Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans

Convertino, Víctor A.; Sather, Tom M.

doi:10.1046/j.1365-2281.2000.00244.x

Cited by 65 publications

(68 citation statements)

References 27 publications

(37 reference statements)

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“…Understanding cerebral hemodynamic responses to blood loss is an essential target for improving survival to hemorrhagic injury, and developing effective therapeutic interventions (35). As there is considerable variability in survival time following hemorrhagic injuries (40), as well as tolerance to simulated hemorrhage (7,15,24,26), it is crucial to determine the role of cerebral blood flow (CBF) and oxygenation on the ability to tolerate severe blood loss.Lower body negative pressure (LBNP) has been extensively utilized as an experimental technique to induce physiologically significant central hypovolemia, and can be used to simulate preshock hemorrhage in humans (4, 9, 44, 51). Two recent studies reported comparable hemodynamic responses to LBNP and blood loss up to 1,000 ml in humans (21, 36) and 25% loss of total blood volume in baboons (17).…”

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“…able variability in survival time following hemorrhagic injuries (40), as well as tolerance to simulated hemorrhage (7,15,24,26), it is crucial to determine the role of cerebral blood flow (CBF) and oxygenation on the ability to tolerate severe blood loss.…”

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The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

Kay

Rickards

2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Kay VL, Rickards CA. The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia. Am J Physiol Regul Integr Comp Physiol 310: R375-R383, 2016. First published December 16, 2015 doi:10.1152/ajpregu.00367.2015Tolerance to central hypovolemia is highly variable, and accumulating evidence suggests that protection of anterior cerebral blood flow (CBF) is not an underlying mechanism. We hypothesized that individuals with high tolerance to central hypovolemia would exhibit protection of cerebral oxygenation (ScO2), and prolonged preservation of CBF in the posterior vs. anterior cerebral circulation. Eighteen subjects (7 male/11 female) completed a presyncope-limited lower body negative pressure (LBNP) protocol (3 mmHg/min onset rate). ScO2 (via near-infrared spectroscopy), middle cerebral artery velocity (MCAv), posterior cerebral artery velocity (PCAv) (both via transcranial Doppler ultrasound), and arterial pressure (via finger photoplethysmography) were measured continuously. Subjects who completed Ն70 mmHg LBNP were classified as high tolerant (HT; n ϭ 7) and low tolerant (LT; n ϭ 11) if they completed Յ60 mmHg LBNP. The minimum difference in LBNP tolerance between groups was 193 s (LT ϭ 1,243 Ϯ 185 s vs. HT ϭ 1,996 Ϯ 212 s; P Ͻ 0.001; Cohen's d ϭ 3.8). Despite similar reductions in mean MCAv in both groups, ScO2 decreased in LT subjects from Ϫ15 mmHg LBNP (P ϭ 0.002; Cohen's dϭ1.8), but was maintained at baseline values until Ϫ75 mmHg LBNP in HT subjects (P Ͻ 0.001; Cohen's d ϭ 2.2); ScO2 was lower at Ϫ30 and Ϫ45 mmHg LBNP in LT subjects (P Յ 0.02; Cohen's d Ն 1.1). Similarly, mean PCAv decreased below baseline from Ϫ30 mmHg LBNP in LT subjects (P ϭ 0.004; Cohen's d ϭ 1.0), but remained unchanged from baseline in HT subjects until Ϫ75 mmHg (P ϭ 0.006; Cohen's d ϭ 2.0); PCAv was lower at Ϫ30 and Ϫ45 mmHg LBNP in LT subjects (P Յ 0.01; Cohen's d Ն 0.94). Individuals with higher tolerance to central hypovolemia exhibit prolonged preservation of CBF in the posterior cerebral circulation and sustained cerebral tissue oxygenation, both associated with a delay in the onset of presyncope.posterior cerebral artery; middle cerebral artery; lower body negative pressure HEMORRHAGE DUE TO TRAUMA IS one of the leading causes of morbidity and mortality worldwide in both the civilian and military settings (1, 2, 13, 22, 32). A major factor contributing to death and disability from severe blood loss is poor tissue perfusion and oxygenation of the vital organs (1, 13, 22). Prolonged cerebral hypoperfusion can lead to neuronal cell death, and if the patient survives, long-term cognitive impairment and physical disability (32). Understanding cerebral hemodynamic responses to blood loss is an essential target for improving survival to hemorrhagic injury, and developing effective therapeutic interventions (35). As there is considerable variability in survival time following hemorrhagic injuries (40), as well as tolerance to simulated hemorrhage (7,15,24,26), it is crucial to determine the rol...

