TY - JOUR
T1 - Time course of compensatory physiological responses to central hypovolemia in high-and low-tolerant human subjects
AU - Xiang, Lusha
AU - Hinojosa-Laborde, Carmen
AU - Ryan, Kathy L.
AU - Rickards, Caroline A.
AU - Convertino, Victor A.
N1 - Funding Information:
This study was funded by the United States Army Medical Research and Materiel Command.
Publisher Copyright:
© 2018 American Physiological Society. All rights reserved.
PY - 2018/8/20
Y1 - 2018/8/20
N2 - Lower body negative pressure (LBNP) simulates hemorrhage in human subjects. Most subjects (67%) exhibited high tolerance (HT) to hypovolemia, while the remainder (33%) had low tolerance (LT). To investigate the mechanisms for decompensation to central hypovolemia in HT and LT subjects, we characterized the time course of total peripheral resistance (TPR), heart rate (HR), and muscle sympathetic nerve activity (MSNA) during LBNP to tolerance determined by the onset of decompensation (presyncope, PS). We hypothesized that 1) maximum (Max) TPR, HR, and MSNA would coincide, and 2) PS would result from simultaneous decreases in TPR, HR, and MSNA in LT and HT subjects but occur earlier in LT than in HT subjects. Max TPR was lower and occurred earlier in LT (n = 59) than in HT (n = 113) subjects (LT: 24 ± 1 mmHg·min·1−1 at 756 ± 31 s; HT: 28 ± 1 mmHg·min·1−1 at 1,265 ± 37 s, P < 0.01). Max TPR occurred several minutes before PS. During subsequent decrease in TPR, HR and MSNA continued to increase. Max HR (LT: 111 ± 2 beat/min at 923 ± 27 s; HT: 130 ± 2 beats/min at 1489 ± 23 s, P < 0.01) occurred several seconds before PS. Higher MSNA (P < 0.01) was attained in HT (n = 10; 51 ± 5 bursts/min at max TPR; 54 ± 5 bursts/min at max HR) than LT subjects (n = 4; 41 ± 8 bursts/min at max TPR; 39 ± 8 bursts/min at max HR). The onset of cardiovascular decompensation is a biphasic process in which vasodilation occurs before bradycardia and sympathetic withdrawal. This pattern was similar in LT and HT but occurred earlier in LT subjects. We conclude that sudden bradycardia plays a critical role in the determination of tolerance to central hypovolemia.
AB - Lower body negative pressure (LBNP) simulates hemorrhage in human subjects. Most subjects (67%) exhibited high tolerance (HT) to hypovolemia, while the remainder (33%) had low tolerance (LT). To investigate the mechanisms for decompensation to central hypovolemia in HT and LT subjects, we characterized the time course of total peripheral resistance (TPR), heart rate (HR), and muscle sympathetic nerve activity (MSNA) during LBNP to tolerance determined by the onset of decompensation (presyncope, PS). We hypothesized that 1) maximum (Max) TPR, HR, and MSNA would coincide, and 2) PS would result from simultaneous decreases in TPR, HR, and MSNA in LT and HT subjects but occur earlier in LT than in HT subjects. Max TPR was lower and occurred earlier in LT (n = 59) than in HT (n = 113) subjects (LT: 24 ± 1 mmHg·min·1−1 at 756 ± 31 s; HT: 28 ± 1 mmHg·min·1−1 at 1,265 ± 37 s, P < 0.01). Max TPR occurred several minutes before PS. During subsequent decrease in TPR, HR and MSNA continued to increase. Max HR (LT: 111 ± 2 beat/min at 923 ± 27 s; HT: 130 ± 2 beats/min at 1489 ± 23 s, P < 0.01) occurred several seconds before PS. Higher MSNA (P < 0.01) was attained in HT (n = 10; 51 ± 5 bursts/min at max TPR; 54 ± 5 bursts/min at max HR) than LT subjects (n = 4; 41 ± 8 bursts/min at max TPR; 39 ± 8 bursts/min at max HR). The onset of cardiovascular decompensation is a biphasic process in which vasodilation occurs before bradycardia and sympathetic withdrawal. This pattern was similar in LT and HT but occurred earlier in LT subjects. We conclude that sudden bradycardia plays a critical role in the determination of tolerance to central hypovolemia.
KW - Blood pressure
KW - Cardiac output
KW - Heart rate
KW - Hypovolemia
KW - Stroke volume
KW - Sympathetic activity
KW - Tolerance
KW - Total peripheral resistance
UR - http://www.scopus.com/inward/record.url?scp=85052086941&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.00361.2017
DO - 10.1152/ajpregu.00361.2017
M3 - Article
C2 - 29668322
AN - SCOPUS:85052086941
SN - 0363-6119
VL - 315
SP - R408-R416
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 2
ER -