg in normals to 68 +/- 4 mmHg in PAB, 65 +/- 5 mmHg in PAB plus losartan and 62 +/- 3 mmHg in PAB plus captopril. RV-to-body weight ratio increased from 0.52 +/- 0.04 g/kg in normals to 1.11 +/- 0.06 g/kg in PAB, 1.06 +/- 0.06 g/kg in PAB plus losartan and 1.06 +/- 0.06 g/kg in PAB plus captopril. Thus 1) pharmacological modulation of the RAS with losartan and captopril did not change the extent of the hemodynamic overload or the hypertrophic response induced by PAB; 2) neither RAS activation nor angiotensin II receptor stimulation is an obligatory and necessary component of the signaling pathway that acts as an intermediary coupling load to the hypertrophic response; and 3) load, independent of the RAS, is capable of stimulating cardiac growth.

Non-NASA Center↗
NASA NTRS2003

Differences in the hemodynamic response to event-related motor and visual paradigms as measured by near-infrared spectroscopy

Several current brain imaging techniques rest on the assumption of a tight coupling between neural activity and hemodynamic response. The nature of this neurovascular coupling, however, is not completely understood. There is some evidence for a decoupling of these processes at the onset of neural activity, which manifests itself as a momentary increase in the relative concentration of deoxyhemoglobin (HbR). The existence of this early component of the hemodynamic response function, however, is controversial, as it is inconsistently found. Near infrared spectroscopy (NIRS) allows quantification of levels of oxyhemoglobin (HbO(2)) and HbR during task performance in humans. We acquired NIRS data during performance of simple motor and visual tasks, using rapid-presentation event-related paradigms. Our results demonstrate that rapid, event-related NIRS can provide robust estimates of the hemodynamic response without artifacts due to low-frequency signal components, unlike data from blocked designs. In both the motor and visual data the onset of the increase in HbO(2) occurs before HbR decreases, and there is a poststimulus undershoot. Our results also show that total blood volume (HbT) drops before HbO(2) and undershoots baseline, raising a new issue for neurovascular models. We did not find early deoxygenation in the motor data using physiologically plausible values for the differential pathlength factor, but did find one in the visual data. We suggest that this difference, which is consistent with functional magnetic resonance imaging (fMRI) data, may be attributable to different capillary transit times in these cortices.

NASA Program Biomedical Research and Countermeasur↗
NASA NTRS1998

Effects of 12 days exposure to simulated microgravity on central circulatory hemodynamics in the rhesus monkey

Central circulatory hemodynamic responses were measured before and during the initial 9 days of a 12-day 10 degrees head-down tilt (HDT) in 4 flight-sized juvenile rhesus monkeys who were surgically instrumented with a variety of intrathoracic catheters and blood flow sensors to assess the effects of simulated microgravity on central circulatory hemodynamics. Each subject underwent measurements of aortic and left ventricular pressures, and aortic flow before and during HDT as well as during a passive head-up postural test before and after HDT. Heart rate, stroke volume, cardiac output, and left ventricular end-diastolic pressure were measured, and dP/dt and left ventricular elastance was calculated from hemodynamic measurements. The postural test consisted of 5 min of supine baseline control followed by 5 minutes of 90 degrees upright tilt (HUT). Heart rate, stroke volume, cardiac output, and left ventricular end-diastolic pressure showed no consistent alterations during HDT. Left ventricular elastance was reduced in all animals throughout HDT, indicating that cardiac compliance was increased. HDT did not consistently alter left ventricular +dP/dt, indicating no change in cardiac contractility. Heart rate during the post-HDT HUT postural test was elevated compared to pre-HDT while post-HDT cardiac output was decreased by 52% as a result of a 54% reduction in stroke volume throughout HUT. Results from this study using an instrumented rhesus monkey suggest that exposure to microgravity may increase ventricular compliance without alternating cardiac contractility. Our project supported the notion that an invasively-instrumented animal model should be viable for use in spaceflight cardiovascular experiments to assess potential changes in myocardial function and cardiac compliance.

