开腹手术所致手术中氧化应激反应的预防

背景有观点认为,各种活性氧成分早期即参与了手术应激和损伤,但尚未得到证实;医疗手段对氧化应激反应的作用也不明确。方法测定血中氢过氧化物的水平,作为细胞损伤的氧化应激指标;同时测定血浆铁还原能力,作为总抗氧化能力的指标。拟行乙状结肠切除术的患者分为4组：七氰烷麻醉下开腹乙状结肠切除术组;七氟烷麻醉下腹腔镜乙状结肠切除术组;丙泊酚麻醉下开腹乙状结肠切除术组;丙泊酚麻醉下腹腔镜乙状结肠切除术组。结果七氟烷开腹乙状结肠切除术组患者的血浆铁还原能力显着降低,由387mmol／L降至153mmol／L,氢过氧化物水平没有变化,这表明手术中患者的氧化应激反应有所增加。氢过氧化物,是一种典型的细胞氧化产物,它并没有明显变化,可能是由于手术中增加的氧化应澈反应还不足以损伤细胞。七氟烷腹腔镜乙状结肠切除术组中,氢过氧化物水平和铁还原能力都没有明显改变,表明腹腔镜手术不会增加手术的氧化应激反应。丙泊酚麻醉2个组,氢过氧化物术毕都明显下降,分别为120±73UCarr和144±107UCarr（1UCarr=0．8mg／L H2O2）。结论开腹手术会增加手术中的氧化应激反应,腹腔镜手术则不会;丙泊酚作为抗氧化剂能够有效地减少手术中的氧化应激反应。     

Monocyte and neutrophil activity after minor surgical stress

Background/Purpose: Surgical stress produces changes in the immune status of patients. In adults, major surgery causes immunosuppression, whereas minor operations stimulate immune responses. In children, the immunologic response to surgery has not been elucidated completely. The authors investigated the effects of minor surgery on immune response by analyzing neutrophil and monocyte phagocytosis and oxidative burst activity. Methods: Sixteen children undergoing elective minor surgery were enrolled. Blood samples were collected before the operation (at time of induction of anesthesia), at the end of operation, and 72 hours after surgery. Neutrophil and monocyte phagocytosis and oxidative burst activity were studied using a flow cytometric method. Results: Phagocytosis and oxidative burst increased significantly at the end of the operation, both in neutrophils (7.4% and 14.3%, respectively) and monocytes (11.6% and 27%, respectively). The increase was only significant for monocytes (17.5%) 72 hours after surgery. White cell count did not show any significant changes. There was no significant correlation between phagocytosis, oxidative burst activity, and white cell count or neutrophil and monocyte count. Conclusions: This study shows that minor surgery in children induces immune activation by increasing neutrophil and monocyte phagocytosis and oxidative burst activity. Further studies are required to understand the molecular basis of these findings.     

Surgical stress and the small intestine: role of oxygen free radicals.

BACKGROUND: Any surgical procedure can be associated with altered intestinal function. The mechanism involved in these changes at the cellular level during surgical stress has not been worked out. This study looked at the biochemical and functional alterations, along with ultrastructural changes, in the intestine during surgical stress in a simple rat model. METHODS: Surgical stress was induced by opening the abdominal wall and handling the intestine as during laparotomy. The effect of oxidative stress on the enterocyte and altered intestinal permeability as well as the ultrastructural changes to the mucosa were studied. RESULTS: Surgical stress results in oxidative stress on enterocytes, as evidenced by increased xanthine oxidase and decreased catalase activity along with altered thiol redox status. This was associated with increased intestinal permeability and widened intercellular spaces. These changes were prominent at 60 minutes after laparotomy and returned to normal by 24 hours. CONCLUSIONS: Mild intestinal handling is capable of inducing oxidative stress in enterocytes; this could be one of the mechanisms by which intestinal mucosal alterations occur during surgical stress.     

