Effect of Dibutyryl Cyclic Adenosine Monophosphate on Skeletal Muscle Reperf usion Injury in the Rat

Abstract

To clarify the action of dibutyryl cyclic adenosine monophosphate (DBcAMP) on reperfused ischemic muscle, experiments were conducted using the hindlimbs of 18 male Lewis rats. At the midportion of the thigh all tissues except for the femoral artery and vein were transected, and a route for continuous intravenous infusion was secured in a contralateral limb vein. After inducing total ischemia by clamping the femoral artery and vein with a vascular clamp for 4 h, the limb was reperfused for 1 h. Blood flow was then compared using the hydrogen gas clearance method in a group in which DBcAMP 10 mg was continuously infused from a vein in the contralateral hindlimb from 1 h prior to the induction of ischemia to 1 h after the completion of ischemia (DBcAMP group), a group in which saline was infused in the same manner (control group), and a group which was subjected to biopsy alone (biopsy group). The percent change in blood flow was significantly higher in the DBcAMP group than in the control group at 15 and 30 min after the release of the clamp. Adenosine triphosphate (ATP), phosphocreatine (PCr), and lipid peroxide (LPO) were measured in tissue samples obtained 1 h after reperfusion. Serum LPO was measured in blood samples collected at the same time. ATP values were higher in the DBcAMP group than in the control group. PCr was significantly higher in the DBcAMP group than in the control group. LPO levels in skeletal muscle tissue did not differ significantly between the DBcAMP and control groups. In contrast, serum LPO levels were significantly lower in the DBcAMP group than the control group. On morphologic analysis the control and DBcAMP groups showed normal vascular endothelial cells and absence of the ‘no-reflow’ phenomenon. These data confirm that in this reperfusion model the administration of DBcAMP enhances the viability of skeletal muscle cells. Moreover, mediated by an effect on vascular endothelial cells this agent is thought to be of help in mitigating the vascular endothelial cell injury occurring in acute ischemic injury. DBcAMP may be a useful agent in mitigating skeletal muscle ischemia-reperfusion injury.

Dexmedetomidine Reduces the Ischemia-Reperfusion Injury Markers During Upper Extremity Surgery With Tourniquet

“…This superoxide ion then leads to the generation of hydrogen peroxide and the hydroxyl radical, both of which are toxic to cells by lipid peroxidation of the cell membranes. 4,22 Reactive oxygen species or lipid peroxides are short-lived and difficult to measure directly. Thus, MDA and HPX as lipid peroxidation degradation products are frequently assayed as reflecting lipid peroxidation level.…”

“…3 Ischemia also causes an increase in intracellular hypoxanthine (HPX) as a result of adenosine triphosphate breakdown. 4 Therefore, MDA and HPX have been described as sensitive markers of ischemia-reperfusion injury.…”

The Effects of 6% Hydroxyethyl Starch on Ischemia - Reperfusion Injury in Total Knee Arthroplasty with Tourniquet Application

“…When oxygen is reentered with reperfusion, hypoxanthine concentration is increased with high activity of the xanthine oxidase. This increased xanthine oxidase during ischemia leads to production of reactive oxygen species and cellular injury [10].…”

The effect of ketamine on acute muscular ischaemia reperfusion in rats

“…Lipid peroxidation occurring during ischaemiareperfusion is a chain reaction leading to oxidation of polyunsaturated fatty acids which, in turn, disrupts the structure of biological membranes and produces toxic metabolites such as malondialdehyde (MDA) [5]. Although skeletal muscle is fairly resistant to ischaemic injury, ischaemia-reperfusion injury in the skeletal muscle has been documented in previous studies [3,4,6]. The occurrence of lipid peroxidation causing widespread tissue damage in skeletal muscle ischaemia-reperfusion was first reported by Lindsey and colleagues [7].…”

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