Mechanisms of postspaceflight orthostatic hypotension: low α1-adrenergic receptor responses before flight and central autonomic dysregulation postflight

2004 ◽  
Vol 286 (4) ◽  
pp. H1486-H1495 ◽  
Author(s):  
Janice V. Meck ◽  
Wendy W. Waters ◽  
Michael G. Ziegler ◽  
Heidi F. deBlock ◽  
Paul J. Mills ◽  
...  

Although all astronauts experience symptoms of orthostatic intolerance after short-duration spaceflight, only ∼20% actually experience presyncope during upright posture on landing day. The presyncopal group is characterized by low vascular resistance before and after flight and low norepinephrine release during orthostatic stress on landing day. Our purpose was to determine the mechanisms of the differences between presyncopal and nonpresyncopal groups. We studied 23 astronauts 10 days before launch, on landing day, and 3 days after landing. We measured pressor responses to phenylephrine injections; norepinephrine release with tyramine injections; plasma volumes; resting plasma levels of chromogranin A (a marker of sympathetic nerve terminal release), endothelin, dihydroxyphenylglycol (DHPG, an intracellular metabolite of norepinephrine); and lymphocyte β2-adrenergic receptors. We then measured hemodynamic and neurohumoral responses to upright tilt. Astronauts were separated into two groups according to their ability to complete 10 min of upright tilt on landing day. Compared with astronauts who were not presyncopal on landing day, presyncopal astronauts had 1) significantly smaller pressor responses to phenylephrine both before and after flight; 2) significantly smaller baseline norepinephrine, but significantly greater DHPG levels, on landing day; 3) significantly greater norepinephrine release with tyramine on landing day; and 4) significantly smaller norepinephrine release, but significantly greater epinephrine and arginine vasopressin release, with upright tilt on landing day. These data suggest that the etiology of orthostatic hypotension and presyncope after spaceflight includes low α1-adrenergic receptor responsiveness before flight and a remodeling of the central nervous system during spaceflight such that sympathetic responses to baroreceptor input become impaired.

1996 ◽  
Vol 81 (5) ◽  
pp. 2134-2141 ◽  
Author(s):  
Janice M. Fritsch-Yelle ◽  
Peggy A. Whitson ◽  
Roberta L. Bondar ◽  
Troy E. Brown

Fritsch-Yelle, Janice M., Peggy A. Whitson, Roberta L. Bondar, and Troy E. Brown. Subnormal norepinephrine release relates to presyncope in astronauts after spaceflight. J. Appl. Physiol. 81(5): 2134–2141, 1996.—Postflight orthostatic intolerance is experienced by virtually all astronauts but differs greatly in degree of severity. We studied cardiovascular responses to upright posture in 40 astronauts before and after spaceflights lasting up to 16 days. We separated individuals according to their ability to remain standing without assistance for 10 min on landing day. Astronauts who could not remain standing on landing day had significantly smaller increases in plasma norepinephrine levels with standing than did those who could remain standing (105 ± 41 vs. 340 ± 62 pg/ml; P = 0.05). In addition, they had significantly lower standing peripheral vascular resistance (23 ± 3 vs. 34 ± 3 mmHg ⋅ l−1⋅ min; P = 0.02) and greater decreases in systolic (−28 ± 4 vs. −11 ± 3 mmHg; P = 0.002) and diastolic (−14 ± 7 vs. 3 ± 2 mmHg; P = 0.0003) pressures. The presyncopal group also had significantly lower supine (16 ± 1 vs. 21 ± 2 mmHg ⋅ l−1⋅ min; P = 0.04) and standing (23 ± 2 vs. 32 ± 2 mmHg ⋅ l−1⋅ min; P = 0.038) vascular resistance, supine (66 ± 2 vs. 73 ± 2 mmHg; P = 0.008) and standing (69 ± 4 vs. 77 ± 2 mmHg; P = 0.007) diastolic pressure, and supine (109 ± 3 vs. 114 ± 2 mmHg; P = 0.05) and standing (99 ± 4 vs. 108 ± 3 mmHg; P = 0.006) systolic pressures before flight. This is the first study to clearly document these differences among presyncopal and nonpresyncopal astronauts after spaceflight and also offer the possibility of preflight prediction of postflight susceptibility. These results clearly point to hypoadrenergic responsiveness, possibly centrally mediated, as a contributing factor in postflight orthostatic intolerance. They may provide insights into autonomic dysfunction in Earthbound patients.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Chaisith Sivakorn ◽  
Polrat Wilairatana ◽  
Srivicha Krudsood ◽  
Marcus J. Schultz ◽  
Tachpon Techarang ◽  
...  