NASA Discipline Cardiopulmonary↗
NASA NTRS1994

Body position does not affect the hemodynamic response to venous air embolism in dogs

Current therapy for massive venous air embolism (VAE) includes the use of the left lateral recumbent (LLR) position. This recommendation is based on animal studies, conducted 50 yr ago, which looked primarily at survival. Little is known, however, about the concomitant hemodynamic response after VAE in various body positions. The purpose of this study was to investigate the hemodynamic and cardiovascular changes in various body positions after VAE. Twenty-two mechanically ventilated supine mongrel dogs received a venous air infusion of 2.5 mL/kg at a rate of 5 mL/s. One minute after the infusion, 100% oxygen ventilation was commenced and the body position of the dogs was changed to either the LLR (n = 6), the LLR with the head 10 degrees down (LLR-10 degrees; n = 6) or the right lateral recumbent (RLR; n = 5) position. Five dogs were maintained in the supine position (SUP; n = 5). One dog died in every group except in the SUP group, where all the dogs recovered. There were no significant differences among the various body positions in terms of heart rate, mean arterial pressure, pulmonary artery pressure, central venous pressure, left ventricular end-diastolic pressure, or cardiac output. The acute hemodynamic changes occurring during the first 5-15 min after VAE recovered to 80% of control within 60 min. Our data suggest that body repositioning does not influence the cardiovascular response to VAE. Specifically, our data do not support the recommendation of repositioning into the LLR position for the treatment of VAE.

Non-NASA Center↗
NASA NTRS1994

Cerebral versus systemic hemodynamics during graded orthostatic stress in humans

BACKGROUND: Orthostatic syncope is usually attributed to cerebral hypoperfusion secondary to systemic hemodynamic collapse. Recent research in patients with neurocardiogenic syncope has suggested that cerebral vasoconstriction may occur during orthostatic hypotension, compromising cerebral autoregulation and possibly contributing to the loss of consciousness. However, the regulation of cerebral blood flow (CBF) in such patients may be quite different from that of healthy individuals, particularly when assessed during the rapidly changing hemodynamic conditions associated with neurocardiogenic syncope. To be able to interpret the pathophysiological significance of these observations, a clear understanding of the normal responses of the cerebral circulation to orthostatic stress must be obtained, particularly in the context of the known changes in systemic and regional distributions of blood flow and vascular resistance during orthostasis. Therefore, the specific aim of this study was to examine the changes that occur in the cerebral circulation during graded reductions in central blood volume in the absence of systemic hypotension in healthy humans. We hypothesized that cerebral vasoconstriction would occur and CBF would decrease due to activation of the sympathetic nervous system. We further hypothesized, however, that the magnitude of this change would be small compared with changes in systemic or skeletal muscle vascular resistance in healthy subjects with intact autoregulation and would be unlikely to cause syncope without concomitant hypotension. METHODS AND RESULTS: To test this hypothesis, we studied 13 healthy men (age, 27 +/- 7 years) during progressive lower body negative pressure (LBNP). We measured systemic flow (Qc is cardiac output; C2H2 rebreathing), regional forearm flow (FBF; venous occlusion plethysmography), and blood pressure (BP; Finapres) and calculated systemic (SVR) and forearm (FVR) vascular resistances. Changes in brain blood flow were estimated from changes in the blood flow velocity in the middle cerebral artery (VMCA) using transcranial Doppler. Pulsatility (systolic minus diastolic/mean velocity) normalized for systemic arterial pressure pulsatility was used as an index of distal cerebral vascular resistance. End-tidal PACO2 was closely monitored during LBNP. From rest to maximal LBNP before the onset of symptoms or systemic hypotension, Qc and FBF decreased by 29.9% and 34.4%, respectively. VMCA decreased less, by 15.5% consistent with a smaller decrease in CBF. Similarly, SVR and FVR increased by 62.8% and 69.8%, respectively, whereas pulsatility increased by 17.2%, suggestive of a mild degree of small-vessel cerebral vasoconstriction. Seven of 13 subjects had presyncope during LBNP, all associated with a sudden drop in BP (29 +/- 9%). By comparison, hyperventilation alone caused greater changes in VMCA (42 +/- 2%) and pulsatility but never caused presyncope. In a separate group of 3 subjects, superimposition of hyperventilation during highlevel LBNP caused a further decrease in VMCA (31 +/- 7%) but no change in BP or level of consciousness. CONCLUSIONS: We conclude that cerebral vasoconstriction occurs in healthy humans during graded reductions in central blood volume caused by LBNP. However, the magnitude of this response is small compared with changes in SVR or FVR during LBNP or other stimuli known to induce cerebral vasoconstriction (hypocapnia). We speculate that this degree of cerebral vasoconstriction is not by itself sufficient to cause syncope during orthostatic stress. However, it may exacerbate the decrease in CBF associated with hypotension if hemodynamic instability develops.