Ventilatorinduzierte diaphragmale Dysfunktion in der Kardiochirurgie

Mechanical ventilation is life-saving for patients with respiratory failure or the necessity for deep sedation. The resulting inactivation of the diaphragm has been revealed to induce myofiber atrophy of around 30?% after 18 h of mechanical ventilation and a contractile deficit of up to 50?%. These profound changes are rooted in a disturbed cellular homeostasis which arises from an increase in oxidative stress and results in cellular apoptosis. This article gives an overview of the major pathomechanisms, the influence of comorbidities in cardiac surgery patients and possible treatment options.     

Oxidative-induced calcium mobilization is dependent on annexin VI release from lipid rafts

BACKGROUND: Oxidative stress results in macrophage reprogramming through the formation of focal adhesion-like complexes on lipid rafts. Although the cellular mechanisms responsible for this reprogramming remain unknown, oxidative stress is known to result in a transient increase in intracellular calcium. This transient flux is thought to occur through the membrane dissociation of the calcium-bound protein annexin VI. The purpose of this study is to clarify the source of the calcium, and determine if it is responsible for the formation of focal adhesion-like complexes during oxidative stress through the activation of calcium/calmodulin dependent protein kinase II (CaMK II). METHODS: THP-1 cells were stimulated with hydrogen peroxide. Selected cells were pretreated with methyl beta-cyclodextrin (MbetaCD), a cholesterol-depleting agent; 1,2-bis aminophenoxy ethane-N,N,N',N'-tetraacetic acid, an intracellular calcium chelator; or autocamtide 2-related inhibitory peptide, a CaMK II inhibitor. Intracellular calcium flux was determined by a Fluo-3 technique. Lipid raft and cellular protein were extracted and analyzed for active CaMK II, annexin VI, and components of focal adhesion-like complexes. RESULTS: Hydrogen peroxide exposure led to mobilization of annexin VI from lipid rafts to the cytosol, which was followed by an increase in cytosolic calcium, phosphorylation of CaMK II, and formation of focal adhesion-like complexes. Cholesterol depletion from lipid rafts attenuated all of these effects. 1,2-bis Aminophenoxy ethane-N,N,N',N'-tetraacetic acid and autocamtide 2-related inhibitory peptide pretreatment attenuated CaMK II phopshorylation and formation of focal ahdesionlike complexes. CONCLUSIONS: Macrophage reprogramming during oxidative stress occurs through the cytosolic mobilization of annexin VI from lipid rafts. As a result, bound calcium dissociates, resulting in the activation of CaMK II and the formation of focal adhesion-like complexes.     

Inhibition of the neutrophil oxidative response by propofol: preserved in vivo function despite in vitro inhibition

BACKGROUND AND OBJECTIVE: Propofol has been shown to inhibit a variety of functions of neutrophils in vitro, but there is a lack of in vivo data. To analyse the effects of propofol on neutrophil function in vivo we chose to investigate cataract surgery since it represents a small surgical procedure with minimal immunomodulatory effects induced by surgery. We sought to analyse any immunosuppressive effects of propofol after short-term administration in vivo in comparison to local anaesthesia as well as to in vitro effects of propofol. METHODS: The study was designed as an open randomized trial enrolling 20 patients undergoing general or local anaesthesia. The neutrophil oxidative response and propofol plasma concentration were assessed prior, during and after anaesthesia. Neutrophil function was determined flow cytometrically based on dihydrorhodamine 123 oxidation. RESULTS: Propofol concentrations which yielded a marked suppression in vitro did not alter the neutrophil oxidative response during cataract surgery in vivo. However, after local anaesthesia the neutrophil oxidative response declined to 37%, compared to the control response prior to anaesthesia. CONCLUSIONS: Although we could detect the well established suppression of neutrophil function by propofol in vitro it was not evident in vivo. This may be due to compensating effects on neutrophil function during surgery in vivo. The decline in the neutrophil oxidative response in the local anaesthesia group might be due to increased stress and catecholamine concentrations or a direct interaction of local anaesthetics with neutrophil intracellular signalling.     

