Gut epithelial apoptosis after severe burn: Effects of gut hypoperfusion

Peter I. Ramzy, Steven Wolf, Oivind Irtun, David W. Hart, James C. Thompson, David Herndon

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Background: Severe cutaneous burn causes transient mesenteric vasoconstriction and altered gut mucosal integrity. We recently showed that burn also increases gut epithelial cell death by apoptosis. The goal of this study was to determine whether changes in gut perfusion after burn contribute to burn-associated gut apoptosis. Study Design: We first correlated superior mesenteric artery blood flow with measurement of gut perfusion at the tissue level by laser doppler in four nonburned rats before, during, and after arterial damping to validate our measurements of gut per fusion. We then characterized gut perfusion sequentially over time after burn; gut perfusion was measured 3 cm from the ligament of Treitz before burn and hourly for 6 hours. A group of control rats underwent the exact same protocol without the burn to exclude effects of anesthesia and laparotomy on tissue per fusion (n = 4). We studied a third group of rats with hypoperfusion of the same duration and magnitude induced mechanically without burn (n = 7). Sections of the proximal gut from all three groups (control without burn, burn, and hypoperfusion without burn) were examined for epithelial apoptosis. Results: Linear regression analysis demonstrated a strong correlation between superior roesenteric artery blood flow and intestinal tissue per fusion measured by laser doppler under both low and high flow conditions (r = 0.85). Laser doppler measurements of gut perfusion after burn showed deceased gut per fusion that was maximal at 2 hours postburn (p < 0.05), and that persisted for 4 hours (p < 0.05). By 6 hours, gut perfusion returned to baseline. Apoptosis increased significantly in the burn group (2.11 ± 0.17%) compared with control (0.52 ± 0.2%) and the mechanically decreased perfusion group (0.51 ± .03) (p < 0.001). Conclusions: We conclude that burn-induced gut hypoperfusion is insufficient to cause burn-related increased gut epithelial apoptosis. We speculate that the signal for increased gut epithelial apoptosis is primarily related to proinflammatory mediators induced by the burn wound. (C) 2000 by the American College of Surgeons.

Original languageEnglish (US)
Pages (from-to)281-287
Number of pages7
JournalJournal of the American College of Surgeons
Volume190
Issue number3
DOIs
StatePublished - Mar 2000

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Perfusion
Apoptosis
Burns
Lasers
Control Groups
Superior Mesenteric Artery
Vasoconstriction
Ligaments
Laparotomy
Linear Models
Cell Death
Anesthesia
Arteries
Epithelial Cells
Regression Analysis
Skin
Wounds and Injuries

ASJC Scopus subject areas

  • Surgery

Cite this

Gut epithelial apoptosis after severe burn : Effects of gut hypoperfusion. / Ramzy, Peter I.; Wolf, Steven; Irtun, Oivind; Hart, David W.; Thompson, James C.; Herndon, David.

In: Journal of the American College of Surgeons, Vol. 190, No. 3, 03.2000, p. 281-287.

Research output: Contribution to journalArticle

Ramzy, Peter I. ; Wolf, Steven ; Irtun, Oivind ; Hart, David W. ; Thompson, James C. ; Herndon, David. / Gut epithelial apoptosis after severe burn : Effects of gut hypoperfusion. In: Journal of the American College of Surgeons. 2000 ; Vol. 190, No. 3. pp. 281-287.
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abstract = "Background: Severe cutaneous burn causes transient mesenteric vasoconstriction and altered gut mucosal integrity. We recently showed that burn also increases gut epithelial cell death by apoptosis. The goal of this study was to determine whether changes in gut perfusion after burn contribute to burn-associated gut apoptosis. Study Design: We first correlated superior mesenteric artery blood flow with measurement of gut perfusion at the tissue level by laser doppler in four nonburned rats before, during, and after arterial damping to validate our measurements of gut per fusion. We then characterized gut perfusion sequentially over time after burn; gut perfusion was measured 3 cm from the ligament of Treitz before burn and hourly for 6 hours. A group of control rats underwent the exact same protocol without the burn to exclude effects of anesthesia and laparotomy on tissue per fusion (n = 4). We studied a third group of rats with hypoperfusion of the same duration and magnitude induced mechanically without burn (n = 7). Sections of the proximal gut from all three groups (control without burn, burn, and hypoperfusion without burn) were examined for epithelial apoptosis. Results: Linear regression analysis demonstrated a strong correlation between superior roesenteric artery blood flow and intestinal tissue per fusion measured by laser doppler under both low and high flow conditions (r = 0.85). Laser doppler measurements of gut perfusion after burn showed deceased gut per fusion that was maximal at 2 hours postburn (p < 0.05), and that persisted for 4 hours (p < 0.05). By 6 hours, gut perfusion returned to baseline. Apoptosis increased significantly in the burn group (2.11 ± 0.17{\%}) compared with control (0.52 ± 0.2{\%}) and the mechanically decreased perfusion group (0.51 ± .03) (p < 0.001). Conclusions: We conclude that burn-induced gut hypoperfusion is insufficient to cause burn-related increased gut epithelial apoptosis. We speculate that the signal for increased gut epithelial apoptosis is primarily related to proinflammatory mediators induced by the burn wound. (C) 2000 by the American College of Surgeons.",
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