AbstractImpaired autonomic control of postural homeostasis resulting in orthostatic hypotension has been described in falciparum malaria. However, severe orthostatic intolerance in Plasmodium vivax has been rarely reported. A case of non-immune previously healthy Thai woman presenting with P. vivax infection with well-documented orthostatic hypotension is described. In addition to oral chloroquine and intravenous artesunate, the patient was treated with fluid resuscitation and norepinephrine. During hospitalization, her haemodynamic profile revealed orthostatic hypotension persisting for another three days after microscopic and polymerase chain reaction confirmed parasite clearance. Potential causes are discussed.


2021 ◽  
Vol 8 ◽  
pp. 100071
Author(s):  
Elena M. Christopoulos ◽  
Jennifer Tran ◽  
Sarah L. Hillebrand ◽  
Peter W. Lange ◽  
Rebecca K. Iseli ◽  
...  

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 642
Author(s):  
Bianca Brix ◽  
Olivier White ◽  
Christian Ure ◽  
Gert Apich ◽  
Paul Simon ◽  
...  

Background: Lymphedema arises due to a malfunction of the lymphatic system, leading to extensive tissue swelling. Complete decongestive therapy (CDT), which is a physical therapy lasting for 3 weeks and includes manual lymphatic drainages (MLD), leads to fluid mobilization and increases in plasma volume. Here, we investigated hemodynamic responses induced by these fluid shifts due to CDT and MLD. Methods: Hemodynamic parameters were assessed continuously during a sit-to-stand test (5 min baseline, 5 min of standing, and 5 min of recovery). This intervention was repeated on days 1, 2, 7, 14, and 21 of CDT, before and after MLD. Volume regulatory hormones were assessed in plasma samples. Results: A total number of 13 patients took part in this investigation. Resting diastolic blood pressure significantly decreased over three weeks of CDT (p = 0.048). No changes in baseline values were shown due to MLD. However, MLD led to a significant decrease in heart rate during orthostatic loading over all epochs on therapy day 14, as well as day 21. Volume regulatory hormones did not show changes over lymphedema therapy. Conclusion: We did not observe any signs of orthostatic hypotension at rest, as well as during to CDT, indicating that lymphedema patients do not display an elevated risk of orthostatic intolerance. Although baseline hemodynamics were not affected, MLD has shown to have potential beneficial effects on hemodynamic responses to a sit-to-stand test in patients undergoing lymphedema therapy.


1992 ◽  
Vol 25 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Motohisa Kaneko ◽  
Tomoyuki Kanno ◽  
Kyoichi Honda ◽  
Hirobumi Mashiko ◽  
Nobuyoshi Oosuga ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-8
Author(s):  
Qianli Tang ◽  
Qiuyan Jiang ◽  
Suren R. Sooranna ◽  
Shike Lin ◽  
Yuanyuan Feng ◽  
...  

To observe the effects of electroacupuncture on pain threshold of laboring rats and the expression of norepinephrine transporter andα2 adrenergic receptor in the central nervous system to determine the mechanism of the analgesic effect of labor. 120 pregnant rats were divided into 6 groups: a control group, 4 electroacupuncture groups, and a meperidine group. After interventions, the warm water tail-flick test was used to observe pain threshold. NE levels in serum, NET, andα2AR mRNA and protein expression levels in the central nervous system were measured. No difference in pain threshold was observed between the 6 groups before intervention. After intervention, increased pain thresholds were observed in all groups except the control group with a higher threshold seen in the electroacupuncture groups. Serum NE levels decreased in the electroacupuncture and MP groups. Increases in NET andα2AR expression in the cerebral cortex and decreases in enlarged segments of the spinal cord were seen. Acupuncture increases uptake of NE via cerebral NET and decreases its uptake by spinal NET. The levels ofα2AR are also increased and decreased, respectively, in both tissues. This results in a decrease in systemic NE levels and may be the mechanism for its analgesic effects.