NASA Discipline Cardiopulmonary↗
NASA NTRS1993

Hemodynamic and hormonal responses to lower body negative pressure in men with varying profiles of strength and aerobic power

Hemodynamic, cardiac, and hormonal responses to lower-body negative pressure (LBNP) were examined in 24 healthy men to test the hypothesis that responsiveness of reflex control of blood pressure during orthostatic challenge is associated with interactions between strength and aerobic power. Subjects underwent treadmill tests to determine peak oxygen uptake (VO2max) and isokinetic dynamometer tests to determine knee extensor strength. Based on predetermined criteria, subjects were classified into one of four fitness profiles of six subjects each, matched for age, height, and body mass: (a) low strength/average aerobic fitness, (b) low strength/high aerobic fitness, (c) high strength/average aerobic fitness, and (d) high strength/high aerobic fitness. Following 90 min of 0.11 rad (6 degrees) head-down tilt (HDT), each subject underwent graded LBNP to -6.7 kPa or presyncope, with maximal duration 15 min, while hemodynamic, cardiac, and hormonal responses were measured. All groups exhibited typical hemodynamic, hormonal, and fluid shift responses during LBNP, with no intergroup differences between high and low strength characteristics. Subjects with high aerobic power exhibited greater (P < 0.05) stroke volume and lower (P < 0.05) heart rate, vascular peripheral resistance, and mean arterial pressure during rest, HDT, and LBNP. Seven subjects, distributed among the four fitness profiles, became presyncopal. These subjects showed greatest reduction in mean arterial pressure during LBNP, had greater elevations in vasopressin, and lesser increases in heart rate and peripheral resistance. Neither VO2max nor leg strength were associated with fall in arterial pressure or with syncopal episodes. We conclude that interactions between aerobic and strength fitness characteristics do not influence responses to LBNP challenge.

Norepinephrine/blood↗
NASA NTRS1993

Body position does not affect the hemodynamic response to venous air embolism in dogs

Current therapy for massive venous air embolism (VAE) includes the use of the left lateral recumbent (LLR) position. This recommendation is based on animal studies, conducted 50 years ago, which looked primarily at survival. Little is known, however, about the concomitant hemodynamic response after VAE in various body positions. The purpose of this study was to investigate the hemodynamic and cardiovascular changes in various body positions after VAE. Twenty-two mechanically ventilated supine mongrel dogs received a venous air infusion of 2.5 mL/kg at a rate of 5 mL/s. One minute after the infusion, 100% oxygen ventilation was commenced and the body position of the dogs was changed to either the LLR (n = 6), the LLR with the head 10 deg down (LLR-10 deg; n = 6) or the right lateral recumbent (RLR; n = 5) position. Five dogs were maintained in the supine position (SUP; n = 5). One dog died in every group except in the SUP group, where all the dogs recovered. There were no significant differences among the various body positions in terms of heart rate, mean arterial pressure, pulmonary artery pressure, central venous pressure, left ventricular end-diastolic pressure, or cardiac output. The acute hemodynamic changes occurring during the first 5-15 min after VAE recovered to 80% of control within 60 min. Our data suggest that body repositioning does not influence the cardiovascular response to VAE. Specifically, our data do not support the recommendation of repositioning into the LLR position for the treatment of VAE.

