Lactate improves cardiac efficiency after hemorrhagic shock

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

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

This study was undertaken to examine the role of lactate on cardiac function and metabolism after severe acute hemorrhagic shock. Anesthetized, nonheparinized rats were bled to a mean arterial pressure of 25-30 mm Hg for 1 h; controls were not bled. Their hearts were removed, and cardiac work and efficiency (work/oxygen consumption) were measured in the isolated working heart mode for 60 min. The hearts were perfused with one of five substrate combinations: 1) glucose (11 mM), 2) glucose + 0.4 mM palmitate, 3) glucose + 0.4 mM palmitate + 8.0 mM lactate, 4) glucose + 1.2 mM palmitate, or 5) glucose + 1.2 mM palmitate + 8.0 mM lactate. After perfusion, hearts were freeze-clamped, and tissue contents of free coenzyme-A (CoA), acetyl CoA, and succinyl CoA were measured, as was myocardial pyruvate dehydrogenase (PDH) activity. The addition of 8.0 mM lactate significantly improved cardiac work in shocked hearts perfused with 0.4 mM palmitate and increased cardiac efficiency in the presence of either 0.4 mM or 1.2 mM palmitate. Compared to control hearts, shocked hearts exhibited a 20-30% decrease in PDH activity. Shocked hearts perfused with lactate demonstrated no increase in acetyl CoA content but did have a significant increase in tissue succinyl CoA compared to control hearts perfused with lactate or shocked hearts perfused without lactate. In the heart recovering from severe hemorrhagic shock, lactate improves cardiac efficiency in the presence of free fatty acids, possibly by a anaplerosis of the tricarboxylic acid cycle.

Original languageEnglish (US)
Pages (from-to)215-221
Number of pages7
JournalShock
Volume14
Issue number2
StatePublished - Aug 2000
Externally publishedYes

Fingerprint

Hemorrhagic Shock
Lactic Acid
Palmitates
Glucose
Acetyl Coenzyme A
Pyruvic Acid
Oxidoreductases
Citric Acid Cycle
Coenzymes
Nonesterified Fatty Acids
Oxygen Consumption
Arterial Pressure
Perfusion

Keywords

  • Cardiac efficiency
  • Fatty acids
  • Hemorrhage
  • Lactate
  • Myocardial metabolism
  • Shock
  • Trauma
  • Tricarboxylic acid cycle

ASJC Scopus subject areas

  • Physiology
  • Critical Care and Intensive Care Medicine

Cite this

Kline, J., Thornton, L. R., Lopaschuk, G. D., Barbee, R. W., & Watts, J. A. (2000). Lactate improves cardiac efficiency after hemorrhagic shock. Shock, 14(2), 215-221.

Lactate improves cardiac efficiency after hemorrhagic shock. / Kline, Jeffrey; Thornton, Lisa R.; Lopaschuk, Gary D.; Barbee, R. Wayne; Watts, John A.

In: Shock, Vol. 14, No. 2, 08.2000, p. 215-221.

Research output: Contribution to journalArticle

Kline, J, Thornton, LR, Lopaschuk, GD, Barbee, RW & Watts, JA 2000, 'Lactate improves cardiac efficiency after hemorrhagic shock', Shock, vol. 14, no. 2, pp. 215-221.
Kline J, Thornton LR, Lopaschuk GD, Barbee RW, Watts JA. Lactate improves cardiac efficiency after hemorrhagic shock. Shock. 2000 Aug;14(2):215-221.
Kline, Jeffrey ; Thornton, Lisa R. ; Lopaschuk, Gary D. ; Barbee, R. Wayne ; Watts, John A. / Lactate improves cardiac efficiency after hemorrhagic shock. In: Shock. 2000 ; Vol. 14, No. 2. pp. 215-221.
@article{3ee1494276ff4612a18ddbda8c690c00,
title = "Lactate improves cardiac efficiency after hemorrhagic shock",
abstract = "This study was undertaken to examine the role of lactate on cardiac function and metabolism after severe acute hemorrhagic shock. Anesthetized, nonheparinized rats were bled to a mean arterial pressure of 25-30 mm Hg for 1 h; controls were not bled. Their hearts were removed, and cardiac work and efficiency (work/oxygen consumption) were measured in the isolated working heart mode for 60 min. The hearts were perfused with one of five substrate combinations: 1) glucose (11 mM), 2) glucose + 0.4 mM palmitate, 3) glucose + 0.4 mM palmitate + 8.0 mM lactate, 4) glucose + 1.2 mM palmitate, or 5) glucose + 1.2 mM palmitate + 8.0 mM lactate. After perfusion, hearts were freeze-clamped, and tissue contents of free coenzyme-A (CoA), acetyl CoA, and succinyl CoA were measured, as was myocardial pyruvate dehydrogenase (PDH) activity. The addition of 8.0 mM lactate significantly improved cardiac work in shocked hearts perfused with 0.4 mM palmitate and increased cardiac efficiency in the presence of either 0.4 mM or 1.2 mM palmitate. Compared to control hearts, shocked hearts exhibited a 20-30{\%} decrease in PDH activity. Shocked hearts perfused with lactate demonstrated no increase in acetyl CoA content but did have a significant increase in tissue succinyl CoA compared to control hearts perfused with lactate or shocked hearts perfused without lactate. In the heart recovering from severe hemorrhagic shock, lactate improves cardiac efficiency in the presence of free fatty acids, possibly by a anaplerosis of the tricarboxylic acid cycle.",
keywords = "Cardiac efficiency, Fatty acids, Hemorrhage, Lactate, Myocardial metabolism, Shock, Trauma, Tricarboxylic acid cycle",
author = "Jeffrey Kline and Thornton, {Lisa R.} and Lopaschuk, {Gary D.} and Barbee, {R. Wayne} and Watts, {John A.}",
year = "2000",
month = "8",
language = "English (US)",
volume = "14",
pages = "215--221",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Lactate improves cardiac efficiency after hemorrhagic shock

