Ischemic preconditioning of free muscle flaps: An experimental study

Microsurgery ◽  
2005 ◽  
Vol 25 (7) ◽  
pp. 524-531 ◽  
Author(s):  
Claudiu F. Marian ◽  
Lucian P. Jiga ◽  
Mihai Ionac
Keyword(s):  
Experimental Study ◽  
Ischemic Preconditioning ◽  
Muscle Flaps

Noninvasive remote ischemic preconditioning for global protection of skeletal muscle against infarction

2003 ◽  
Vol 285 (4) ◽  
pp. H1435-H1443 ◽  
Author(s):  
Patrick D. Addison ◽  
Peter C. Neligan ◽  
Homa Ashrafpour ◽  
Asim Khan ◽  
Anguo Zhong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protective Effect ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Ischemic Preconditioning ◽  
Bolus Injection ◽  
Remote Ischemic Preconditioning ◽  
Intravenous Bolus ◽  
Muscle Flaps ◽  
Intravenous Bolus Injection

The aim of this study was to investigate the efficacy and mechanism of action of a noninvasive remote ischemic preconditioning (IPC) technique for the protection of multiple distant skeletal muscles against ischemic necrosis (infarction). It was observed in the pig that three cycles of 10-min occlusion and reperfusion in a hindlimb by tourniquet application reduced the infarction of latissimus dorsi (LD), gracilis (GC), and rectus abdominis (RA) muscle flaps by 55%, 60%, and 55%, respectively, compared with their corresponding control ( n = 6, P < 0.01) when they were subsequently subjected to 4 h of ischemia and 48 h of reperfusion. This infarct-protective effect of remote IPC in LD muscle flaps was abolished by an intravenous bolus injection of the nonselective opioid receptor antagonist naloxone (3 mg/kg) 10 min before remote IPC and a continuous intravenous infusion (3 mg/kg) during remote IPC and by an intravenous bolus injection of the selective δ1-opioid receptor antagonist 7-benzylidenealtrexone maleate (3 mg/kg). However, this infarct-protective effect of remote IPC was not affected by an intravenous bolus injection of the ganglionic blocker hexamethonium chloride (20 mg/kg) or the nonspecific adenosine receptor antagonist 8-( p-sulfophenyl)theophylline (10 mg/kg) or by a local intra-arterial injection of the adenosine1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (3 mg/muscle flap) given 10 min before remote IPC. It was also observed that this remote IPC of skeletal muscle against infarction was associated with a slower rate of muscle ATP depletion during the 4 h of sustained ischemia and a reduced muscle neutrophilic myeloperoxidase activity after 1.5 h of reperfusion. These observations led us to speculate that noninvasive remote IPC by brief cycles of occlusion and reperfusion in a pig hindlimb is effective in global protection of skeletal muscle against infarction. This infarct-protective effect is most likely triggered by the activation of opioid receptors in the skeletal muscle, and remote IPC is associated with an energy-sparing effect during sustained ischemia and attenuation of neutrophil accumulation during reperfusion.

Role and mechanism of PKC in ischemic preconditioning of pig skeletal muscle against infarction

2000 ◽  
Vol 279 (2) ◽  
pp. R666-R676 ◽  
Author(s):  
Richard A. Hopper ◽  
Christopher R. Forrest ◽  
Huai Xu ◽  
Anguo Zhong ◽  
Wei He ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Muscle Blood Flow ◽  
Signal Transduction Pathway ◽  
Muscle Flap ◽  
Polymyxin B ◽  
Myeloperoxidase Activity ◽  
Muscle Flaps ◽  
Arterial Blood