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The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

Kay

Rickards

2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, similar BP responses during HUT were reported in healthy subjects by Gabbett et al [29], who conducted a 90°HUT test on young males, and observed that a BP overshoot in an early stage of HUT to about 10 mmHg above the supine value. It has been widely accepted that considerable individual variations exist in orthostatic tolerance [25,26,30,31]. Accordingly, we assume that the BP overshoot response observed in both subject groups probably reflects great individual variations in orthostatic tolerance.…”

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“…Furthermore, DSBP was significantly higher during the first 2 min of HUT in the nurse group than in the control group. Orthostatic tolerance depends on physical factors such as height, plasma volume, arterial and cardiopulmonary baroreflex sensitivity, cardiac filling, or stroke volume [18,[24][25][26]. Furthermore, brain blood flow is a critical factor for syncope [27,28].…”

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Arterial blood pressure response to head-up tilt test and orthostatic tolerance in nurses

Onizuka

Niimi²,

Sato

et al. 2015

Environ Health Prev Med

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Objectives High tolerance to postural changes was examined in nurses. Methods Twelve female nurses and 12 healthy controls underwent a 70°head-up tilt (HUT) test for 10 min. Blood pressure (BP), heart rate (HR), pulse pressure, and hormone levels were measured. Baroreceptor sensitivity (BRS) was calculated using a sequence technique. Results HR increased during HUT in both subject groups, with no difference between groups. Systolic BP was rapidly increased by HUT in both subject groups, and was higher in the nurse group than in the control group during the first 2 min of HUT. Pulse pressure decreased during 1-2.5 min of HUT in the control group, but there was no decrease in the nurse group. BRS was decreased by HUT in the nurse group, while it tended to be decreased in the control group. Both during baseline and HUT, BRS was lower in the nurse group than in the control group. Plasma noradrenaline increased with HUT, and the increase was greater in the nurse group than in the control group. Conclusions Although nurse subjects had a lower BRS during HUT than control subjects, they were able to effectively maintain BP during HUT, suggesting that nurse subjects had higher orthostatic tolerance. The better maintenance of BP in nurse subjects appeared to be associated with a compensatory mechanism other than the arterial baroreflex and/or a hemodynamic mechanism.

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Cerebral Blood‐Flow Regulation During Hemorrhage

Rickards

2015

Comprehensive Physiology

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Massive uncontrolled blood loss can occur under a variety of conditions including trauma, as a complication of childbirth or surgery, ruptured ulcers, clotting disorders, and hemorrhagic fevers. Across the continuum of hemorrhage, loss of blood volume is a significant challenge to the maintenance of cerebral perfusion. During the initial stages of hemorrhage, reflex mechanisms are activated to protect cerebral perfusion, but persistent blood loss will eventually reduce global cerebral blood flow and the delivery of metabolic substrates, leading to generalized cerebral ischemia, hypoxia, and ultimately, neuronal cell death. Cerebral blood flow is controlled by various regulatory mechanisms, including prevailing arterial pressure, intracranial pressure, arterial blood gases, neural activity, and metabolic demand. Hemorrhage represents a unique physiological stress to the brain, as it influences each of these regulatory mechanisms, resulting in complex interplay that ultimately challenges the ability of the brain to maintain adequate perfusion. Early studies of actual hemorrhage in humans employed blood loss protocols up to 1000 mL, but did not include any measurements of cerebral blood flow. As ethical considerations necessarily constrain the use of human volunteers for massive blood loss studies that induce irreversible shock, most of what is known about cerebral blood-flow responses to hemorrhage has been determined from animal models. Limitations of species differences regarding regulatory mechanisms, anatomy, and the effect of anesthesia, however, must be considered. Advances in monitoring technologies, and a recent renewed interest in understanding cerebral blood-flow regulation in humans, however, is rapidly accelerating knowledge in this field.

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Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans

Cited by 65 publications

References 27 publications

The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

Arterial blood pressure response to head-up tilt test and orthostatic tolerance in nurses

Cerebral Blood‐Flow Regulation During Hemorrhage

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