Protease activation during surgical stress in the rat small intestine

BACKGROUND: Surgical stress affects intestinal permeability and our earlier study using a rat model indicated that oxidative stress plays an important role in this process. Proteases are important mediators of cellular damage and are known to be activated in oxidative stress. This study looked at protease activity in enterocytes after surgical stress. METHODS: Surgical stress was induced by opening the abdominal wall and handling the intestine as done during laparotomy, in normal and xanthine oxidase-deficient rats. Enterocytes at various stages of differentiation were isolated and protease activity and protection offered by xanthine oxidase inhibitors were determined. Mitochondria and cytosol were prepared from total isolated enterocytes at different periods after surgical stress and protease activation was studied. RESULTS: Surgical stress induced activation of proteases in both the villus and crypt cells. Protease activation is seen in both mitochondria and cytosol, and similar to the other alterations in mucosal cells, protease activation was maximum 60 min after stress, returning to normal by 24 h. Thiol compounds modulate protease activity in both mitochondria and cytosol and the activation is not seen in xanthine oxidase-deficient animals. CONCLUSIONS: Surgical stress induces activation of proteases in villus and crypt cells of the small intestine. Both mitochondrial and cytosolic proteases are activated and free radicals generated by xanthine oxidase may mediate protease activation after surgical stress in the intestine.     

Does prolonged pneumoperitoneum affect oxidative stress compared with open surgical procedures?

BACKGROUND AND PURPOSE: As laparoscopic surgery has evolved, it has become part of the urologic surgical armamentarium and is now used to perform more complex procedures. Carbon dioxide, used to create pneumoperitoneum, produces physiologic changes in various organs, including the kidneys. Such changes are associated with altered redox status because of the release of free radicals and changes in oxidative stress signals. It is unknown whether prolonged pneumoperitoneum is associated with an increase in oxidative stress compared with open surgery. The objective of this study was to compare oxidative stress in patients undergoing urologic laparoscopic and open operations. PATIENTS AND METHODS: Urine samples were obtained immediately preoperatively, immediately postoperatively, and at 6 and 18 hours after surgery from 10 patients who underwent urologic laparoscopic surgery and 10 patients who underwent open surgery. Concentrations of the oxidative stress marker isoprostane (8- iso-prostaglandin F2a) were measured, and the results were analyzed with respect to clinical factors associated with the type of surgery. RESULTS: Urinary isoprostane concentrations (mean +/- SEM) in the laparoscopic and open groups showed an increase immediately after surgery to 189.0 +/- 64.2% and 141.1 +/- 45.8% of the preoperative values, respectively. A decrease in isoprostane was subsequently observed in both groups at 6 hours postoperatively, with preoperative values restored at 18 hours postoperatively (126.3 +/- 19.7% and 89.5 +/- 55.9% at 6 and 18 hours, respectively, in the laparoscopic group and 130.7 +/- 41.6% and 88.7 +/- 20.4% at 6 and 18 hours, respectively, in the open-surgery group). Although in both groups the peak PGF 2a concentration was observed immediately (0 hours) postoperatively, no significant differences were observed between the groups at 0, 6, and 18 hours. In the laparoscopic-surgery group, the mean increase tended to be higher and the decrease to be less prolonged than in the open-surgery group. CONCLUSION: Oxidative stress, as measured by urinary 8-iso-prostaglandin F2a, is produced by both laparoscopic and open urologic surgery. The findings of our nonrandomized study suggest a pattern of increased oxidative stress postoperatively with either type of surgery, with subsequent return almost to preoperative levels. Prolonged laparoscopic operative time did not affect oxidative stress levels.     

Clinical and hormonal response to general anaesthesia in patients affected by different degrees of mental retardation.

