Acute microvascular action of vascular endothelial growth factor in skeletal muscle ischemia/reperfusion injury.

Background: The purpose of this study was to investigate the acute action of vascular endothelial growth factor (VEGF) in the microcirculation of skeletal muscle subject to ischemia/reperfusion in vivo and to determine the role of nitric oxide synthase in VEGF-induced microvascular protection.

Methods: A vascular pedicle isolated rat cremaster muscle model coupled with local intraarterial infusion technique was used. Each muscle underwent 4 hours of zero-flow warm ischemia followed by 2 hours of reperfusion.

NOS upregulation attenuates vascular endothelial dysfunction in the late phase of ischemic preconditioning in skeletal muscle.

Previously, we have demonstrated a late phase protection of ischemic preconditioning in the microcirculation of cremaster muscle. This microvascular protection was blocked by a non-specific NOS inhibitor. The purpose of present study was to evaluate endothelial function in the terminal arteriole of cremaster muscle after 24-h of ischemic preconditioning followed by 4-h warm ischemia and to evaluate eNOS and iNOS gene and protein expression at 24 h after ischemic preconditioning in the cremaster muscle.

Ischemic preconditioning-induced microvascular protection at a distance.

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.

Microvascular protection induced by late preconditioning was abolished in STZ-induced acute diabetic rats.

The authors attempted to determine whether ischemic preconditioning (IPC) can provide microvascular protection in skeletal muscle of diabetic rats against injury from a subsequent (24 hr later) prolonged period of ischemia and reperfusion. Male Sprague Dawley rats weighting 80 to 100 g were injected intraperitoneally with either streptozotocin (STZ, 65 mg/kg) or vehicle (sodium citrate, pH 4.5).

Role of PKC in the late phase of microvascular protection induced by preconditioning.

Introduction: We hypothesized that the late phase of microvascular protection induced by ischemic preconditioning or by adenosine is protein kinase C (PKC) dependent.

Materials And Methods: The cremaster muscle of male Sprague-Dawley rats underwent 45 min of ischemic preconditioning and, 24 h later, 4 h of warm ischemia followed by 60 min of reperfusion. To mimic the effects of IPC, adenosine (ADO; an adenosine receptor agonist) or 4-phorbol 12-myristate 13-acetate (PMA; a PKC activator) was delivered to the vascular network of the cremaster 24 h before the prolonged ischemia via local intra-arterial infusion.