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Minerva Anestesiologica 2001 May;67(5):387-92

Copyright © 2009 EDIZIONI MINERVA MEDICA

language: Italian

The nitric oxide metabolism in the hypoxic, ischemic and reperfused human skeletal muscle cell: clinical and therapeutical observation

Corbucci G. G., Palmerini C. *, Palombari R. **, Lettieri B., Grella E., Velluti C. ***, Chelo C. ***

Università degli Studi - Cagliari Istituto di Anestesia-Rianimazione °II Università degli Studi - Napoli Dipartimento di Anestesia-Rianimazione, Terapia Intensiva *Università degli Studi - Perugia Dipartimento Biologia Cellulare e Molecolare **Dipartimento di Chimica *** Università degli Studi - Cagliari Dipartimento di Ortopedia e Traumatologia


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Back­ground. The bio­chem­i­cal and meta­bol­ic ­role ­played by ­nitric ­oxide (NO) in ­course of oxi­da­tive ­stress due to ­cell hypox­ia, ische­mia and reper­fu­sion has a deter­mi­nant rel­e­vance in the mit­o­chon­dri­al adap­tive chang­es ­which antag­o­nize the irre­ver­sible mor­pho-func­tion­al dam­age. In par­tic­u­lar con­di­tions, ­such as in pro­longed ische­mia and/or exog­e­nous NO sup­ple­men­ta­tion, ­this ele­ment is ­present in the radi­cal­ic ­form (·NOO) con­cur­ring to per­ox­i­da­tive ­cell inju­ry. Aim of ­this ­study was to inves­ti­gate ­these oppo­site NO ­aspects in hypox­ic, ischem­ic and reper­fused ­human skel­e­tal mus­cle tis­sue.
Meth­ods. Skel­e­tal mus­cle sam­ples ­were tak­en dur­ing elec­tive ­knee ortho­pe­dic sur­gery in 10 con­sec­u­tive ­patients. The biop­sies ­were ­obtained ­before, ­after 5±1 min and 58±2 min ­from tour­ni­quet appli­ca­tion and ­then ­after 18±3 min fol­low­ing mus­cle reper­fu­sion. The sam­ples, imme­di­ate­ly fro­zen in liq­uid nitro­gen, ­were ­assayed for endo­cel­lu­lar ­free NO fol­low­ing the gas-amper­o­met­ric meth­od ­described by Pal­me­ri­ni C.
­Results. ­When com­pared ­with nor­mox­ic tis­sues, a sig­nif­i­cant ­decrease in ­free NO con­tent was ­observed in hypox­ic sam­ples. ­After ­about 60 min of pro­longed ische­mia the NO lev­els ­show an evi­dent ­increase, ­while the tis­sue reper­fu­sion ­leads to a pro­gres­sive res­to­ra­tion of phys­io­log­i­cal con­tent in the cel­lu­lar ­free ­nitric ­oxide.
Con­clu­sions. The ­obtained ­data in hypox­ic mus­cle ­cell ­seem to under­line the piv­ot­al ­role ­played by NO in adapt­ing the cyto­chrome c oxi­dase oxi­da­tive activ­ity to low­er O2 bio-avail­abil­ity. On the oth­er ­hand the pro­longed ische­mia ­leads to a con­sis­tent ·NOO gen­er­a­tion trig­gered by oxy­ra­di­cal gen­er­a­tion and Ca2+ intra­cel­lu­lar ­over ­load. ­Even if the tis­sue reoxy­gen­a­tion ­restores the nor­mal NO lev­els it is argu­able ­that the pre-treat­ment of ischem­ic ­cell ­with anti­ox­i­dants, Ca2-antag­o­nist and Desa­meth­a­sone sup­ple­men­ta­tion ­could rep­re­sent a cru­cial and spe­cif­ic ther­a­peu­tic ­approach to crit­i­cal­ly ill ­patient.

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