BACKGROUND: Poor or no clinical signs of psychological distress are usually observed in patients affected by severe or profound mental retardation (MR). The aim of this study was to use clinical and hormonal parameters in order to compare the amount of stress in patients affected by different degrees of MR undergoing general anaesthesia for dental care. METHODS: Nine patients affected by mild or moderate MR (group A: intellective quotient > 35) and 12 affected by severe or profound MR (group B: intellective quotient < 36), undergoing general anaesthesia for dental care, were studied. The reaction to venipuncture before anaesthesia induction and the recovery from anaesthesia were assessed by clinical scores. Cardiac rate and arterial pressure were recorded before and after venipuncture and after removing the endotracheal tube. Cortisol and prolactin, two hormones affected by stress, were determined in plasma the day prior to surgery (1), after anaesthesia induction (2), and after removing the endotracheal tube (3). RESULTS: During venipuncture, group B was significantly less reactive than group A (p < 0.05) and showed no arterial pressure increase while group A presented a significant increase of systolic pressure; conversely, the groups shared the same hormonal pattern at time 2 (cortisol did not change, prolactin increased significantly). Postoperatively A and B groups did not differ regarding cardiac rate and arterial pressure, while a wider range of postoperative scores was observed in group A in which a further prolactin increase was registered at time 3. CONCLUSIONS: Clinical evaluation can underestimate the stress to which patients affected by severe or profound MR are subjected during anaesthesia induction.     

Effect of N-acetylcysteine on antioxidant status in glycerol-induced acute renal failure in rats

Myoglobinuric acute renal failure has three pathogenic mechanisms: tubular obstruction, renal vasoconstriction, and oxidative stress. The latter is generated through the iron released from the group hemo of the myoglobin. Iron induces the formation of high-activity oxygen free radicals that increase oxidative stress and provoke lipid peroxidation and cellular death. This oxidative stress can be measured in several ways, both total or partially with the total antioxidant status or the intermediate enzymes. On the other hand, N-acetylcysteine is a demonstrated substance with antioxidant properties. The aim of the present work was to assess the effect of N-acetylcysteine on the oxidative stress in the glycerol-induced acute renal failure in rats model. We observed that the animals treated with N-acetylcysteine showed an improvement in the antioxidant activity given by an increase in the total antioxidant status and glutathione reductase levels in serum. This improvement was greater when treatment was administered before the induction of rhabdomyolysis. Nevertheless, the observed increase in antioxidant status was only statistically significant for glutathione reductase but not for total antioxidant status. Our results support an important role for N-acetylcysteine in the treatment of this form of acute renal failure, although we think that oxidative stress is not the main pathogenic mechanism of the tubular necrosis induced by rhabdomyolysis, tubular obstruction and renal vasoconstriction being still more important.     

Plasma hypoxanthine levels during crystalloid and blood cardioplegias: warm blood cardioplegia increases hypoxanthine levels with a greater risk of oxidative stress

BACKGROUND: Patients undergoing cardiopulmonary bypass (CPB) are subjected to severe oxidative stress, and frequently show evidence of acute lung injury post surgery. Associations between acute lung injury, oxidative stress, and aberrant ATP catabolism have been made and prompted us to consider whether the purine metabolites xanthine and hypoxanthine alter significantly during CPB when different types of cardioplegia are used. METHODS: Experimental design: retrospective follow up study on stored plasma samples from patients randomly selected to receive either warm blood, cold blood, or crystalloid cardioplegia. Setting: adult intensive care unit of post graduate teaching hospital. Patients: thirty-eight patients undergoing aortic valve replacement, with or without artery grafting. Operation was carried out by a single surgeon. Interventions: all patients received either a homograft aortic valve or a stentless porcine valve. RESULTS: No significant differences in xanthine levels at any time points during CPB, or between the different cardioplegic groups. Hypoxanthine levels were, however, significantly higher in patients receiving warm blood cardioplegia (74.84+/-16.715 microM, p=0.0151), and was most marked at time point 3 when the aortic cross clamp was released. Patients receiving crystalloid cardioplegia showed higher levels of hypoxanthine (44.56+/-10.16 microM) than those receiving cold blood cardioplegia (21.57+/-7.106 microM). CONCLUSIONS: Considering these data together, it suggests that aberrant ATP catabolism, characteristic of ischaemia/reperfusion, is further disturbed during warm blood cardioplegia leading to a marked increase in plasma hypoxanthine levels. This has the potential to further increase oxidative stress during CPB.     

