Ischemic preconditioning-induced microcirculatory protection appears to be a systemic
rather than a local phenomenon. This protection induced by remote ischemic preconditioning
(RIPC) may be attributed to a humoral rather than a neuronal mechanism.
An innervated (Inn, Groups 1 and 4) or denervated (Den, Groups 2 and 3) and vascular
isolated right cremaster of the rat was prepared. Left femoral vessels were clamped
(Groups 1, 2, and 4) for 45 min or unclamped (Group 3) as a control. After 2 hr of
reperfusion in the left lower extremity, 4 hr of ischemia in the right cremaster was
applied in Groups 1, 2, and 3. However, in Group 4, 4 hr of ischemia in the cremaster
muscle was instituted before reperfusion of the left femoral artery was begun. Microcirculatory
responses, including terminal arteriole diameter, capillary perfusion, and endothelium
function were evaluated. Four groups (six rats per group) were designed: Group 1:
RIPC (Inn); Group 2: RIPC (Den); Group 3: sham RIPC (Den); and Group 4: fake RIPC
(Inn).
Ischemia of 45 min followed by 2 hr of reperfusion in the left lower extremity of
the rat induced a significant microvascular protection against subsequent 4-hr ischemia
in both innervated and denervated cremasters. This microvascular protection at a distance
was lost in sham RIPC and in fake RIPC groups.
The results demonstrated that remote protection induced by ischemic preconditioning
is a systemic phenomenon and due to a humoral mechanism.
KEYWORDS
Ischemic preconditioning - ischemia reperfusion - microcirculation
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Wei Z WangM.D.
Division of Plastic Surgery, Department of Surgery, University of Nevada School of
Medicine
2040 W. Charleston Blvd.
Suite 301, Las Vegas, NV 89102