Abstract
Our previous study on human skeletal muscle undergoing ischemia and reperfusion has revealed that granulocytes, which infiltrate the muscle tissue in large numbers, play an important role in mediating fibre injuries by producing superoxide anion (O2-) which is responsible for membrane lipid peroxidation. In the current study five patients undergoing aortic reconstructive surgery were given acetyl-carnitine (2 mg/kg i.v. plus 1 mg/kg/min for 30 min) prior to the induction of ischemia. Muscle biopsies and blood samples were examined: a) after anaesthesia; b) at the end of ischemia; and c) 30 min after reperfusion, with the aim of elucidating whether acetylcarnitine could prevent the infiltration and/or the activation of granulocytes and eventually skeletal muscle injuries. During ischemia and reperfusion complement activation recruited numerous granulocytes into the muscle tissue, but, contrary to the untreated samples, the ability for O2--generation of these cells remained at low levels and was comparable to that of ischemia even when molecular O2- was reintroduced to the tissue. Accordingly, the morphological changes of the postischemic muscle fibers were substantially reduced when compared to the untreated samples, in fact, the mitochondrial swelling was only moderate and the intramitochondrial dense bodies were small and scarce. The current findings support a positive role of acetyl-carnitine in ameliorating the ischemia-reperfusion (I-R)-induced damage of human skeletal muscle.
| Original language | English |
|---|---|
| Pages (from-to) | 683-690 |
| Number of pages | 8 |
| Journal | Histology and Histopathology |
| Volume | 9 |
| Issue number | 4 |
| Publication status | Published - 1994 |
| Externally published | Yes |
Keywords
- Acetyl-carnitine
- Granulocytes
- Ischemia-reperfusion syndrome
- Skeletal muscle
Fingerprint
Dive into the research topics of 'Ischemia-reperfusion of human skeletal muscle during aortoiliac surgery: Effects of acetylcarnitine'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver