Intraperitoneal resuscitation improves intestinal blood flow following hemorrhagic shock.
OBJECTIVE
To study the effects of peritoneal resuscitation from hemorrhagic shock.


BACKGROUND
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.
Zakaria
El Rasheid
el R
Department of Surgery, University of Louisville, Louisville, KY 40292, USA.
Garrison
R Neal
RN
Spain
David A
DA
Matheson
Paul J
PJ
Harris
Patrick D
PD
Richardson
J David
JD
D000818:Animals; D004730:Endothelium, Vascular / Q000187:drug effects*; D005440:Fluid Therapy / Q000379:methods*; D005950:Glucose Solution, Hypertonic / Q000008:administration & dosage*; D007263:Infusions, Parenteral; D007422:Intestines / Q000098:blood supply* / Q000502:physiology; D007511:Ischemia; D008297:Male; D023421:Models, Animal; D009102:Multiple Organ Failure / Q000209:etiology / Q000517:prevention & control; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation / Q000379:methods*; D012771:Shock, Hemorrhagic / Q000150:complications / Q000188:drug therapy*; D013152:Splanchnic Circulation / Q000187:drug effects*; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000517:prevention & control
D005950:Glucose Solution, Hypertonic