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The Journal of Cardiovascular Surgery 2001 October;42(5):605-10


lingua: Inglese

Biomolecular and biochemical response of myocardial cell to ischemia and reperfusion in the course of heart surgery

Ricchi A., Cardu G., Lettieri B. °, Fusar-Poli D. E. *, Tacchini C. *, Bernelli-Zazzera A. *, Corbucci G. G. **

From the Cardiosurgery Department A. Brotzu Hospital, Cagliari, Italy *Institute of General Pathology CNR Center for the Study of Cell Pathology University of Milan, Milan, Italy **Institute of Anaesthesia, Resuscitation University of Cagliari, Cagliari, Italy °Institute of Anaesthesia, Intensive Care University of Naples, Naples, Italy


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 syn­the­ses 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 mal­o­nal­de­hyde (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 Cox­i­dase (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 char­ac­ter­ize the 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 by 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 con­vin­cible ­that reoxy­gen­a­tion, as actu­al­ly ­employed in clin­i­cal prac­tice, com­pro­mis­es the integ­rity of the ­cells.

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