Circulation ◽  
2000 ◽  
Vol 102 (1) ◽  
pp. 96-103 ◽  
Author(s):  
Chang-seng Liang ◽  
Naomi Kenmotsu Rounds ◽  
Erdan Dong ◽  
Suzanne Y. Stevens ◽  
Junya Shite ◽  
...  

2001 ◽  
Vol 281 (2) ◽  
pp. R375-R380 ◽  
Author(s):  
Heidi L. Collins ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo

We tested the hypothesis that central arginine vasopressin (AVP) mediates postexercise reductions in arterial pressure (AP) and heart rate (HR). To test this hypothesis, nine spontaneously hypertensive rats (SHR) were instrumented with a 22-gauge stainless steel guide cannula in the right lateral cerebral ventricle and with a carotid arterial catheter. After the rats recovered, AP and HR were assessed before and after a single bout of dynamic exercise with the central administration of vehicle or the selective AVP V1-receptor antagonist d(CH3)5Tyr(Me)-AVP (AVP-X). AP and HR were significantly decreased below preexercise values with central administration of vehicle [ P < 0.05, change (Δ)−21 ± 4 mmHg and Δ−20 ± 6 beats/min, respectively]. In sharp contrast, after exercise with central administration of AVP-X, both AP (Δ+8 ± 5 mmHg) and HR (Δ+24 ± 9 beats/min) were not significantly different from preexercise values ( P > 0.05). Furthermore, AVP-X at rest did not significantly alter AP (181 ± 11 vs. 178 ± 11 mmHg, P > 0.05) or HR (328 ± 24 vs. 331 ± 22 beats/min, P > 0.05). Thus central blockade of AVP V1 receptors prevented postexercise reductions in AP and HR. These data suggest that AVP, acting within the central nervous system, mediates postexercise reductions in AP and HR in the SHR.


1993 ◽  
Vol 264 (4) ◽  
pp. H1259-H1268 ◽  
Author(s):  
N. Uemura ◽  
D. E. Vatner ◽  
Y. T. Shen ◽  
J. Wang ◽  
S. F. Vatner

The goal of this study was to determine whether enhanced vascular responsiveness during the development of perinephritic hypertension is selective or nonspecific. The effects of graded infusions of norepinephrine (NE), phenylephrine (PE), angiotensin II (ANG II), and vasopressin (VP) were examined on mean arterial pressure, total peripheral resistance (TPR), and aortic pressure-diameter relationships in conscious dogs. NE increased TPR significantly greater (P < 0.01) in hypertension than normotension, as did PE infusion, whereas ANG II and VP increased TPR similarly before and after hypertension. Analysis of aortic pressure-diameter relationships also demonstrated significant (P < 0.05) shifts in response to NE and PE, but not ANG II and VP, during the development of hypertension. In normotensive dogs, low doses of ANG II infusion also enhanced the vasoconstrictor response not only to NE and PE but also to VP. In contrast to what was observed in hypertension, in the presence of ANG II infusion after ganglionic blockade, enhanced responses to PE and NE were no longer observed. The alpha 1-adrenergic receptor density in membrane preparations from aortic tissue, as determined by [3H]prazosin binding, was higher (P < 0.05) in hypertensive dogs than control dogs. Thus the vascular responsiveness in the aorta and resistance vessels is enhanced to alpha 1-adrenergic stimulation, but not to all vasoconstrictors, during developing perinephritic hypertension. The mechanism appears to involve increased alpha 1-adrenergic receptor density.


1962 ◽  
Vol 203 (5) ◽  
pp. 961-963 ◽  
Author(s):  
Mohinder P. Sambhi ◽  
Max H. Weil ◽  
Vasant N. Udhoji

Pressor responses produced by intravenous injections of graded doses of norepinephrine were recorded in ten normal subjects before and after pharmacologic doses of glucocorticoids. Two subjects had been pretreated with 9α-fluorocortisol. Although a considerable variation was found in the responsiveness to repeated norepinephrine injections, variance analysis demonstrated that administration of adrenal cortical hormones and their analogues did not significantly alter the response. These observations do not support the hypothesis that acute administration of corticosteroids in large doses potentiates the pressor effects of catecholamines in the human subject with normal adrenal function.


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