Protein kinase C (PKC) inhibitors, chelerythrine (Chel, 0.6 mg) and polymyxin B (Poly B, 1.0 mg), and PKC activators, phorbol 12-myristate 13-acetate (PMA, 0.05 mg) and 1-oleoyl-2-acetyl glycerol (OAG, 0.1 mg), were used as probes to investigate the role of PKC in mediation of ischemic preconditioning (IPC) of noncontracting pig latissimus dorsi (LD) muscles against infarction in vivo. These drugs were delivered to each LD muscle flap (8 × 12 cm) by 10 min of local intra-arterial infusion. It was observed that LD muscle flaps sustained 43 ± 5% infarction when subjected to 4 h of global ischemia and 24 h of reperfusion. IPC with three cycles of 10 min ischemia-reperfusion reduced muscle infarction to 25 ± 3% ( P < 0.05). This anti-infarction effect of IPC was blocked by Chel (42 ± 7%) and Poly B (37 ± 2%) and mimicked by PMA (19 ± 10%) and OAG (14 ± 5%) treatments ( P < 0.05), given 10 min before 4 h of ischemia. In addition, the ATP-sensitive K+ (KATP) channel antagonist sodium 5-hydroxydecanoate attenuated ( P < 0.05) the anti-infarction effect of IPC (37 ± 2%), PMA (44 ± 17%), and OAG (46 ± 9%). IPC, OAG, and Chel treatment alone did not affect mean arterial blood pressure or muscle blood flow assessed by 15-μm radioactive microspheres. Western blot analysis of muscle biopsies obtained before (baseline) and after IPC demonstrated seven cytosol-associated isoforms, with nPKCɛ alone demonstrating progressive cytosol-to-membrane translocation within 10 min after the final ischemia period of IPC. Using differential fractionation, it was observed that nPKCɛ translocated to a membrane compartment other than the sarcolemma and/or sarcoplasmic reticulum. Furthermore, IPC and preischemic OAG but not postischemic OAG treatment reduced ( P < 0.05) muscle myeloperoxidase activity compared with time-matched ischemic controls during 16 h of reperfusion after 4 h of ischemia. Taken together, these observations indicate that PKC plays a central role in the anti-infarction effect of IPC in pig LD muscles, most likely through a PKC-KATPchannel-linked signal-transduction pathway.

Role of ATP-sensitive K+ channels in ischemic preconditioning of skeletal muscle against infarction

1997 ◽  
Vol 273 (1) ◽  
pp. H44-H51 ◽  
Author(s):  
C. Y. Pang ◽  
P. Neligan ◽  
H. Xu ◽  
W. He ◽  
A. Zhong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Energy Charge ◽  
Katp Channels ◽  
High Energy ◽  
Intraarterial Infusion ◽  
Muscle Flaps ◽  
Charge Potential

We studied the role and mechanism of ATP-sensitive K+ (KATP) channels in ischemic preconditioning (IPC) of skeletal muscle against infarction in vivo. Surgically denervated, noncontractile latissimus dorsi muscle flaps in pentobarbitone-anesthetized pigs were assigned to nine groups: control; IPC (3 cycles of 10-min ischemia/reperfusion); preischemic lemakalim (LMK, 0.18 mg/muscle); postischemic LMK; sodium 5-hydroxydecanoate (5-HD, 27 mg/muscle) before IPC; glibenclamide (Glib 0.3 mg/kg iv) before IPC; 5-HD before preischemic LMK; 5-HD before ischemia; and Glib before ischemia. Except for Glib, all drugs were delivered to each muscle by 10-min local intraarterial infusion to avoid systemic effects. All muscle flaps underwent 4 h of global ischemia. Infarction was assessed at 48 h of reperfusion. In a separate study, muscle biopsies were taken before, during, and after ischemia for assay of high-energy phosphate and lactate contents and myeloperoxidase (MPO) activity. It was observed that muscle infarction in the IPC (24 +/- 2%) and preischemic LMK (21 +/- 2%) groups were smaller (P < 0.05) than that in the control (42 +/- 2%). The anti-infarction effect of IPC and LMK was blocked by 5-HD or Glib. IPC and preischemic LMK caused a higher (P < 0.05) muscle content of ATP and energy charge potential, a lower (P < 0.05) muscle content of lactate during ischemia, and a lower (P < 0.05) muscle MPO activity throughout 16 h of reperfusion compared with the control. These observations indicated for the first time that KATP channels are also involved in the anti-infarction effect of IPC in noncontractile skeletal muscle in vivo. Presently, the cause and importance of energy-sparing and neutrophil-inhibitory effects of IPC and LMK are not known.

scholarly journals Exploring Spinal Cord Protection by Remote Ischemic Preconditioning: An Experimental Study

2017 ◽  
Vol 103 (3) ◽  
pp. 804-811 ◽  
Author(s):  
Johanna Herajärvi ◽  
Tuomas Anttila ◽  
Henna Sarja ◽  
Caius Mustonen ◽  
Henri Haapanen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Experimental Study ◽  
Ischemic Preconditioning ◽  
Remote Ischemic Preconditioning ◽  
Spinal Cord Protection
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