Heart function after severe hemorrhagic shock

Jeffrey Kline, Lisa R. Thornton, Gary D. Lopaschuk, R. Wayne Barbee, John A. Watts

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Objective: Test whether brief deep hemorrhagic hypotension or prolonged moderate hemorrhagic hypotension impairs intrinsic heart function. Methods: Pentobarbital-anesthetized, non-anticoagulated rats were cannulated via the carotid artery. This study focuses on three main groups: 1) hemorrhage to a mean arterial blood pressure (MAP)=25 mm Hg for 1 h (1 h severe shock), 2) hemorrhage to MAP=40 mm Hg for 3 h (3 h moderate shock), 3) no hemorrhage (control). Hearts were either freeze-clamped in-situ for tissue analysis (n=6 per group) or were removed to study in vitro cardiac function and efficiency using a working heart perfusion (n=12 per group, glucose (11 mM)/palmitate (0.4 mM), 3% BSA buffer). Following perfusion, hearts were freeze-clamped and analyzed for free CoA, acetyl-, succinyl-, and malonyl-CoA, ATP content and for TNF-α content. Results: Isolated working hearts obtained following 1 h of severe shock generated 20% less hydraulic work than hearts obtained from control rats or rats subjected to 3 h of moderate shock. The cardiac efficiency (work/O2 consumption) was also significantly reduced with 1 h severe shock (0.76 ± 0.07 after 15 min perfusion) versus control (0.96 ± 0.06) or 3 h prolonged shock (1.10 ± 0.09). Myocardial Co-A ester, ATP and TNF-α concentrations were not different between control and shocked hearts, although TNF-α concentrations increased significantly in all hearts during ex vivo perfusion. Conclusions: Depth of hypotension is more important than duration in causing intrinsic cardiac dysfunction. This post-hemorrhagic cardiac dysfunction is not a result of substrate limitation to the heart, nor myocardial TNF-α accumulation, but is more likely a result of impaired transfer of energy from molecular oxygen into external cardiac work.

Original languageEnglish (US)
Pages (from-to)454-461
Number of pages8
JournalShock
Volume12
Issue number6
StatePublished - Dec 1999
Externally publishedYes

Fingerprint

Hemorrhagic Shock
Shock
Arterial Pressure
Perfusion
Hypotension
Hemorrhage
Adenosine Triphosphate
Malonyl Coenzyme A
Acetyl Coenzyme A
Palmitates
Energy Transfer
Pentobarbital
Carotid Arteries
Buffers
Esters
Oxygen
Glucose

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Physiology

Cite this

Kline, J., Thornton, L. R., Lopaschuk, G. D., Barbee, R. W., & Watts, J. A. (1999). Heart function after severe hemorrhagic shock. Shock, 12(6), 454-461.

Heart function after severe hemorrhagic shock. / Kline, Jeffrey; Thornton, Lisa R.; Lopaschuk, Gary D.; Barbee, R. Wayne; Watts, John A.

In: Shock, Vol. 12, No. 6, 12.1999, p. 454-461.

Research output: Contribution to journalArticle

Kline, J, Thornton, LR, Lopaschuk, GD, Barbee, RW & Watts, JA 1999, 'Heart function after severe hemorrhagic shock', Shock, vol. 12, no. 6, pp. 454-461.
Kline J, Thornton LR, Lopaschuk GD, Barbee RW, Watts JA. Heart function after severe hemorrhagic shock. Shock. 1999 Dec;12(6):454-461.
Kline, Jeffrey ; Thornton, Lisa R. ; Lopaschuk, Gary D. ; Barbee, R. Wayne ; Watts, John A. / Heart function after severe hemorrhagic shock. In: Shock. 1999 ; Vol. 12, No. 6. pp. 454-461.
@article{f50607ff42804c68aa8f5d6ef3263706,
title = "Heart function after severe hemorrhagic shock",
abstract = "Objective: Test whether brief deep hemorrhagic hypotension or prolonged moderate hemorrhagic hypotension impairs intrinsic heart function. Methods: Pentobarbital-anesthetized, non-anticoagulated rats were cannulated via the carotid artery. This study focuses on three main groups: 1) hemorrhage to a mean arterial blood pressure (MAP)=25 mm Hg for 1 h (1 h severe shock), 2) hemorrhage to MAP=40 mm Hg for 3 h (3 h moderate shock), 3) no hemorrhage (control). Hearts were either freeze-clamped in-situ for tissue analysis (n=6 per group) or were removed to study in vitro cardiac function and efficiency using a working heart perfusion (n=12 per group, glucose (11 mM)/palmitate (0.4 mM), 3{\%} BSA buffer). Following perfusion, hearts were freeze-clamped and analyzed for free CoA, acetyl-, succinyl-, and malonyl-CoA, ATP content and for TNF-α content. Results: Isolated working hearts obtained following 1 h of severe shock generated 20{\%} less hydraulic work than hearts obtained from control rats or rats subjected to 3 h of moderate shock. The cardiac efficiency (work/O2 consumption) was also significantly reduced with 1 h severe shock (0.76 ± 0.07 after 15 min perfusion) versus control (0.96 ± 0.06) or 3 h prolonged shock (1.10 ± 0.09). Myocardial Co-A ester, ATP and TNF-α concentrations were not different between control and shocked hearts, although TNF-α concentrations increased significantly in all hearts during ex vivo perfusion. Conclusions: Depth of hypotension is more important than duration in causing intrinsic cardiac dysfunction. This post-hemorrhagic cardiac dysfunction is not a result of substrate limitation to the heart, nor myocardial TNF-α accumulation, but is more likely a result of impaired transfer of energy from molecular oxygen into external cardiac work.",
author = "Jeffrey Kline and Thornton, {Lisa R.} and Lopaschuk, {Gary D.} and Barbee, {R. Wayne} and Watts, {John A.}",
year = "1999",
month = "12",
language = "English (US)",
volume = "12",
pages = "454--461",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Heart function after severe hemorrhagic shock

