Glutathione deficiency increases organ dysfunction after hemorrhagic shock

Malcolm K. Robinson, Jan D. Rounds, Roy W. Hong, Danny O. Jacobs, Douglas W. Wilmore

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

Background. Reactive oxygen metabolites contribute to tissue destruction in a wide variety of diseases. Glutathione, a potent endogenous antioxidant, neutralizes the destructive potential of free radicals, but this tripeptide may be depleted during illness. We hypothesized that glutathione deficiency would amplify organ dysfunction after shock in rats. Methods. Rats received either diethyl maleate to deplete tissue glutathione or a control solution intraperitoneally. The animals were subsequently bled to and maintained at a mean arterial pressure of 40 mm Hg for 30 minutes and then fully resuscitated. Sham animals underwent blood pressure monitoring only. Tissue glutathione, liver and renal function tests, organ bacterial content, and mortality rates were determined 4 and 24 hours after shock. Results. Normal rats subjected to shock and sham animals had similar laboratory chemistry results, organ culture results, and mortality rates. However, glutathione-depleted animals subjected to shock had elevated liver and renal function tests, increased organ bacteria, and a dramatic increase in mortality rates compared with control shock and sham animals. Conclusions. We conclude that glutathione deficiency predisposes animals to organ failure and death after an otherwise nonlethal period of hypotension. Because glutathione deficiency is associated with severe injury and sepsis, treatment strategies that maintain glutathione stores may decrease the incidence of multisystem organ failure.

Original languageEnglish (US)
Pages (from-to)140-149
Number of pages10
JournalSurgery
Volume112
Issue number2
StatePublished - 1992
Externally publishedYes

Fingerprint

Hemorrhagic Shock
Glutathione
Shock
diethyl maleate
Liver Function Tests
Mortality
Animal Structures
Kidney
Organ Culture Techniques
Hypotension
Free Radicals
Sepsis
Arterial Pressure
Antioxidants
Oxygen
Blood Pressure
Bacteria
Incidence
Wounds and Injuries

ASJC Scopus subject areas

  • Surgery

Cite this

Robinson, M. K., Rounds, J. D., Hong, R. W., Jacobs, D. O., & Wilmore, D. W. (1992). Glutathione deficiency increases organ dysfunction after hemorrhagic shock. Surgery, 112(2), 140-149.

Glutathione deficiency increases organ dysfunction after hemorrhagic shock. / Robinson, Malcolm K.; Rounds, Jan D.; Hong, Roy W.; Jacobs, Danny O.; Wilmore, Douglas W.

In: Surgery, Vol. 112, No. 2, 1992, p. 140-149.

Research output: Contribution to journalArticle

Robinson, MK, Rounds, JD, Hong, RW, Jacobs, DO & Wilmore, DW 1992, 'Glutathione deficiency increases organ dysfunction after hemorrhagic shock', Surgery, vol. 112, no. 2, pp. 140-149.
Robinson MK, Rounds JD, Hong RW, Jacobs DO, Wilmore DW. Glutathione deficiency increases organ dysfunction after hemorrhagic shock. Surgery. 1992;112(2):140-149.
Robinson, Malcolm K. ; Rounds, Jan D. ; Hong, Roy W. ; Jacobs, Danny O. ; Wilmore, Douglas W. / Glutathione deficiency increases organ dysfunction after hemorrhagic shock. In: Surgery. 1992 ; Vol. 112, No. 2. pp. 140-149.
@article{0af2fa88df45459ea23146c4b7bc2856,
title = "Glutathione deficiency increases organ dysfunction after hemorrhagic shock",
abstract = "Background. Reactive oxygen metabolites contribute to tissue destruction in a wide variety of diseases. Glutathione, a potent endogenous antioxidant, neutralizes the destructive potential of free radicals, but this tripeptide may be depleted during illness. We hypothesized that glutathione deficiency would amplify organ dysfunction after shock in rats. Methods. Rats received either diethyl maleate to deplete tissue glutathione or a control solution intraperitoneally. The animals were subsequently bled to and maintained at a mean arterial pressure of 40 mm Hg for 30 minutes and then fully resuscitated. Sham animals underwent blood pressure monitoring only. Tissue glutathione, liver and renal function tests, organ bacterial content, and mortality rates were determined 4 and 24 hours after shock. Results. Normal rats subjected to shock and sham animals had similar laboratory chemistry results, organ culture results, and mortality rates. However, glutathione-depleted animals subjected to shock had elevated liver and renal function tests, increased organ bacteria, and a dramatic increase in mortality rates compared with control shock and sham animals. Conclusions. We conclude that glutathione deficiency predisposes animals to organ failure and death after an otherwise nonlethal period of hypotension. Because glutathione deficiency is associated with severe injury and sepsis, treatment strategies that maintain glutathione stores may decrease the incidence of multisystem organ failure.",
author = "Robinson, {Malcolm K.} and Rounds, {Jan D.} and Hong, {Roy W.} and Jacobs, {Danny O.} and Wilmore, {Douglas W.}",
year = "1992",
language = "English (US)",
volume = "112",
pages = "140--149",
journal = "Surgery",
issn = "0039-6060",
publisher = "Mosby Inc.",
number = "2",