Effect of l‐carnitine on oxidative stress and platelet activation after major surgery

Background: The surgical/anesthesia trauma is associated with an increased production of reactive oxygen species (ROS). This enhanced oxidative stress leads to cell damage resulting in various complications such as sepsis, myocardial injury and increased mortality. The aim of this study was to investigate the role of antioxidant treatment with l‐ carnitine in oxidative stress and platelet activation in patients undergoing major abdominal surgery. Methods: Forty patients scheduled for abdominal surgery were randomly allocated to l‐ carnitine, administered with a rapid infusion (0.05 g/kg) diluted in 250 ml of saline solution, vs. placebo treatment just before the surgical intervention. At baseline and after treatment, oxidative stress was evaluated by detection of circulating levels of soluble NOX2‐derived peptide (sNOX2‐dp), a marker of NADPH oxidase activation, and by analyzing platelet ROS formation. Platelet activation was studied by dosing sCD40L. Results: We observed an increase of soluble sNOX2‐dp, sCD40L and ROS production in the placebo group compared with the baseline after the surgical intervention. Conversely, in the l‐ carnitine‐treated group, sNOX2‐dp, sCD40L and ROS production did not significantly differ from the baseline. A linear correlation analysis showed that Δ of ROS correlated with Δ of sNOX2 (R_s=0.817; P<0.001) and Δ of sCD40L (R_s=0.780; P<0.001). Multiple linear regression analysis showed that the only independent predictive variable associated with Δ of ROS was Δ of serum NOX2 levels (SE=0.05; standardized coefficient β=1.075; P<0.001). Conclusion: Our findings suggest that l‐ carnitine could be helpful in modulating oxidative stress and platelet activation during major abdominal surgery‐dependent oxidative damage.     

Effect of N‐Acetylcysteine on Antioxidant Status in Glycerol‐Induced Acute Renal Failure in Rats

Myoglobinuric acute renal failure has three pathogenic mechanisms: tubular obstruction, renal vasoconstriction, and oxidative stress. The latter is generated through the iron released from the group hemo of the myoglobin. Iron induces the formation of high‐activity oxygen free radicals that increase oxidative stress and provoke lipid peroxidation and cellular death. This oxidative stress can be measured in several ways, both total or partially with the total antioxidant status or the intermediate enzymes. On the other hand, N‐acetylcysteine is a demonstrated substance with antioxidant properties. The aim of the present work was to assess the effect of N‐acetylcysteine on the oxidative stress in the glycerol‐induced acute renal failure in rats model. We observed that the animals treated with N‐acetylcysteine showed an improvement in the antioxidant activity given by an increase in the total antioxidant status and glutathione reductase levels in serum. This improvement was greater when treatment was administered before the induction of rhabdomyolysis. Nevertheless, the observed increase in antioxidant status was only statistically significant for glutathione reductase but not for total antioxidant status. Our results support an important role for N‐acetylcysteine in the treatment of this form of acute renal failure, although we think that oxidative stress is not the main pathogenic mechanism of the tubular necrosis induced by rhabdomyolysis, tubular obstruction and renal vasoconstriction being still more important.     

