Time course of compensatory physiological responses to central hypovolemia in high-and low-tolerant human subjects

Lusha Xiang, Carmen Hinojosa-Laborde, Kathy L. Ryan, Caroline Alice Rickards, Victor A. Convertino

Research output: Contribution to journalArticleResearchpeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)R408-R416
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume315
Issue number2
DOIs
StatePublished - 20 Aug 2018

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Hypovolemia
Vascular Resistance
Heart Rate
Syncope
Myocardium
Lower Body Negative Pressure
Bradycardia
Central Tolerance
Vasodilation
Hemorrhage
Muscles

Keywords

  • Blood pressure
  • Cardiac output
  • Heart rate
  • Hypovolemia
  • Stroke volume
  • Sympathetic activity
  • Tolerance
  • Total peripheral resistance

Cite this

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title = "Time course of compensatory physiological responses to central hypovolemia in high-and low-tolerant human subjects",
abstract = "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.",
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Time course of compensatory physiological responses to central hypovolemia in high-and low-tolerant human subjects. / Xiang, Lusha; Hinojosa-Laborde, Carmen; Ryan, Kathy L.; Rickards, Caroline Alice; Convertino, Victor A.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 315, No. 2, 20.08.2018, p. R408-R416.

Research output: Contribution to journalArticleResearchpeer-review

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 Alice

AU - Convertino, Victor A.

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

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U2 - 10.1152/ajpregu.00361.2017

DO - 10.1152/ajpregu.00361.2017

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SP - R408-R416

JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

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