TY - JOUR
T1 - Autonomic mechanisms associated with heart rate and vasoconstrictor reserves
AU - Convertino, Victor A.
AU - Rickards, Caroline A.
AU - Ryan, Kathy L.
N1 - Funding Information:
Acknowledgments We thank the experimental subjects for their cheerful cooperation, as well as Mr Gary Muniz for his superb technical assistance and Drs John McManus, Girish Sethuraman, Keith Berry, Steven Glorsky and Robert Gerhardt for their assistance with physical examinations and medical monitoring of the subjects. This research was supported by funding from the US Army Combat Casualty Care Research Program. The opinions or assertions contained herein are the private views of the author and are not to be construed as official or as reflecting the views of the US Department of the Army or the US Department of Defense.
PY - 2012/6
Y1 - 2012/6
N2 - Introduction Hemorrhage is accompanied by baroreflexmediated 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 RRISAP 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 B 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.
AB - Introduction Hemorrhage is accompanied by baroreflexmediated 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 RRISAP 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 B 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.
KW - Cardiac vagal control
KW - Hemorrhage
KW - Lower body negative pressure
KW - Sympathetic nerve activity
UR - http://www.scopus.com/inward/record.url?scp=84863718572&partnerID=8YFLogxK
U2 - 10.1007/s10286-011-0151-5
DO - 10.1007/s10286-011-0151-5
M3 - Article
C2 - 22083580
AN - SCOPUS:84863718572
SN - 0959-9851
VL - 22
SP - 123
EP - 130
JO - Clinical Autonomic Research
JF - Clinical Autonomic Research
IS - 3
ER -