Vasoactive mediators and splanchnic perfusion.
OBJECTIVE
To provide an overview of the splanchnic hemodynamic response to circulatory shock.


METHODS
Previous studies performed in our own laboratory, as well as a computer-assisted search of the English language literature (MEDLINE, 1966 to 1991), followed by a selective review of pertinent articles.


METHODS
Studies were selected that demonstrated relevance to the splanchnic hemodynamic response to circulatory shock, either by investigating the pathophysiology or documenting the sequelae. Article selection included clinical studies as well as studies in appropriate animal models.


METHODS
Pertinent data were abstracted from the cited articles.


RESULTS
The splanchnic hemodynamic response to circulatory shock is characterized by a selective vasoconstriction of the mesenteric vasculature mediated largely by the renin-angiotensin axis. This vasospasm, while providing a natural selective advantage to the organism in mild-to-moderate shock (preserving relative perfusion of the heart, kidneys, and brain), may, in more severe shock, cause consequent loss of the gut epithelial barrier, or even hemorrhagic gastritis, ischemic colitis, or ischemic hepatitis. From a physiologic standpoint, nonpulsatile cardiopulmonary bypass, a controlled form of circulatory shock, has been found experimentally to significantly increase circulating levels of angiotensin II, the hormone responsible for this selective splanchnic vasoconstriction.


CONCLUSIONS
While angiotensin II has been viewed primarily as the mediator responsible for the increased total vascular resistance seen during (and after) cardiopulmonary bypass, it may also cause the disproportionate decrease in mesenteric perfusion, as measured in human subjects by intraluminal gastric tonometry and galactose clearance by the liver, as well as the consequent development of the multiple organ failure syndrome seen in 1% to 5% of patients after cardiac surgery.
Reilly
P M
PM
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD.
Bulkley
G B
GB
D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D006439:Hemodynamics; D006801:Humans; D007422:Intestines / Q000098:blood supply; D007511:Ischemia / Q000150:complications / Q000503:physiopathology; D012769:Shock / Q000150:complications / Q000503:physiopathology*; D013152:Splanchnic Circulation / Q000502:physiology*; D014661:Vasoconstriction
D000804:Angiotensin II