Intraperitoneal Resuscitation Improves Intestinal Blood Flow Following Hemorrhagic Shock

El Rasheid Zakaria, R. Neal Garrison, David A. Spain, Paul J. Matheson, Patrick D. Harris, J. David Richardson, Timothy Fabian, Lewis M. Flint, Loring W. Rue, Basil A. Pruitt, John A. Mannick, Gregory B. Bulkley, H. Biemann Othersen, F. Charles Brunicardi

Research output: Contribution to journalArticle

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Abstract

Objective: To study the effects of peritoneal resuscitation from hemorrhagic shock. Summary Background Data: Methods for conventional resuscitation (CR) from hemorrhagic shock (HS) often fail to restore adequate intestinal blood flow, and intestinal ischemia has been implicated in the activation of the inflammatory response. There is clinical evidence that intestinal hypoperfusion is a major factor in progressive organ failure following HS. This study presents a novel technique of peritoneal resuscitation (PR) that improves visceral perfusion. Methods: Male Sprague-Dawley rats were bled to 50% of baseline mean arterial pressure (MAP) and resuscitated with shed blood plus 2 equal volumes of saline (CR). Groups were 1) sham, 2) HS + CR, and 3) HS + CR + PR with a hyperosmolar dextrose-based solution (Delflex 2.5%). Groups 1 and 2 had normal saline PR. In vivo videomicroscopy and Doppler velocimetry were used to assess terminal ileal microvascular blood flow. Endothelial cell function was assessed by the endothelium-dependent vasodilator acetylcholine. Results: Despite restored heart rate and MAP to baseline values, CR animals developed a progressive intestinal vasoconstriction and tissue hypoperfusion compared to baseline flow. PR induced an immediate and sustained vasodilation compared to baseline and a marked increase in average intestinal blood flow during the entire 2-hour post-resuscitation period. Endothelial-dependent dilator function was preserved with PR. Conclusions: Despite the restoration of MAP with blood and saline infusions, progressive vasoconstriction and compromised intestinal blood flow occurs following HS/CR. Hyperosmolar PR during CR maintains intestinal blood flow and endothelial function. This is thought to be a direct effect of hyperosmolar solutions on the visceral microvessels. The addition of PR to a CR protocol prevents the splanchnic ischemia that initiates systemic inflammation.

Original languageEnglish (US)
Pages (from-to)704-713
Number of pages10
JournalAnnals of Surgery
Volume237
Issue number5
DOIs
StatePublished - May 1 2003

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Hemorrhagic Shock
Resuscitation
Arterial Pressure
Vasoconstriction
Ischemia
Endothelium-Dependent Relaxing Factors
Video Microscopy
Viscera
Rheology
Microvessels

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Zakaria, E. R., Garrison, R. N., Spain, D. A., Matheson, P. J., Harris, P. D., Richardson, J. D., ... Brunicardi, F. C. (2003). Intraperitoneal Resuscitation Improves Intestinal Blood Flow Following Hemorrhagic Shock. Annals of Surgery, 237(5), 704-713. https://doi.org/10.1097/00000658-200305000-00013

Intraperitoneal Resuscitation Improves Intestinal Blood Flow Following Hemorrhagic Shock. / Zakaria, El Rasheid; Garrison, R. Neal; Spain, David A.; Matheson, Paul J.; Harris, Patrick D.; Richardson, J. David; Fabian, Timothy; Flint, Lewis M.; Rue, Loring W.; Pruitt, Basil A.; Mannick, John A.; Bulkley, Gregory B.; Othersen, H. Biemann; Brunicardi, F. Charles.

In: Annals of Surgery, Vol. 237, No. 5, 01.05.2003, p. 704-713.

Research output: Contribution to journalArticle

Zakaria, ER, Garrison, RN, Spain, DA, Matheson, PJ, Harris, PD, Richardson, JD, Fabian, T, Flint, LM, Rue, LW, Pruitt, BA, Mannick, JA, Bulkley, GB, Othersen, HB & Brunicardi, FC 2003, 'Intraperitoneal Resuscitation Improves Intestinal Blood Flow Following Hemorrhagic Shock', Annals of Surgery, vol. 237, no. 5, pp. 704-713. https://doi.org/10.1097/00000658-200305000-00013
Zakaria ER, Garrison RN, Spain DA, Matheson PJ, Harris PD, Richardson JD et al. Intraperitoneal Resuscitation Improves Intestinal Blood Flow Following Hemorrhagic Shock. Annals of Surgery. 2003 May 1;237(5):704-713. https://doi.org/10.1097/00000658-200305000-00013
Zakaria, El Rasheid ; Garrison, R. Neal ; Spain, David A. ; Matheson, Paul J. ; Harris, Patrick D. ; Richardson, J. David ; Fabian, Timothy ; Flint, Lewis M. ; Rue, Loring W. ; Pruitt, Basil A. ; Mannick, John A. ; Bulkley, Gregory B. ; Othersen, H. Biemann ; Brunicardi, F. Charles. / Intraperitoneal Resuscitation Improves Intestinal Blood Flow Following Hemorrhagic Shock. In: Annals of Surgery. 2003 ; Vol. 237, No. 5. pp. 704-713.
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abstract = "Objective: To study the effects of peritoneal resuscitation from hemorrhagic shock. Summary Background Data: Methods for conventional resuscitation (CR) from hemorrhagic shock (HS) often fail to restore adequate intestinal blood flow, and intestinal ischemia has been implicated in the activation of the inflammatory response. There is clinical evidence that intestinal hypoperfusion is a major factor in progressive organ failure following HS. This study presents a novel technique of peritoneal resuscitation (PR) that improves visceral perfusion. Methods: Male Sprague-Dawley rats were bled to 50{\%} of baseline mean arterial pressure (MAP) and resuscitated with shed blood plus 2 equal volumes of saline (CR). Groups were 1) sham, 2) HS + CR, and 3) HS + CR + PR with a hyperosmolar dextrose-based solution (Delflex 2.5{\%}). Groups 1 and 2 had normal saline PR. In vivo videomicroscopy and Doppler velocimetry were used to assess terminal ileal microvascular blood flow. Endothelial cell function was assessed by the endothelium-dependent vasodilator acetylcholine. Results: Despite restored heart rate and MAP to baseline values, CR animals developed a progressive intestinal vasoconstriction and tissue hypoperfusion compared to baseline flow. PR induced an immediate and sustained vasodilation compared to baseline and a marked increase in average intestinal blood flow during the entire 2-hour post-resuscitation period. Endothelial-dependent dilator function was preserved with PR. Conclusions: Despite the restoration of MAP with blood and saline infusions, progressive vasoconstriction and compromised intestinal blood flow occurs following HS/CR. Hyperosmolar PR during CR maintains intestinal blood flow and endothelial function. This is thought to be a direct effect of hyperosmolar solutions on the visceral microvessels. The addition of PR to a CR protocol prevents the splanchnic ischemia that initiates systemic inflammation.",
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AU - Zakaria, El Rasheid

