Vestibular and Cardiovascular Responses After Long-Duration Spaceflight

2020 ◽  
Vol 91 (8) ◽  
pp. 621-627
Author(s):  
Nandini Deshpande ◽  
Steven S. Laurie ◽  
Stuart M. C. Lee ◽  
Chris A. Miller ◽  
Ajitkumar P. Mulavara ◽  
...  

BACKGROUND: The vestibulo-sympathetic reflex operates during orthostatically challenging movements to initiate cardiovascular responses in advance of a baroreceptor-mediated response. The objective of this study was to determine whether there was an association between changes in vestibular function and cardiovascular responses during a prone-to-stand movement in astronauts after return from long-duration spaceflight.METHODS: Thirteen crewmembers who participated in International Space Station missions were tested before spaceflight and 1 d after landing. Vestibular function was evaluated by computerized dynamic posturography while their head was erect and while they performed dynamic head tilts. Heart rate and mean arterial blood pressure were measured while the subjects were in prone and standing positions.RESULTS: The 21.4% increase in the astronauts’ heart rate during the prone to stand maneuver after spaceflight correlated significantly with their spaceflight-induced 48.7% decrease in postural stability during dynamic head tilts. The larger mean arterial pressure in the prone position after spaceflight compared to preflight (+7%) also correlated with the postflight decrease in postural stability during dynamic head tilts.CONCLUSION: These results indicate that an appropriate vestibular function is important to evoke optimum vestibulo-sympathetic response during orthostatically challenging voluntary movements performed after spaceflight. They also suggest that there may be a greater need to generate an anticipatory cardiovascular response after spaceflight.Deshpande N, Laurie SS, Lee SMC, Miller CA, Mulavara AP, Peters BT,Reschke MF, Stenger MB, Taylor LC, Wood SJ, Clément GR, Bloomberg JJ. Vestibular and cardiovascular responses after long-duration spaceflight. Aerosp Med Hum Perform. 2020; 91(8):621–627.

1999 ◽  
Vol 7 (1) ◽  
pp. 20-31 ◽  
Author(s):  
Elizabeth Thompson ◽  
Theo H. Versteegh ◽  
Tom J. Overend ◽  
Trevor B. Birmingham ◽  
Anthony A. Vandervoort

Our purpose was to describe heart rate (HR), mean arterial blood pressure (MAP), and perceived exertion (RPE) responses to submaximal isokinetic concentric (CON) and eccentric (ECC) exercise at the same absolute torque output in older adults. Peak torques for ECC and CON knee extension were determined in healthy older males (n = 13) and females (n = 7). Subjects then performed separate, randomly ordered, 2-min bouts of CON and ECC exercise. Heart rate and MAP increased (p < .001) from resting values throughout both exercise bouts. CON exercise elicited a significantly greater cardiovascular response than ECC exercise after 60 s. Peak HR, MAP, and RPE after CON exercise were greater than after ECC exercise (p < .01). At the same absolute torque output, isokinetic CON knee extension exercise resulted in a significantly greater level of cardiovascular stress than ECC exercise. These results are relevant to resistance testing and exercise in older people.


1998 ◽  
Vol 274 (3) ◽  
pp. R814-R821 ◽  
Author(s):  
James C. Schadt ◽  
Eileen M. Hasser

Chronically instrumented, conscious rabbits were used to test the hypothesis that sensory stimulation with an air jet or oscillation produces differential hemodynamic changes that may be appropriate for an active or a passive behavioral response, respectively. Both stressors increased arterial pressure, central venous pressure, and hindquarters blood flow and produced visceral vasoconstriction. Neither stimulus altered hindquarters conductance. Although air jet increased heart rate and cardiac output, oscillation did not. The two stressors affected arterial baroreflex control of heart rate differently. Oscillation reset arterial pressure to a higher level with no change in heart rate maximum or minimum, whereas air jet reset both heart rate and arterial pressure to higher levels. Neither stressor affected baroreflex sensitivity. We conclude that the conscious rabbit shows at least two distinct cardiovascular responses when exposed to acute stressors. Air jet produces a cardiovascular response including tachycardia, which resembles the defense reaction and appears appropriate for active defense or flight. The response to oscillation, on the other hand, appears better suited for a passive response such as “freezing” behavior. During exposure to either stressor, the baroreflex is altered to allow simultaneous increases in heart rate and arterial blood pressure, but the sensitivity is maintained, allowing normal moment to moment control of heart rate.


