In recent years we have witnessed a major development in medical sciences. We perform more and more complicated surgical procedures that require temporary ischemia. This complication arises following stroke, myocardial infarction, acute limb ischemia, mesenteric embolism, or organ replantation and transplantation [1, 2]. Provided that the ischemia has not been too prolonged, restoration of blood flow can salvage hypoperfused tissue. However, tissue damage can actually be increased during reperfusion by a group of pathogenetic mechanisms widely known as ischemia-reperfusion injury (IRI). This interesting process is triggered by commencement of blood circulation. In unfavorable conditions despite restoration of blood flow we observe no-reflow phenomenon. IRI complicates fate of transplanted and replanted limbs. It is a serious problem in acute limb ischemia where not so rarely it leads to limb loss or to whole organism complication like singly or multiple organ failure or even death.

Pathophysiology of ischemia reperfusion injury is very complex and not fully understood. Many hypotheses of vicious circle of IRI have been discussed for recent years. Well documented events during IRI is leukocyte attachment to endothelial cells, leukocyte migration to perivascular space where they release oxygen radicals and enzymes [3, 4]. Another events occurring during IRI is intravascular fibrin deposition and extravascular compartment edema [5]. One of key events in IRI cascade is translocation of phosphatidylserine in anoxic conditions to the surface of endothelial cells providing an attachment site for leukocytes and platelets [6]. This attachment impedes blood flow through the microvasculature and results in leukocyte activation and degranulation.

One of important research methods in understanding IRI is direct in-vivo observation of microcirculatory hemodynamics, vascular pathophysiology and leukocyte-endothelial interactions. Among many in-vivo observation methods a model of cremaster muscle is unique in field of IRI [7–10].

The first to introduce the cremaster muscle model in histological and electron microscopy studies on inflammation were Majno and Palade [7]. This model modified by Grant for use in microcirculatory observation by in vivo microscopy [8]. Baez was the first to open the cremaster muscle and to detach the testicle from the flap to spread out the flap and transilluminate it under a microscope [9]. The next step in improvement of the model was a tissue bath to provide better control of the microcirculatory environment introduced Miller and Wiegman [10]. This model was further developed by Siemionow in such a way that the cremaster muscle was completely isolated on its neurovascular pedicle, as an island flap [11]. As a result of this modification flap circulation is solely dependent on one feeding artery and one outflowing vein, excluding all other sources of vascular supply. This model simulates the conditions encountered during clinical surgery, where the main vasculature is interrupted resulting in total downstream tissue ischemia. These microcirculatory observations of the muscle flap made during ischemia and reperfusion expands significantly our ability to study microcirculation in relation to flap hemodynamics, reactivity of the microvessels, leukocyte-endothelial interactions and endothelial permeability [1, 11, 12].

Major advantage of the cremaster muscle flap is structural and functional similarity to other skeletal muscles. Thus, all changes observed in the microcirculation of this small flap could be applied to limb replantation or transplantation, muscle flaps used in clinical microsurgery as well as to vascular surgery. It allows observation and quantitative measurements of vasospasm, vessel diameters, formation of thrombus or emboli, capillary perfusion, leukocytes – endothelial interaction and endothelial damage. Interesting and valuable modification is a cremaster chamber model for chronic observation of the microcirculation and it’s response to IRI [12]. This model has been used to describe relation of thrombus formation at the anastomosis site of feeding vessels with decrease in capillary perfusion. To ease preparation of the model and avoid accessory parameters related with anastomosis, cremaster muscle flap is also used for vascular pedicle clamp related IRI [13]. In this setting flap is subjected to microcirculatory observation before vascular pedicle is clamped and during reperfusion 2–6 h later [14, 15]. This model may be also used for non-acute IRI in states of reduced blood flow. To induce reduced blood flow ligature is put on one or both of main flap vessels. Rat cremaster flap is also applicable to test local and remote pre or post ischemic conditioning.

For recent years many pharmacological compounds of different mechanism of action like, free radicals scavengers, antithrombotic agents, L-E adhesion inhibitors, immunosuppressive drugs and many other have been tested to alleviate IRI [13–19].