Mehlhorn, Uwe↗
NASA NTRS2001

Short-term hemodynamic performance of the mitral Carpentier-Edwards PERIMOUNT pericardial valve. Carpentier-Edwards PERIMOUNT Investigators

BACKGROUND: Although long-term durability data exist, little data are available concerning the hemodynamic performance of the Carpentier-Edwards PERIMOUNT pericardial valve in the mitral position. METHODS: Sixty-nine patients who were implanted with mitral PERIMOUNT valves at seven international centers between January 1996 and February 1997 consented to participate in a short-term echocardiography follow-up. Echocardiographs were collected at a mean of 600+/-133 days after implantation (range, 110 to 889 days); all underwent blinded core lab analysis. RESULTS: At follow-up, peak gradients were 9.09+/-3.43 mm Hg (mean, 4.36+/-1.79 mm Hg) and varied inversely with valve size (p < 0.05). The effective orifice areas were 2.5+/-0.6 cm2 and tended to increase with valve size (p = 0.08). Trace mitral regurgitation (MR) was common (n = 48), 9 patients had mild MR, 1 had moderate MR, none had severe MR. All MR was central (n = 55) or indeterminate (n = 3). No paravalvular leaks were observed. Mitral regurgitation flow areas were 3.4+/-2.8 cm2 and were without significant volumes. CONCLUSIONS: In this multicenter study, these mitral valves are associated with trace, although physiologically insignificant, central MR. Despite known echocardiographic limitations, the PERIMOUNT mitral valves exhibit similar hemodynamics to other prosthetic valves.

Clinical Trial↗
NASA NTRS2000

Hemodynamic and symptomatic effects of acute interventions on tilt in patients with postural tachycardia syndrome

A variety of approaches have been used to alleviate symptoms in postural tachycardia syndrome (POTS). Drugs reported to be of benefit include midodrine, propranolol, clonidine, and phenobarbital. Other measures used include volume expansion and physical countermaneuvers. These treatments may influence pathophysiologic mechanisms of POTS such as alpha-receptor dysfunction, beta-receptor supersensitivity, venous pooling, and brainstem center dysfunction. The authors prospectively studied hemodynamic indices and symptom scores in patients with POTS who were acutely treated with a variety of interventions. Twenty-one subjects who met the criteria for POTS were studied (20 women, 1 man; mean age, 28.7 +/- 6.8 y; age range, 14-39 y). Patients were studied with a 5-minute head-up tilt protocol, ECG monitoring, and noninvasive beat-to-beat blood pressure monitoring, all before and after the administration of an intervention (intravenous saline, midodrine, propranolol, clonidine, or phenobarbital). The hemodynamic indices studied were heart rate (ECG) and systolic, mean, and diastolic blood pressure. Patients used a balanced verbal scale to record any change in their symptoms between the tilts. Symptom scores improved significantly after the patients received midodrine and saline. Midodrine and propranolol reduced the resting heart rate response to tilt (p <0.005) and the immediate and 5-minute heart rate responses to tilt (p <0.002). Clonidine accentuated the immediate decrease in blood pressure on tilt up (p <0.05). It was concluded that midodrine and intravenous saline are effective in decreasing symptoms on tilt in patients with POTS when given acutely. Effects of treatments on heart rate and blood pressure responses generally reflected the known pharmacologic mechanisms of the agents.

Non-NASA Center↗
NASA NTRS1999

Rapid tachyphylaxis to hemodynamic effects of PACAP-27 after inhibition of nitric oxide synthesis

The vasodilator effects of pituitary adenylate cyclase-activating polypeptide (PACAP)-27 are subject to tachyphylaxis in rats treated with the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). We examined whether this tachyphylaxis could be prevented by administration of the putative endothelium-derived nitrosyl factor S-nitroso-L-cysteine (L-SNC) and whether L-SNC may exert its effects via increases in cGMP levels in vascular smooth muscle. Five doses of PACAP-27 (2 nmol/kg iv) produced pronounced vasodilator responses in saline-treated rats. These responses were not subject to tachyphylaxis. The first injection of PACAP-27 (2 nmol/kg iv) in L-NAME-treated (50 micromol/kg iv) rats produced vasodilator responses similar to those in saline-treated rats, whereas subsequent injections produced progressively smaller responses. The injection of L-SNC (1,200 nmol/kg iv) before each injection of PACAP-27 prevented tachyphylaxis to the Gs protein-coupled receptor agonist in L-NAME-treated rats, whereas equihypotensive doses of the NO donor sodium nitroprusside (100 micrograms/kg iv) did not. The injection of the membrane-permeant cGMP analog 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate (8-CPT-cGMP; 30 micromol/kg iv) to L-NAME-treated rats restored resting hemodynamic values to pre-L-NAME levels but did not prevent the development of tachyphylaxis to PACAP-27. These results suggest that nitrosyl factors prevent the development of tachyphylaxis to the hemodynamic actions of PACAP-27. These nitrosyl factors may act independently of their ability to generate cGMP in vascular smooth muscle.

