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A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care

Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
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Minerva Anestesiologica 2000 July-August;66(7-8):523-30


language: English

Adaptive changes in response to acute hypoxia, ischemia and reperfusion in human cardiac cell

Corbucci G. G.

From the Institute of Anaesthesia and Intensive Care University of Cagliari


Background. Previous stud­ies ­have ­shown ­that bio­mo­lec­u­lar and bio­chem­i­cal adap­tive chang­es antag­o­nize oxi­da­tive dam­age due to hypox­ia and ische­mia in myo­car­dial ­cells. The aim of our ­study was to ver­i­fy in ­human ischem­ic and reper­fused car­diac tis­sue the rela­tion­ship ­between mit­o­chon­dri­al ­enzyme activ­ities and the acti­va­tion of HSP70 and c-fos syn­the­sis in the con­text of a cytop­ro­tec­tive mech­a­nism. Nitric ­oxide (NO) mod­ulat­ing ­effects on mit­o­chon­dri­al res­pir­a­to­ry ­chain ­enzyme activ­ities in ischem­ic and reper­fused tis­sue ­were inves­ti­gat­ed (pre­lim­i­nary ­report).
Methods. During elec­tive cor­o­nary ­artery ­bypass graft­ing, in 30 con­sec­u­tive ­patients ven­tri­cle sam­ples ­were tak­en one ­before aor­tic clamp­ing the sec­ond ­after 55±8 min ischem­ic peri­od and the ­third 34±5 ­after ­final reper­fu­sion. Coronary ­sinus ­blood sam­ples ­were tak­en in par­allel to ­assess ­free rad­i­cal ­release meas­ured by mal­o­n­dialde­hyde (MDA) lev­els. In a ­small num­ber of ­patients (N=5) ­nitric ­oxide tis­sue lev­els ­were ana­lyzed.
Results. When com­pared ­with nor­mox­ic tis­sue, a sig­nif­i­cant ­decrease in cyto­chrome ox­i­dase (COX) and suc­ci­nate Cyt-c reduc­tase (SCR) activ­ities in ischem­ic and reper­fused sam­ples ­were ­observed. The acti­va­tion of HSP70-72 and c-fos tran­scrip­tion fac­tor was evi­dent in cours­es of ische­mia and reper­fu­sion. Blood MDA lev­els under­line the con­cept ­that oxy­ra­di­cal gen­er­a­tion char­ac­teriz­es per­ox­i­da­tive dam­age in reoxy­gen­at­ed myo­car­dial tis­sue ­while adap­tive chang­es ­which ­occur in ischem­ic ­cells ­seem to antag­o­nize the oxy­ra­di­cal inju­ry.
Conclusions. In the ­course of ­heart sur­gery the myo­car­dial ­cell ­seems to pre­vent ischem­ic dam­age acti­vat­ing ­some pecu­liar bio­mo­lec­u­lar and bio­chem­i­cal adap­tive chang­es ­which per­mit the rever­sibil­ity of the oxi­da­tive inju­ry. In con­trast it ­appears evi­dent ­that mas­sive and rap­id reoxy­gen­a­tion of the car­diac tis­sue ­leads to per­ox­i­da­tive dam­age due to oxy­ra­di­cal gen­er­a­tion. Nitric ­oxide ­seems to ­play a cru­cial ­role in cel­lu­lar adap­ta­tion to ische­mia ­even if fur­ther stud­ies ­will be need­ed to elu­ci­date ­these find­ings. From the ­data ­obtained in ­this ­work we can­not ­draw cer­tain con­clu­sions in ­terms of ­human car­diac ­cell adap­ta­tion to ische­mia where­as it ­seems con­vinc­ing ­that reoxy­gen­a­tion, as actu­al­ly ­employed in clin­i­cal prac­tice, com­pro­mis­es the integ­rity of the ­cells.

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