1965 ◽  
Vol 43 (2) ◽  
pp. 327-337
Author(s):  
M. A. Chiong ◽  
J. D. Hatcher

Cardiovascular responses to the intravenous administration of adrenaline were measured as a means of assessing cardiovascular reactivity in intact anaesthetized dogs, before and at 3 hours and 3 days after the rapid production of anaemia by a dextran-for-blood exchange. Three types of experiments were carried out. In experiments A and B, 2.0 and 5.0 μg/kg of adrenaline (respectively) were injected intravenously before and at both periods after exchange, and the changes in arterial blood pressure were assessed. In experiment B the changes in the arterial plasma concentration of potassium and sodium were also measured. In experiment C, several cardiovascular parameters, including cardiac output (Fick method), arterial pressure, and heart rate, were measured before and at the end of a 15-minute infusion of adrenaline in a dose of 0.2 μg/kg minute. In all three experiments, evidence of a reduced cardiovascular response to adrenaline was found when the dogs were anaemic; and in experiment B the adrenaline-induced hyperkalaemia and hyponatraemia were found to be significantly reduced during anaemia.The mechanism of the hyporeactivity to adrenaline during anaemia is not clear, but may include changes in blood volume, electrolyte disturbances, and severe anoxia.


2013 ◽  
Vol 305 (2) ◽  
pp. R164-R170 ◽  
Author(s):  
D. Xu ◽  
J. K. Shoemaker ◽  
A. P. Blaber ◽  
P. Arbeille ◽  
K. Fraser ◽  
...  

Limited data are available to describe the regulation of heart rate (HR) during sleep in spaceflight. Sleep provides a stable supine baseline during preflight Earth recordings for comparison of heart rate variability (HRV) over a wide range of frequencies using both linear, complexity, and fractal indicators. The current study investigated the effect of long-duration spaceflight on HR and HRV during sleep in seven astronauts aboard the International Space Station up to 6 mo. Measurements included electrocardiographic waveforms from Holter monitors and simultaneous movement records from accelerometers before, during, and after the flights. HR was unchanged inflight and elevated postflight [59.6 ± 8.9 beats per minute (bpm) compared with preflight 53.3 ± 7.3 bpm; P < 0.01]. Compared with preflight data, HRV indicators from both time domain and power spectral analysis methods were diminished inflight from ultralow to high frequencies and partially recovered to preflight levels after landing. During inflight and at postflight, complexity and fractal properties of HR were not different from preflight properties. Slow fluctuations (<0.04 Hz) in HR presented moderate correlations with movements during sleep, partially accounting for the reduction in HRV. In summary, substantial reduction in HRV was observed with linear, but not with complexity and fractal, methods of analysis. These results suggest that periodic elements that influence regulation of HR through reflex mechanisms are altered during sleep in spaceflight but that underlying system complexity and fractal dynamics were not altered.


1987 ◽  
Vol 62 (3) ◽  
pp. 1186-1191 ◽  
Author(s):  
J. W. Kozelka ◽  
G. W. Christy ◽  
R. D. Wurster

The ascending spinal pathways mediating somatocardiovascular reflexes during exercise were studied in unanesthetized dogs by placing lesions in the lumbar spinal cord. After training to run on a treadmill with hindlimbs only, 20 dogs were anesthetized and instrumented using sterile surgical techniques. To chronically record heart rate and arterial blood pressure, the aorta was cannulated via the omocervical artery. To test the intactness of descending spinal sympathetic pathways, reflex pressor responses to baroreceptor hypotension were produced by bilateral carotid arterial occlusion using pneumatic vessel occluders placed around the common carotid arteries. To generate transient ischemic exercise (120 s), a pneumatic occluder was placed around the left iliac artery. Eight to 10 days after instrumentation, blood pressure and heart rate were monitored at rest and during hindlimb running with and without simultaneous iliac arterial occlusion. The modest pressor response and tachycardia elicited by hindlimb exercise were markedly augmented by simultaneous hindlimb ischemia (i.e., iliac arterial occlusion). Lesion placement in the dorsolateral sulcus area and the dorsolateral funiculus at L2 significantly reduced the blood pressure and heart rate responses to simultaneous exercise occlusion. The cardiovascular responses to nonischemic exercise and bilateral carotid arterial occlusion were not altered by such spinal sections. It is concluded that in the dog the ascending spinal pathways mediating cardiovascular responses to ischemic exercise are located in the lateral funiculus, including the dorsolateral sulcus area and dorsolateral funiculus.


2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.


1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.