NASA Discipline Regulatory Physiology↗
NASA NTRS1977

Hemodynamic Studies of the Legs Under Weightlessness

Significant among the medical findings following prolonged space flight are reduced orthostatic tolerance and ergometric work capacity. Changes in hemodynamics of the legs with increased blood pooling and reduction in cardiac output must be considered one of the most probable causes of these effects. Concern for the above plus the observed marked tissue changes occurring in the legs during flight prompted the addition of several procedures to evaluate hemodynamic changes in the leg; resting arterial blood flow, venous compliance and muscle pumping were investigated. In so far as possible, the initial reaction to pressure in the smallest possible vein segment was examined.

William E Thornton↗
NASA NTRS1992

Hemodynamic responses to seated and supine lower body negative pressure - Comparison with +Gz acceleration

The hemodynamic responses to LBNP in seated subjects and in subjects in supine body positions were compared and were correlated with hemodynamic changes which occurred during a simulated (by centrifugation) Shuttle reentry acceleration with a slow onset rate of 0.002 G/s and during gradual onset exposures to +3 Gz and +4 Gz. Results demonstrate that seated LBNP at a level of -40 mm Hg can serve as a static simulator for changes in the heart rate and in mean blood pressure induced by gradual onset acceleration stress occurring during Shuttle reentry. The findings also provide a rationale for using LBNP during weightlessness as a means of imposing G-loading on the circulation prior to reentry.

Polese, Alvese↗
NASA NTRS1991

Acute hemodynamic response to weightlessness during parabolic flight

The effect of a short exposure to weightlessness on hemodynamic parameters of humans was investigated in seven subjects flown aboard the KC-135 aircraft. Particular attention is given to the relationships among various hemodynamic responses to hypergravic and hypogravic states, observed for four different postures: semisupine, supine, standing, and sitting. Results are presented on changes in the thoracic fluid index, heart rate, cardiac index, and the coefficient of variation of the R-R intervals. High values of the coefficient of variation were found at the onset of 0-G, suggesting that vagal cardiac neural activity increases in all positions except supine (where a small decrease was registered).

Mukai, Chiaki N.↗
NASA NTRS1993

Evaluation of bioimpedance for the measurement of physiologic variables as related to hemodynamic studies in space flight

Orthostatic intolerance, following space flight, has received substantial attention because of the possibility that it compromises astronaut safety and reduces the ability of astronauts to function at peak performance levels upon return to a one-g environment. Many pre- and post-flight studies are performed to evaluate changes in hemodynamic responses to orthostatic challenges after shuttle missions. The purpose of this present project is to validate bioimpedance as a means to acquire stroke volume and other hemodynamic information in these studies. In this study, ten male and ten female subjects were subjected to simultaneous measurements of thoracic bioimpedance and Doppler ultrasonic velocimetry under supine, 10 degree head down and 30 degree head up conditions. Paired measurements were made during six periods of five seconds breath holding, over a two minute period, for each of the three positions. Stroke volume was calculated by three bioimpedance techniques and ultrasonic Doppler.