5-Aminoisoquinolinone reduces renal injury and dysfunction caused by experimental ischemia/reperfusion

BACKGROUND: Poly (ADP-ribose) polymerase (PARP), a nuclear enzyme activated by strand breaks in DNA, plays an important role in the development of ischemia/reperfusion (I/R) injury. The aim of this study was to investigate the effects of a water-soluble and potent PARP inhibitor, 5-aminoisoquinolinone (5-AIQ), on the renal injury and dysfunction caused by oxidative stress of the rat kidney in vitro and in vivo. METHODS: Primary cultures of rat renal proximal tubular cells, subjected to oxidative stress caused by hydrogen peroxide (H2O2), were incubated with increasing concentrations of 5-AIQ (0.01 to 1 mmol/L) after which PARP activation, cellular injury, and cell death were measured. In in vivo experiments, anesthetized male Wistar rats were subjected to renal bilateral ischemia (45 minutes) followed by reperfusion (6 hours) in the absence or presence of 5-AIQ (0.3 mg/kg) after which renal dysfunction, injury and PARP activation were assessed. RESULTS: Incubation of proximal tubular cells with H2O2 caused a substantial increase in PARP activity, cellular injury, and cell death, which were all significantly reduced in a concentration-dependent by 5-AIQ [inhibitory concentration 50 (IC50) approximately 0.03 mmol/L]. In vivo, renal I/R resulted in renal dysfunction, injury, and PARP activation, primarily in the proximal tubules of the kidney. Administration of 5-AIQ significantly reduced the biochemical and histologic signs of renal dysfunction and injury and markedly reduced PARP activation caused by I/R. CONCLUSION: This study demonstrates that 5-AIQ is a potent, water soluble inhibitor of PARP activity, which can significantly reduce (1) cellular injury and death caused to primary cultures of rat proximal tubular cells by oxidative stress in vitro, and (2) renal injury and dysfunction caused by I/R of the kidney of the rat in vivo.     

The influence of laparoscopic surgery on postoperative polymorphonuclear leukocyte function

Background: Laparoscopic surgery is thought to result in a better preservation of patients' immunological defenses. Polymorphonuclear leukocytes (PMN) are the most important effector cells in the elimination of pathogenic microorganisms. Because little is known about their function after laparoscopic surgery, we studied PMN phagocytosis, antigen expression, and oxygen radical production. Methods: In this study, 17 patients scheduled for Nissen fundoplication were randomly assigned to undergo either a laparoscopic or conventional procedure. To study phagocytic capacity, PMN were incubated with fluorescein isothiocyanate (FITC)-labeled Staphylococcus aureus. Plasma opsonic capacity was measured by comparing PMN phagocytosis in the presence of patients' own plasma with phagocytosis in the presence of control plasma. Cellular activation was measured by the expression of various cell surface markers and by assessment of PMA-stimulated oxidative burst. Results: Phagocytosis by PMN in the presence of patients' plasma was significantly lower 2 h after the conventional operation. No decrease in phagocytosis was observed when control plasma was used, indicating a decreased opsonic capacity of plasma after conventional surgery. No changes were observed after laparoscopic surgery. Furthermore, CD11b expression was significantly lower after the laparoscopic approach, indicating a blunted cellular activation. A significantly lower PMA-stimulated oxidative burst further confirmed the tempered stimulation after laparoscopic surgery. Conclusions: Laparoscopic surgery results in a preservation of the plasma opsonic capacity, and thereby the ability of PMN to phagocytose bacteria. Moreover, the postoperative cellular activation is reduced. The preserved phagocytosis and the blunted activation may prevent the development of postoperative infectious complications. Received: 12 February 1999/Accepted: 30 September 1999/Online publication: 9 August 2000     

The tension-free vaginal tape procedure in women with previous failed stress incontinence surgery.