AU - Kline, Jeffrey

AU - Thornton, Lisa R.

AU - Lopaschuk, Gary D.

AU - Barbee, R. Wayne

AU - Watts, John A.

PY - 2000/8

Y1 - 2000/8

N2 - This study was undertaken to examine the role of lactate on cardiac function and metabolism after severe acute hemorrhagic shock. Anesthetized, nonheparinized rats were bled to a mean arterial pressure of 25-30 mm Hg for 1 h; controls were not bled. Their hearts were removed, and cardiac work and efficiency (work/oxygen consumption) were measured in the isolated working heart mode for 60 min. The hearts were perfused with one of five substrate combinations: 1) glucose (11 mM), 2) glucose + 0.4 mM palmitate, 3) glucose + 0.4 mM palmitate + 8.0 mM lactate, 4) glucose + 1.2 mM palmitate, or 5) glucose + 1.2 mM palmitate + 8.0 mM lactate. After perfusion, hearts were freeze-clamped, and tissue contents of free coenzyme-A (CoA), acetyl CoA, and succinyl CoA were measured, as was myocardial pyruvate dehydrogenase (PDH) activity. The addition of 8.0 mM lactate significantly improved cardiac work in shocked hearts perfused with 0.4 mM palmitate and increased cardiac efficiency in the presence of either 0.4 mM or 1.2 mM palmitate. Compared to control hearts, shocked hearts exhibited a 20-30% decrease in PDH activity. Shocked hearts perfused with lactate demonstrated no increase in acetyl CoA content but did have a significant increase in tissue succinyl CoA compared to control hearts perfused with lactate or shocked hearts perfused without lactate. In the heart recovering from severe hemorrhagic shock, lactate improves cardiac efficiency in the presence of free fatty acids, possibly by a anaplerosis of the tricarboxylic acid cycle.

AB - This study was undertaken to examine the role of lactate on cardiac function and metabolism after severe acute hemorrhagic shock. Anesthetized, nonheparinized rats were bled to a mean arterial pressure of 25-30 mm Hg for 1 h; controls were not bled. Their hearts were removed, and cardiac work and efficiency (work/oxygen consumption) were measured in the isolated working heart mode for 60 min. The hearts were perfused with one of five substrate combinations: 1) glucose (11 mM), 2) glucose + 0.4 mM palmitate, 3) glucose + 0.4 mM palmitate + 8.0 mM lactate, 4) glucose + 1.2 mM palmitate, or 5) glucose + 1.2 mM palmitate + 8.0 mM lactate. After perfusion, hearts were freeze-clamped, and tissue contents of free coenzyme-A (CoA), acetyl CoA, and succinyl CoA were measured, as was myocardial pyruvate dehydrogenase (PDH) activity. The addition of 8.0 mM lactate significantly improved cardiac work in shocked hearts perfused with 0.4 mM palmitate and increased cardiac efficiency in the presence of either 0.4 mM or 1.2 mM palmitate. Compared to control hearts, shocked hearts exhibited a 20-30% decrease in PDH activity. Shocked hearts perfused with lactate demonstrated no increase in acetyl CoA content but did have a significant increase in tissue succinyl CoA compared to control hearts perfused with lactate or shocked hearts perfused without lactate. In the heart recovering from severe hemorrhagic shock, lactate improves cardiac efficiency in the presence of free fatty acids, possibly by a anaplerosis of the tricarboxylic acid cycle.

KW - Cardiac efficiency

KW - Fatty acids

KW - Hemorrhage

KW - Lactate

KW - Myocardial metabolism

KW - Shock

KW - Trauma

KW - Tricarboxylic acid cycle

UR - http://www.scopus.com/inward/record.url?scp=0034241950&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034241950&partnerID=8YFLogxK

M3 - Article

VL - 14

SP - 215

EP - 221

JO - Shock

JF - Shock

SN - 1073-2322

IS - 2

ER -