TY - JOUR
T1 - Mesenteric vasoconstriction in response to hemorrhagic shock
AU - Toung, Thomas
AU - Reilly, Patrick M.
AU - Fuh, Katherine C.
AU - Ferris, Robert
AU - Bulkley, Gregory B.
PY - 2000/4
Y1 - 2000/4
N2 - Previous studies indicate that cardiogenic shock (tamponade) in swine produces selective mesenteric ischemia due to disproportionate mesenteric vasospasm mediated primarily by the reninangiotensin axis. Here, we characterized the systemic and mesenteric hemodynamic responses to hypovolemic shock to better understand the neurohumoral mechanisms controlling this response. Varying degrees of hypovolemic shock were produced by graded levels of hemorrhage, from 12.5 to 50% of the calculated blood volume. Systemic and mesenteric pressures and blood flows were measured, and corresponding vascular resistances were calculated. The hemodynamic responses of the mesenteric vascular bed were compared with those of the systemic (nonmesenteric) vasculature. These experiments were then repeated after confirmed blockade either of the α-adrenergic nervous system (phenoxybenzamine), of vasopressin (Manning compound), or of the renin-angiotensin axis (enalapril). Graded levels of hemorrhage produced corresponding graded, reproducible, steady-state levels of systemic hypotension, hypoperfusion, and peripheral vasoconstriction, i.e., hemorrhagic shock. This was associated with disproportionate degrees of mesenteric ischemia due to disproportionate mesenteric vasoconstriction. The selective component of this mesenteric vasoconstrictive response was not attenuated by α-adrenergic blockade nor by vasopressin blockade but was blocked by ablation of the renin-angiotensin axis with enalapril. Like cardiogenic shock, hemorrhagic shock generates selective mesenteric ischemia by producing a disproportionate mesenteric vasospasm that is mediated primarily by the renin-angiotensin axis.
AB - Previous studies indicate that cardiogenic shock (tamponade) in swine produces selective mesenteric ischemia due to disproportionate mesenteric vasospasm mediated primarily by the reninangiotensin axis. Here, we characterized the systemic and mesenteric hemodynamic responses to hypovolemic shock to better understand the neurohumoral mechanisms controlling this response. Varying degrees of hypovolemic shock were produced by graded levels of hemorrhage, from 12.5 to 50% of the calculated blood volume. Systemic and mesenteric pressures and blood flows were measured, and corresponding vascular resistances were calculated. The hemodynamic responses of the mesenteric vascular bed were compared with those of the systemic (nonmesenteric) vasculature. These experiments were then repeated after confirmed blockade either of the α-adrenergic nervous system (phenoxybenzamine), of vasopressin (Manning compound), or of the renin-angiotensin axis (enalapril). Graded levels of hemorrhage produced corresponding graded, reproducible, steady-state levels of systemic hypotension, hypoperfusion, and peripheral vasoconstriction, i.e., hemorrhagic shock. This was associated with disproportionate degrees of mesenteric ischemia due to disproportionate mesenteric vasoconstriction. The selective component of this mesenteric vasoconstrictive response was not attenuated by α-adrenergic blockade nor by vasopressin blockade but was blocked by ablation of the renin-angiotensin axis with enalapril. Like cardiogenic shock, hemorrhagic shock generates selective mesenteric ischemia by producing a disproportionate mesenteric vasospasm that is mediated primarily by the renin-angiotensin axis.
KW - Angiotensin
KW - Mesenteric ischemia
KW - Renin
KW - Splanchnic circulation
KW - Splanchnic vasoconstriction
KW - Swine
KW - Sympathetic nervous system
KW - Vasopressin
UR - http://www.scopus.com/inward/record.url?scp=0033649264&partnerID=8YFLogxK
U2 - 10.1097/00024382-200004000-00003
DO - 10.1097/00024382-200004000-00003
M3 - Article
C2 - 10774614
AN - SCOPUS:0033649264
SN - 1073-2322
VL - 13
SP - 267
EP - 273
JO - Shock
JF - Shock
IS - 4
ER -