PURPOSE: The tension-free vaginal tape procedure is an increasingly popular choice for treating female urinary stress incontinence. This ongoing, prospective, open label study presents the results of tension-free vaginal tape surgery at 1 year in women who have previously undergone unsuccessful stress incontinence surgery. MATERIALS AND METHODS: A total of 67 women with previous failed surgery for stress urinary incontinence underwent the tension-free vaginal tape procedure. Treatment outcome was categorized as cure, significant improvement or failure based on cystometry findings and urinary pad loss results at 3 months of followup, and on subjective questioning at 3 months and 1 year of followup. RESULTS: At 12 months 54 women (81%) were cured, 4 (6%) were significantly improved and 9 (13%) were no better. No serious morbidity was noted after the procedure. CONCLUSIONS: The tension-free vaginal tape procedure provides the prospect of a success rate similar to that of a conventional sling procedure in patients with previous failed surgery. It has a low rate of operative complications and postoperative morbidity.     

Relationship between energetic stress and pro-apoptotic/cytoprotective kinase mechanisms in intestinal preservation

BACKGROUND: A recent study from our laboratory documented significant improvements in post-transplant viability in an experimental model of intestinal transplantation when a novel, nutrient-rich preservation solution was used during cold storage. The current study investigated the relationship between energetic/oxidative stress responses and fundamental kinase signaling events during the period of organ storage. This relationship may be a key factor contributing to improved graft viability after storage in a nutrient-rich preservation solution. METHODS: Rat small intestine was harvested and flushed intraluminally with University of Wisconsin (UW) solution or an amino acid-rich (AA) solution as follows: Group 1, no luminal flush (clinical control); Group 2, luminal UW solution; Group 3, luminal AA solution. Energetics (ATP, total adenylates), oxidative stress (malondialdehyde), histology, and MAPK (P38, JNK, ERK)/AMPK/Caspase-3 were assessed throughout 12-hour cold storage. RESULTS: P38 and JNK were upregulated strongly in Group 2 after 1- and 12-hour storage. Group 3 exhibited a delayed activation and subsequent downregulation of these pre-apoptotic signals. Between 6 to 12 hours, a strong upregulation of ERK was observed in Group 3. AMPK downregulation correlated with a reduction in AMP/ATP ratio, ERK upregulation, and P38/JNK downregulation in Group 3. After 12-hour storage, histology indicated superior preservation of mucosal architecture in Group 3 tissues. CONCLUSIONS: A nutrient-rich preservation solution abrogates pre-apoptotic signaling (JNK and P38) and upregulates cytoprotective signals (ERK). Our data support the concept of a concerted effort facilitating cellular protection in response to ischemic stress.     

Oxidative stress in patients undergoing cardiac surgery: comparative study of revascularization and valve replacement procedures

OBJECTIVE: The aim of this study was to evaluate the time course of oxidative stress markers in plasma and erythrocyte from patients undergoing open heart surgery with cardiopulmonary bypass (CPB) and to examine whether the type of surgical technique used (valve replacement or coronary revascularization) produces any differences in these makers. PATIENTS AND METHODS: Twenty-two patients undergoing cardiac surgery with CPB were divided in 2 groups (valve replacement or coronary revascularization). We took 5 blood samples at different times during cardiac surgery and analyzed thiobarbituric acid reactive substances (TBARS), alpha-tocopherol, coenzyme Q, and retinol in plasma and TBARS (baseline levels and induced by Fe(2+)-ascorbate oxidation), alpha-tocopherol, coenzyme Q and catalase, superoxide dismutase, and glutathione peroxidase activity in erythrocyte. RESULTS: Plasma alpha-tocopherol content decreased after starting CPB in both groups. In contrast, in erythrocytes there was an increase in the activity or concentration of all of the antioxidants. Erythrocyte TBARS contents, both baseline levels and induced levels, were higher in coronary revascularization group. CONCLUSION: Although both groups suffered an increase in oxidative stress after CPB, this increase was higher in coronary revascularization group and therefore the possibility of post-CPB complications could be more severe in this group. As the groups followed a different pattern of antioxidant response, a different therapeutic approach may be required for each.