}

TY - JOUR

T1 - Glutathione deficiency increases organ dysfunction after hemorrhagic shock

AU - Robinson, Malcolm K.

AU - Rounds, Jan D.

AU - Hong, Roy W.

AU - Jacobs, Danny O.

AU - Wilmore, Douglas W.

PY - 1992

Y1 - 1992

N2 - Background. Reactive oxygen metabolites contribute to tissue destruction in a wide variety of diseases. Glutathione, a potent endogenous antioxidant, neutralizes the destructive potential of free radicals, but this tripeptide may be depleted during illness. We hypothesized that glutathione deficiency would amplify organ dysfunction after shock in rats. Methods. Rats received either diethyl maleate to deplete tissue glutathione or a control solution intraperitoneally. The animals were subsequently bled to and maintained at a mean arterial pressure of 40 mm Hg for 30 minutes and then fully resuscitated. Sham animals underwent blood pressure monitoring only. Tissue glutathione, liver and renal function tests, organ bacterial content, and mortality rates were determined 4 and 24 hours after shock. Results. Normal rats subjected to shock and sham animals had similar laboratory chemistry results, organ culture results, and mortality rates. However, glutathione-depleted animals subjected to shock had elevated liver and renal function tests, increased organ bacteria, and a dramatic increase in mortality rates compared with control shock and sham animals. Conclusions. We conclude that glutathione deficiency predisposes animals to organ failure and death after an otherwise nonlethal period of hypotension. Because glutathione deficiency is associated with severe injury and sepsis, treatment strategies that maintain glutathione stores may decrease the incidence of multisystem organ failure.

AB - Background. Reactive oxygen metabolites contribute to tissue destruction in a wide variety of diseases. Glutathione, a potent endogenous antioxidant, neutralizes the destructive potential of free radicals, but this tripeptide may be depleted during illness. We hypothesized that glutathione deficiency would amplify organ dysfunction after shock in rats. Methods. Rats received either diethyl maleate to deplete tissue glutathione or a control solution intraperitoneally. The animals were subsequently bled to and maintained at a mean arterial pressure of 40 mm Hg for 30 minutes and then fully resuscitated. Sham animals underwent blood pressure monitoring only. Tissue glutathione, liver and renal function tests, organ bacterial content, and mortality rates were determined 4 and 24 hours after shock. Results. Normal rats subjected to shock and sham animals had similar laboratory chemistry results, organ culture results, and mortality rates. However, glutathione-depleted animals subjected to shock had elevated liver and renal function tests, increased organ bacteria, and a dramatic increase in mortality rates compared with control shock and sham animals. Conclusions. We conclude that glutathione deficiency predisposes animals to organ failure and death after an otherwise nonlethal period of hypotension. Because glutathione deficiency is associated with severe injury and sepsis, treatment strategies that maintain glutathione stores may decrease the incidence of multisystem organ failure.

UR - http://www.scopus.com/inward/record.url?scp=0026781166&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026781166&partnerID=8YFLogxK

M3 - Article

C2 - 1641757

AN - SCOPUS:0026781166

VL - 112

SP - 140

EP - 149

JO - Surgery

JF - Surgery

SN - 0039-6060

IS - 2

ER -