1964 ◽  
Vol 207 (3) ◽  
pp. 634-640 ◽  
Author(s):  
Emmett S. Manley ◽  
Clinton B. Nash ◽  
R. A. Woodbury

Dogs under pentobarbital anesthesia were employed in an investigation of the effect of abrupt, severe hypercapnia upon blood pressure, heart rate, and force of myocardial contraction. Electrocardiographic activity and arterial blood pH were also monitored. Hypercapnia was induced for 10-min periods with 15 and 30% CO2 in oxygen. The studies were undertaken in nontreated animals and animals treated with atropine, reserpine, chlorisondamine, P-286, or bilateral adrenalectomy. Severe hypercapnia was shown to be depressant to the cardiovascular parameters evaluated, but blood pressure and contractile force normally demonstrated compensation to this depression. Parasympathetic blockade with atropine did not reduce the depression observed in the nontreated dogs during hypercapnia. Results obtained with other pretreated animals indicate that compensation occurs primarily via sympathetic activation. Adrenal activation may assume importance in compensation to 30% CO2, but intact adrenals were not necessary for survival during hypercapnia. No arrhythmias (excluding bradycardia) were observed during or immediately following exposure to either concentration of CO2.


1992 ◽  
Vol 263 (5) ◽  
pp. R1104-R1109 ◽  
Author(s):  
C. L. Stebbins

Peripheral vasopressin (AVP) can act centrally to sensitize the arterial baroreflex and/or peripherally to attenuate regional blood flow by a direct vascular effect. Because plasma concentrations of AVP increase during exercise, this study examined the possibility that AVP is capable of modulating the reflex cardiovascular response to static muscle contraction. Thus, in anesthetized cats, the pressor [mean arterial pressure (MAP)], myocardial contractile (dP/dt), and heart rate responses to 30-45 s of electrically induced static contraction of the hindlimb muscles were compared before and after intravenous injection of the V1 receptor antagonist d[CH2)5Tyr(Me)]-AVP (V1-x, n = 7), V1-x plus the V2 receptor antagonist [d(CH2)5,D-Phe2,Ile4,Arg8,Ala9]vasopressin (V2-x, n = 5), or the ganglionic blocker hexamethonium chloride (n = 5). In three additional cats, the contraction-induced cardiovascular response was monitored before and after injection of V1-x + V2-x and after hexamethonium. Subsequent to treatment with V1-x, the MAP and dP/dt responses to contraction were augmented by 18 +/- 5 and 22 +/- 10%, respectively (P < 0.05). After injection of V1-x + V2-x, the MAP and dP/dt responses were augmented to a similar extent (32 +/- 6 and 40 +/- 17%, respectively; P < 0.05). However, there was no difference in the magnitude of augmentation of these responses between the two conditions. The heart rate response was not altered by either treatment. Ganglionic blockade eliminated the cardiovascular responses to contraction. Last, when the pressor and contractile responses to contraction were initially augmented by administration of V1-x + V2-x, subsequent ganglionic blockade abolished the entire cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)


1984 ◽  
Vol 56 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
K. J. Dormer

Mongrel dogs (n = 34) were used to record the cardiovascular responses during submaximal exercise-tolerance tests (ETT) before and after the placement of lesions in rostral portions of the cerebellar fastigial nucleus (FN). Sterile surgical procedures were used to implant solid-state pressure transducers into the left ventricle or descending aorta (anesthesia 1% halothane in O2) and multipolar stainless steel electrodes into FN (anesthesia alpha-chloralose 115 mg/kg iv). Heart rate (HR), maximal left ventricular systolic pressure ( LVPmax ) and its first derivative ( dLVP /dt), and mean arterial blood pressure (MAP) were recorded during a motorized treadmill ETT. Electrolytic direct-current or radio-frequency lesions were made through the indwelling FN electrodes, and the ETT was repeated following 10–14 days recovery. Two-way analysis of variance (ANOVA), with repeated measures on one, and one-way ANOVA for simple effects indicated a significant reduction in HR and MAP (P less than 0.01) but not LVPmax and dLVP /dt occurred during exercise as a result of rostral FN lesions. Although the trend for reduced LVPmax and dLVP /dt was also evident, a relatively greater decrease in blood pressure occurred in the peripheral vasculature during exercise. It was concluded that FN acts as a modulator of HR and MAP during dynamic exercise because of the observed deficits, and because FN is known to both send efferent projections to medullary vasomotor areas and receive projections from motor cortex and muscle and joint afferents.


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