AU - Garrison, R. Neal

AU - Spain, David A.

AU - Matheson, Paul J.

AU - Harris, Patrick D.

AU - Richardson, J. David

AU - Fabian, Timothy

AU - Flint, Lewis M.

AU - Rue, Loring W.

AU - Pruitt, Basil A.

AU - Mannick, John A.

AU - Bulkley, Gregory B.

AU - Othersen, H. Biemann

AU - Brunicardi, F. Charles

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N2 - Objective: To study the effects of peritoneal resuscitation from hemorrhagic shock. Summary Background Data: Methods for conventional resuscitation (CR) from hemorrhagic shock (HS) often fail to restore adequate intestinal blood flow, and intestinal ischemia has been implicated in the activation of the inflammatory response. There is clinical evidence that intestinal hypoperfusion is a major factor in progressive organ failure following HS. This study presents a novel technique of peritoneal resuscitation (PR) that improves visceral perfusion. Methods: Male Sprague-Dawley rats were bled to 50% of baseline mean arterial pressure (MAP) and resuscitated with shed blood plus 2 equal volumes of saline (CR). Groups were 1) sham, 2) HS + CR, and 3) HS + CR + PR with a hyperosmolar dextrose-based solution (Delflex 2.5%). Groups 1 and 2 had normal saline PR. In vivo videomicroscopy and Doppler velocimetry were used to assess terminal ileal microvascular blood flow. Endothelial cell function was assessed by the endothelium-dependent vasodilator acetylcholine. Results: Despite restored heart rate and MAP to baseline values, CR animals developed a progressive intestinal vasoconstriction and tissue hypoperfusion compared to baseline flow. PR induced an immediate and sustained vasodilation compared to baseline and a marked increase in average intestinal blood flow during the entire 2-hour post-resuscitation period. Endothelial-dependent dilator function was preserved with PR. Conclusions: Despite the restoration of MAP with blood and saline infusions, progressive vasoconstriction and compromised intestinal blood flow occurs following HS/CR. Hyperosmolar PR during CR maintains intestinal blood flow and endothelial function. This is thought to be a direct effect of hyperosmolar solutions on the visceral microvessels. The addition of PR to a CR protocol prevents the splanchnic ischemia that initiates systemic inflammation.

AB - Objective: To study the effects of peritoneal resuscitation from hemorrhagic shock. Summary Background Data: Methods for conventional resuscitation (CR) from hemorrhagic shock (HS) often fail to restore adequate intestinal blood flow, and intestinal ischemia has been implicated in the activation of the inflammatory response. There is clinical evidence that intestinal hypoperfusion is a major factor in progressive organ failure following HS. This study presents a novel technique of peritoneal resuscitation (PR) that improves visceral perfusion. Methods: Male Sprague-Dawley rats were bled to 50% of baseline mean arterial pressure (MAP) and resuscitated with shed blood plus 2 equal volumes of saline (CR). Groups were 1) sham, 2) HS + CR, and 3) HS + CR + PR with a hyperosmolar dextrose-based solution (Delflex 2.5%). Groups 1 and 2 had normal saline PR. In vivo videomicroscopy and Doppler velocimetry were used to assess terminal ileal microvascular blood flow. Endothelial cell function was assessed by the endothelium-dependent vasodilator acetylcholine. Results: Despite restored heart rate and MAP to baseline values, CR animals developed a progressive intestinal vasoconstriction and tissue hypoperfusion compared to baseline flow. PR induced an immediate and sustained vasodilation compared to baseline and a marked increase in average intestinal blood flow during the entire 2-hour post-resuscitation period. Endothelial-dependent dilator function was preserved with PR. Conclusions: Despite the restoration of MAP with blood and saline infusions, progressive vasoconstriction and compromised intestinal blood flow occurs following HS/CR. Hyperosmolar PR during CR maintains intestinal blood flow and endothelial function. This is thought to be a direct effect of hyperosmolar solutions on the visceral microvessels. The addition of PR to a CR protocol prevents the splanchnic ischemia that initiates systemic inflammation.

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