Autonomic mechanisms associated with heart rate and vasoconstrictor reserves

Convertino, Víctor A.; Rickards, Caroline A.; Ryan, Kathy L.

doi:10.1007/s10286-011-0151-5

Cited by 74 publications

(86 citation statements)

References 41 publications

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“…Since stroke volume and compensatory reserve are both calculated from features of the arterial waveform, there was a high correlation between the two measures. However, consistent with previous observations in humans (6,9,25), data from this study reaffirmed that stroke volume failed to distinguish low-from high-tolerant baboons (Fig. 4A).…”

Section: Discussionsupporting

confidence: 92%

Comparison of compensatory reserve during lower-body negative pressure and hemorrhage in nonhuman primates

Hinojosa‐Laborde

Howard

Mulligan

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Hinojosa-Laborde C, Howard JT, Mulligan J, Grudic GZ, Convertino VA. Comparison of compensatory reserve during lowerbody negative pressure and hemorrhage in nonhuman primates. Am J Physiol Regul Integr Comp Physiol 310: R1154 -R1159, 2016. First published March 30, 2016 doi:10.1152/ajpregu.00304.2015.-Compensatory reserve was measured in baboons (n ϭ 13) during hemorrhage (Hem) and lower-body negative pressure (LBNP) using a machine-learning algorithm developed to estimate compensatory reserve by detecting reductions in central blood volume during LBNP. The algorithm calculates compensatory reserve index (CRI) from normovolemia (CRI ϭ 1) to cardiovascular decompensation (CRI ϭ 0). The hypothesis was that Hem and LBNP will elicit similar CRI values and that CRI would have higher specificity than stroke volume (SV) in predicting decompensation. Blood was removed in four steps: 6.25%, 12.5%, 18.75%, and 25% of total blood volume. Four weeks after Hem, the same animals were subjected to four levels of LBNP that was matched on the basis of their central venous pressure. Data These data support the hypothesis that Hem and LBNP elicited the same CRI response, suggesting that measurement of compensatory reserve is superior to SV as a predictor of cardiovascular decompensation blood loss; central hypovolemia; stroke volume; blood pressure; compensatory mechanisms

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Section: Discussionsupporting

confidence: 92%

Comparison of compensatory reserve during lower-body negative pressure and hemorrhage in nonhuman primates

Hinojosa‐Laborde

Howard

Mulligan

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This notion is consistent with previous observations that individuals with HT to reductions in central blood volume display greater vagal withdrawal and elevations in sympathetic nerve activity. 28 …”

Section: Discussionmentioning

confidence: 97%

“…Perhaps more important is the reserve to withdraw vagal activity during reductions in central blood volume, a phenomenon that is represented by the reduction in BRS from baseline to the point of maximal tolerance (100% LBNP). 23,28 Thus, a lower reserve for cardiac vagal withdrawal of the carotid-cardiac baroreflex can be associated with reduced elevation in HR although the SBP has dropped. 28 The findings of the present study are consistent with this notion that reduced elevation in HR through 80% LBNP tolerance was the primary cause for the lower SI observed in LT subjects and was associated with blunted cardiac vagal withdrawal as indicated by a smaller difference between baseline and maximal BRS compared with HT subjects.…”

Section: Discussionmentioning

confidence: 98%

Physiologic mechanisms underlying the failure of the “shock index” as a tool for accurate assessment of patient status during progressive simulated hemorrhage

Schafer

Sickle²,

Hinojosa‐Laborde³

et al. 2013

Journal of Trauma and Acute Care Surgery

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“…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). It is well established that during the initial stages of progressive central hypovolemia, reflex cardiovascular responses are initiated (e.g., tachycardia, peripheral vasoconstriction) (5,6,15,19,24,38), protecting the vital organs from hypoperfusion. Although traditionally protection of absolute CBF was thought to be essential in determining tolerance to central hypovolemia (24), recent studies have indicated a disconnect between tolerance to LBNP and protection of absolute flow [predominantly assessed by middle cerebral artery velocity (MCAv), an index of global cerebral blood flow] (20, 27, 28, 37).…”

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confidence: 99%

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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Autonomic mechanisms associated with heart rate and vasoconstrictor reserves

Abstract: Our data support the hypothesis that greater physiological reserve capacity for tachycardia and vasoconstriction related to high tolerance to central hypovolemia is associated with greater reserves for sympathoexcitation and cardiac vagal withdrawal.

Cited by 74 publications

References 41 publications

Comparison of compensatory reserve during lower-body negative pressure and hemorrhage in nonhuman primates

Comparison of compensatory reserve during lower-body negative pressure and hemorrhage in nonhuman primates

Physiologic mechanisms underlying the failure of the “shock index” as a tool for accurate assessment of patient status during progressive simulated hemorrhage

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

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