Format

Send to

Choose Destination
See comment in PubMed Commons below
Clin Auton Res. 2012 Jun;22(3):123-30. doi: 10.1007/s10286-011-0151-5. Epub 2011 Nov 15.

Autonomic mechanisms associated with heart rate and vasoconstrictor reserves.

Author information

1
US Army Institute of Surgical Research, 3698 Chambers Pass, Fort Sam Houston, TX 78234-6315, USA. victor.convertino@amedd.army.mil

Abstract

INTRODUCTION:

Hemorrhage is accompanied by baroreflex-mediated tachycardia and vasoconstriction. The difference between baseline and maximum responses is defined as the heart rate (HR) and vasoconstrictor 'reserve'.

OBJECTIVE:

To test the hypothesis that higher HR and vasoconstrictor reserves in subjects with high tolerance (HT) to central hypovolemia is associated with greater reserve for sympathoexcitation and vagal withdrawal compared with low tolerant (LT) subjects.

METHODS:

R-R intervals (RRI), systolic arterial pressure (SAP), estimated stroke volume, and muscle sympathetic nerve activity (MSNA) were measured during lower body negative pressure (LBNP) designed to induce pre-syncope. Subjects with tolerance ≤ 60 mmHg LBNP were classified as LT (n = 22) while subjects who tolerated LBNP levels >60 mmHg were classified as HT (n = 56). Spontaneous cardiac baroreflex sensitivity (BRS) was assessed via RRI-SAP down-down sequences.

RESULTS:

HR reserve in HT subjects (+52 ± 2 bpm) was twofold greater (P < 0.001) than that in LT subjects (+27 ± 3 bpm). Vasoconstrictor reserve in the HT group (+3.4 ± 0.5 pru) was greater (P = 0.04) than that of the LT group (+1.9 ± 0.3 pru). HT subjects demonstrated greater (P ≤ 0.03) BRS reserve (-14.2 ± 1.8 ms/mmHg) and MSNA reserve (+41 ± 2 bursts/min) compared with LT subjects (-7.4 ± 1.7 ms/mmHg and +26 ± 7 bursts/min).

INTERPRETATION:

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.

PMID:
22083580
DOI:
10.1007/s10286-011-0151-5
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center