Taylor, Bruce C.↗
NASA NTRS2000

Bioimpedance Measurement of Segmental Fluid Volumes and Hemodynamics

Bioimpedance has become a useful tool to measure changes in body fluid compartment volumes. An Electrical Impedance Spectroscopic (EIS) system is described that extends the capabilities of conventional fixed frequency impedance plethysmographic (IPG) methods to allow examination of the redistribution of fluids between the intracellular and extracellular compartments of body segments. The combination of EIS and IPG techniques was evaluated in the human calf, thigh, and torso segments of eight healthy men during 90 minutes of six degree head-down tilt (HDT). After 90 minutes HDT the calf and thigh segments significantly (P < 0.05) lost conductive volume (eight and four percent, respectively) while the torso significantly (P < 0.05) gained volume (approximately three percent). Hemodynamic responses calculated from pulsatile IPG data also showed a segmental pattern consistent with vascular fluid loss from the lower extremities and vascular engorgement in the torso. Lumped-parameter equivalent circuit analyses of EIS data for the calf and thigh indicated that the overall volume decreases in these segments arose from reduced extracellular volume that was not completely balanced by increased intracellular volume. The combined use of IPG and EIS techniques enables noninvasive tracking of multi-segment volumetric and hemodynamic responses to environmental and physiological stresses.

Montgomery, Leslie D.↗
NASA NTRS2003

Computational Hemodynamic Simulation of Human Circulatory System under Altered Gravity

A computational hemodynamics approach is presented to simulate the blood flow through the human circulatory system under altered gravity conditions. Numerical techniques relevant to hemodynamics issues are introduced to non-Newtonian modeling for flow characteristics governed by red blood cells, distensible wall motion due to the heart pulse, and capillary bed modeling for outflow boundary conditions. Gravitational body force terms are added to the Navier-Stokes equations to study the effects of gravity on internal flows. Six-type gravity benchmark problems are originally presented to provide the fundamental understanding of gravitational effects on the human circulatory system. For code validation, computed results are compared with steady and unsteady experimental data for non-Newtonian flows in a carotid bifurcation model and a curved circular tube, respectively. This computational approach is then applied to the blood circulation in the human brain as a target problem. A three-dimensional, idealized Circle of Willis configuration is developed with minor arteries truncated based on anatomical data. Demonstrated is not only the mechanism of the collateral circulation but also the effects of gravity on the distensible wall motion and resultant flow patterns.

Kim. Chang Sung↗
NASA NTRS1999

Hemodynamic actions of systemically injected pituitary adenylate cyclase activating polypeptide-27 in the rat

The aims of this study were (1) to characterize the hemodynamic mechanisms underlying the hypotensive effects of pituitary adenylate cyclase activating polypeptide-27 (PACAP-27 0.1-2.0 nmol/kg, i.v.) in pentobarbital-anesthetized rats, and (2) to determine the roles of the autonomic nervous system, adrenal catecholamines and endothelium-derived nitric oxide (NO) in the expression of PACAP-27-mediated effects on hemodynamic function. PACAP-27 produced dose-dependent decreases in mean arterial blood pressure and hindquarter and mesenteric vascular resistances in saline-treated rats. PACAP-27 also produced pronounced falls in mean arterial blood pressure in rats treated with the ganglion blocker, chlorisondamine (5 mg/kg, i.v.). The hypotensive and vasodilator actions of PACAP-27 were not attenuated by the beta-adrenoceptor antagonist, propranolol (1 mg/kg, i.v.), or the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME 50 micromol/kg, i.v.). PACAP-27 produced dose-dependent increases in heart rate whereas the hypotensive response produced by the nitrovasodilator, sodium nitroprusside (10 microg/kg, i.v.), was associated with a minimal tachycardia. The PACAP-27-induced tachycardia was unaffected by chlorisondamine, but was virtually abolished by propranolol. These results suggest that the vasodilator effects of PACAP-27 are due to actions in the microcirculation rather than to the release of adrenal catecholamines and that this vasodilation may not involve the release of endothelium-derived NO. These results also suggest that PACAP-27 produces tachycardia by directly releasing norepinephrine from cardiac sympathetic nerve terminals rather than by direct or baroreceptor reflex-mediated increases in sympathetic nerve activity.

Non-NASA Center↗
NASA NTRS2004

INSD-Hemodynamics

Hemodynamics (potentially will support Digital Astronaut program): Hemodynamics (potentially will support Digital Astronaut program): During long-duration space missions, astronauts have to adapt themselves to.altered circumstance of microgravity. Blood circulation undergoes significant adaptation during and after space flight. The blood flow through an anatomical Circle of Willis configuration is simulated to provide means for studying gravitational effects on the brain circulation.

Cetin, Kiris↗