Beneficial effects of elevating cardiac preload on left-ventricular diastolic function and volume during heat stress: implications toward tolerance during a hemorrhagic insult

TY - JOUR

T1 - Beneficial effects of elevating cardiac preload on left-ventricular diastolic function and volume during heat stress

T2 - implications toward tolerance during a hemorrhagic insult

AU - Brothers, R M

AU - Pecini, Redi

AU - Dalsgaard, Morten

AU - Bundgaard-Nielsen, Morten

AU - Wilson, Thad E

AU - Secher, Niels H

AU - Crandall, Craig G

N1 - Copyright © 2014 the American Physiological Society.

PY - 2014/10/15

Y1 - 2014/10/15

N2 - Volume loading normalizes tolerance to a simulated hemorrhagic challenge in heat-stressed individuals, relative to when these individuals are thermoneutral. The mechanism(s) by which this occurs is unknown. This project tested two unique hypotheses; that is, the elevation of central blood volume via volume loading while heat stressed would 1) increase indices of left ventricular diastolic function, and 2) preserve left ventricular end-diastolic volume (LVEDV) during a subsequent simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Indices of left ventricular diastolic function were evaluated in nine subjects during the following conditions: thermoneutral, heat stress, and heat stress after acute volume loading sufficient to return ventricular filling pressures toward thermoneutral levels. LVEDV was also measured in these subjects during the aforementioned conditions prior to and during a simulated hemorrhagic challenge. Heat stress did not change indices of diastolic function. Subsequent volume infusion elevated indices of diastolic function, specifically early diastolic mitral annular tissue velocity (E') and early diastolic propagation velocity (E) relative to both thermoneutral and heat stress conditions (P < 0.05 for both). Heat stress reduced LVEDV (P < 0.05), while volume infusion returned LVEDV to thermoneutral levels. The reduction in LVEDV to LBNP was similar between thermoneutral and heat stress conditions, whereas the reduction after volume infusion was attenuated relative to both conditions (P < 0.05). Absolute LVEDV during LBNP after volume loading was appreciably greater relative to the same level of LBNP during heat stress alone. Thus, rapid volume infusion during heat stress increased indices of left ventricular diastolic function and attenuated the reduction in LVEDV during LBNP, both of which may serve as mechanisms by which volume loading improves tolerance to a combined hyperthermic and hemorrhagic challenge.

AB - Volume loading normalizes tolerance to a simulated hemorrhagic challenge in heat-stressed individuals, relative to when these individuals are thermoneutral. The mechanism(s) by which this occurs is unknown. This project tested two unique hypotheses; that is, the elevation of central blood volume via volume loading while heat stressed would 1) increase indices of left ventricular diastolic function, and 2) preserve left ventricular end-diastolic volume (LVEDV) during a subsequent simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Indices of left ventricular diastolic function were evaluated in nine subjects during the following conditions: thermoneutral, heat stress, and heat stress after acute volume loading sufficient to return ventricular filling pressures toward thermoneutral levels. LVEDV was also measured in these subjects during the aforementioned conditions prior to and during a simulated hemorrhagic challenge. Heat stress did not change indices of diastolic function. Subsequent volume infusion elevated indices of diastolic function, specifically early diastolic mitral annular tissue velocity (E') and early diastolic propagation velocity (E) relative to both thermoneutral and heat stress conditions (P < 0.05 for both). Heat stress reduced LVEDV (P < 0.05), while volume infusion returned LVEDV to thermoneutral levels. The reduction in LVEDV to LBNP was similar between thermoneutral and heat stress conditions, whereas the reduction after volume infusion was attenuated relative to both conditions (P < 0.05). Absolute LVEDV during LBNP after volume loading was appreciably greater relative to the same level of LBNP during heat stress alone. Thus, rapid volume infusion during heat stress increased indices of left ventricular diastolic function and attenuated the reduction in LVEDV during LBNP, both of which may serve as mechanisms by which volume loading improves tolerance to a combined hyperthermic and hemorrhagic challenge.

KW - Adult

KW - Blood Pressure

KW - Body Temperature Regulation

KW - Diastole

KW - Echocardiography

KW - Fever

KW - Heart

KW - Heart Ventricles

KW - Heat-Shock Response

KW - Hemorrhage

KW - Humans

KW - Lower Body Negative Pressure

KW - Male

KW - Ventricular Function, Left

M3 - Journal article

C2 - 25163916

SN - 0363-6119

VL - 307

SP - R1036-41

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

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

IS - 8

ER -