Abstract
Keywords: reperfusion, ischemia
THE MUSCULAR SYSTEM
Introduction
Ischemia is a state of tissue oxygen deprivation accompanied by a reduced washout of the resulting Metabolites. It leads to muscle cell energy failure, inflammatory reaction, and biochemical alterations. This is a disease that causes serious problems including many limb amputations and mortality. (Harman et al 1948) Reperfusion is the restoration of blood flow to the ischemic tissue. Despite the unequivocal benefit of reperfusion of blood to an ischemic tissue, reperfusion itself can elicit a cascade of adverse reactions that paradoxically injure tissue. When reperfusion is attempted, there is a high free radical production and neutrophil activation, which makes local and systematic lesions more severe making the ischemia worse. Reperfusion injury results in damage to such organs as the skeletal muscle, kidneys, lungs, liver, heart, brain and liver. (Zimmermann BJ et al 1992)
Muscle changes
The skeletal muscle is the tissue in a limb that is most vulnerable to ischemia. Because muscle represents the primary mass of tissue in the extremity, damage to muscle is the most critical aspect of the limb reperfusion syndrome. It has been particularly difficult to tell when muscle dies because gross and microscopic changes are minimal for many hours following muscle death. Tourniquet ischemia was induced in rats using spectrophotometric triphenyltetrazolium chloride. An analysis of the skeletal muscle found that significant muscle injury occurred after three h of ischemia. Following 4, 5, and 6 h of ischemia, the injury was severe, with less than 3% of control functional activity demonstrated at 6 h. It was of interest that following 6 h of ischemia, reperfusion hyperemia was apparent and fluorescence exceeded that of the control limb. Muscle fibers, which are composed of two basic types, demonstrate differences in their vulnerability to ischemia. (Birch-Machin et al 1994) After a longer ischemic interval, diminishing ATP levels correlated closely with worsening muscle necrosis. After 6 h of ischemia, 20% of preischemic ATP remained and complete muscle necrosis resulted.
ISCHEMIA contributes to the pathophysiology of many conditions faced by anesthesiologists, including myocardial infarction, peripheral vascular insufficiency, stroke, and hypovolemic shock. Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion per se may augment tissue injury in excess of that produced by ischemia alone.
Skeletal muscle blood flow measurement
Skeletal muscle blood flow was measured by planting a transonicflow probe in the gastrocnemius muscles. (Takada M et al 1997) The probe was connected to a Transonic Laser Doppler blood flowmeter (BLF21, Transonic System Inc) and PowerLab 8/30 (ADInstruments). Blood flow was recorded by Labchart 6 at baseline and after the application and release of tourniquet. (Haimovici H. Metabolic J Cardiovasc Surg 1979)
Heart
Leukocyte adhesion to damaged endothelium is enhanced in the presence of platelets by a mechanism involving platelet P-selectin. (Nemoto T et al 1993) Thrombus formation may also be enhanced by this interaction. In human studies, P-selectin levels were shown to be significantly increased in plasma in patients with acute myocardial infarct . (Harris K et al 1986) The use of a selectin blocker, an analogue of sialyl Lewis X selectin ligand, inhibited leukocyte and platelet interaction after arterial injury produced by angioplasty in pigs.
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