AU - Kline, Jeffrey

AU - Thornton, Lisa R.

AU - Lopaschuk, Gary D.

AU - Barbee, R. Wayne

AU - Watts, John A.

PY - 1999/12

Y1 - 1999/12

N2 - Objective: Test whether brief deep hemorrhagic hypotension or prolonged moderate hemorrhagic hypotension impairs intrinsic heart function. Methods: Pentobarbital-anesthetized, non-anticoagulated rats were cannulated via the carotid artery. This study focuses on three main groups: 1) hemorrhage to a mean arterial blood pressure (MAP)=25 mm Hg for 1 h (1 h severe shock), 2) hemorrhage to MAP=40 mm Hg for 3 h (3 h moderate shock), 3) no hemorrhage (control). Hearts were either freeze-clamped in-situ for tissue analysis (n=6 per group) or were removed to study in vitro cardiac function and efficiency using a working heart perfusion (n=12 per group, glucose (11 mM)/palmitate (0.4 mM), 3% BSA buffer). Following perfusion, hearts were freeze-clamped and analyzed for free CoA, acetyl-, succinyl-, and malonyl-CoA, ATP content and for TNF-α content. Results: Isolated working hearts obtained following 1 h of severe shock generated 20% less hydraulic work than hearts obtained from control rats or rats subjected to 3 h of moderate shock. The cardiac efficiency (work/O2 consumption) was also significantly reduced with 1 h severe shock (0.76 ± 0.07 after 15 min perfusion) versus control (0.96 ± 0.06) or 3 h prolonged shock (1.10 ± 0.09). Myocardial Co-A ester, ATP and TNF-α concentrations were not different between control and shocked hearts, although TNF-α concentrations increased significantly in all hearts during ex vivo perfusion. Conclusions: Depth of hypotension is more important than duration in causing intrinsic cardiac dysfunction. This post-hemorrhagic cardiac dysfunction is not a result of substrate limitation to the heart, nor myocardial TNF-α accumulation, but is more likely a result of impaired transfer of energy from molecular oxygen into external cardiac work.

AB - Objective: Test whether brief deep hemorrhagic hypotension or prolonged moderate hemorrhagic hypotension impairs intrinsic heart function. Methods: Pentobarbital-anesthetized, non-anticoagulated rats were cannulated via the carotid artery. This study focuses on three main groups: 1) hemorrhage to a mean arterial blood pressure (MAP)=25 mm Hg for 1 h (1 h severe shock), 2) hemorrhage to MAP=40 mm Hg for 3 h (3 h moderate shock), 3) no hemorrhage (control). Hearts were either freeze-clamped in-situ for tissue analysis (n=6 per group) or were removed to study in vitro cardiac function and efficiency using a working heart perfusion (n=12 per group, glucose (11 mM)/palmitate (0.4 mM), 3% BSA buffer). Following perfusion, hearts were freeze-clamped and analyzed for free CoA, acetyl-, succinyl-, and malonyl-CoA, ATP content and for TNF-α content. Results: Isolated working hearts obtained following 1 h of severe shock generated 20% less hydraulic work than hearts obtained from control rats or rats subjected to 3 h of moderate shock. The cardiac efficiency (work/O2 consumption) was also significantly reduced with 1 h severe shock (0.76 ± 0.07 after 15 min perfusion) versus control (0.96 ± 0.06) or 3 h prolonged shock (1.10 ± 0.09). Myocardial Co-A ester, ATP and TNF-α concentrations were not different between control and shocked hearts, although TNF-α concentrations increased significantly in all hearts during ex vivo perfusion. Conclusions: Depth of hypotension is more important than duration in causing intrinsic cardiac dysfunction. This post-hemorrhagic cardiac dysfunction is not a result of substrate limitation to the heart, nor myocardial TNF-α accumulation, but is more likely a result of impaired transfer of energy from molecular oxygen into external cardiac work.

UR - http://www.scopus.com/inward/record.url?scp=0033258467&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033258467&partnerID=8YFLogxK

M3 - Article

C2 - 10588514

AN - SCOPUS:0033258467

VL - 12

SP - 454

EP - 461

JO - Shock

JF - Shock

SN - 1073-2322

IS - 6

ER -