Effects of intracisternal tramadol on cerebral and spinal neuronal cells in rat.

BACKGROUND: The aim was to investigate whether tramadol had toxic effect on cerebral neurons and/or spinal cord neurons when it was administered into the cerebrospinal fluid. Due to lipid peroxidation (LPO) and myeloperoxidation (MPO) levels are not specific predictors of neuronal damage, these biochemical markers of tissue damage were evaluated together with the histopathological findings of apoptosis. METHODS: Forty eight Wistar rats were anesthetized and the right femoral artery was cannulated. Mean arterial pressures, and heart rates, arterial carbon dioxide tension, arterial oxygen tension, blood pH were recorded. When the free cerebrospinal fluid flow was seen; 0.04 mL normal saline (Group Sham) or diluted tramadol in 0.04 mL volume (Group T1, T2, T0.5 and T0.1) was administered within 30 seconds from the posterior craniocervical junction of rats. For the Control Group, the free cerebrospinal fluid flow was seen but nothing was injected in it. After 7 days, following the sacrification of the rats, brain tissue, cervical and lumber segments of spinal cord were collected for the histopathological and biochemical examination. RESULTS: There was not a statistically significant difference among all groups regarding the brain LPO levels (P=0.485). The LPO levels of the cervical segment of spinal cord and the lumbar segment of spinal cord were also similar (P=0.146, P=0.939, respectively). The mean MPO levels of the cervical and the lumbar segments of spinal cord were similar among all groups (P=0.693, P=0.377, respectively). There were not any statistically significant difference regarding the total number of red neurons of the brain tissue and the cervical and lumbar segments of spinal cord among all groups (P=0.264, P=0.202, P=0.780, respectively). CONCLUSION: Tramadol had no neurotoxic effect on brain and on spinal cord tissue when administered by the intracisternal route in cerebrospinal fluid in rats.

Protective effect of dexamethasone on fetal rat skin in experimental intrauterine ischaemia/reperfusion injury.

BACKGROUND: Perinatal asphyxia is an important cause of injury to fetal tissues such as the brain, heart, liver and gastrointestinal system. Fetal skin has also been shown to be vulnerable to intrauterine injury after intrauterine ischaemia/reperfusion (I/R) injury. AIM: To examine the effect of dexamethasone on fetal skin in intrauterine I/R injury in rats. METHODS: The response of rat fetal skin to I/R injury and maternal dexamethasone treatment were assessed by determining thiobarbituric acid reactive substances (TBARS), and myeloperoxidase (MPO) and nitric oxide (NO) metabolites. We also examined the ultrastructural changes of fetal skin. Bilateral utero-ovarian artery clamping was performed to produce ischaemia for 30 min in rats at day 19 of pregnancy, and reperfusion was achieved by removing the clamps for 60 min before fetal tissue was collected. The treatment group was given dexamethasone intraperitoneally 20 min before I/R was performed. RESULTS: TBARS, MPO and NO all increased significantly in fetal rat skin after I/R injury. Levels of TBARS, MPO and NO were significantly lower in the dexamethasone-treated group than in the I/R-only group. I/R injury produced ultrastructural damage in the epidermis. Oedema and mitochondrial damage were less severe in the dexamethasone-treated group. CONCLUSIONS: Maternal treatment with dexamethasone may have a protective effect on fetal skin in cases of I/R injury.

Effect of intrauterine ischaemia-reperfusion injury on rat skin.

INTRODUCTION: It was previously demonstrated that decreased maternal blood flow might create impairment in skin development. The aim of this study was to show by means of lipid peroxidation the effect of intrauterine ischaemia-reperfusion injury on fetal rat skin. METHODS: In total, 24 female Spraque-Dawley rats, 19 days pregnant, were used. They were separated into three groups (n = 8): a control group, a sham-operated group and an experimental group. Laparotomy was performed on all three groups. In the sham-operated and experimental groups, utero-ovarian artery dissection was performed in addition. In the experimental group, fetal ischaemia was induced by clamping the utero-ovarian artery bilaterally for 30 min, and reperfusion was achieved by removing the clamps for 60 min. At the end of the experiment, the fetuses were removed by caesarean section and skin specimens were taken from the fetuses. Lipid peroxidation in the skin tissues was determined as thiobarbituric acid reactive substance (TBARS) concentration for each fetal rat. One-way ANOVA and post hoc tests were used for statistical analysis. RESULTS: The level of TBARS was significantly increased in the fetal rat skin after ischaemia-reperfusion injury compared with the control group. CONCLUSION: Lipid peroxidation has an important role in intrauterine ischaemia-reperfusion-induced fetal skin damage in rats.

Neuroprotective effect of melatonin on experimental peripheral nerve injury: an electron microscopic and biochemical study.

BACKGROUND AND STUDY AIMS: Melatonin is an important antioxidant agent with a protective role in the prevention of oxidative stress. We designed an experimental study which focused on the potential neuroprotective effect of melatonin on peripheral nerve injury. MATERIALS AND METHODS: Sciatic nerve injury was induced in the mid thigh region of 30 male Wistar rats by clip compression. Melantonin was injected intraperitoneally in 15 of the 30 rats. Electron microscope and biochemical studies were performed to assess the potential beneficial effect of melatonin on peripheral nerve regeneration. Changes to cellular organelles, myelin lamellae and axons were studied. RESULTS: There was a significant difference between the melatonin and nerve injury groups. Rats treated with melatonin demonstrated significant structural protection of the myelin lamellae compared to the nerve injury group. Axonal shrinkage and myelin changes were not prominent histopathologically in melatonin-treated group. Biochemical analysis confirmed the neuroprotective effects of melatonin with significantly lower lipid peroxidation and myeloperoxidase activity measurements in the melatonin-treated group compared to the neural injury group. The results indicate that melatonin can improve neural healing. CONCLUSION: With its neuroprotective effect, as demonstrated in this experimental peripheral nerve injury, melatonin might be used successfully in clinical practice. Further studies on the correct dosage and possible side effects are necessary.

Possible impact of inflammatory status on C-telopeptide pyridinoline cross-links of type I collagen and osteocalcin levels around oral implants with peri-implantitis: a controlled clinical trial.

Detection of progression level of peri-implantitis may help in the prevention of oral implant failure. C-telopeptide pyridinoline crosslinks of Type I collagen (ICTP) and osteocalcin (OC) are specific markers of bone turnover and bone degradation. Determination of the ICTP and OC levels in the peri-implant sulcus fluid (PISF) may predict the metabolic and/or inflammatory changes in the peri-implant bone. The aim of this clinical study was to evaluate ICTP and OC levels in the PISF for oral implants with and without peri-implant bone destruction and correlate these levels with the traditional clinical peri-implant parameters (probing depth, plaque index, gingival index and gingival bleeding time index) and radiographic bone level measurements. Fifteen patients with 30 peri-implant sites with bone destruction (radiographic bone loss) and health were included. Clinical parameters were measured and PISF was collected from the sites. Peri-implant sulcus fluid ICTP and OC levels were detected by radioimmunoassay technique from PISF samples. All clinical parameters demonstrated a significant increase in peri-implantitis sites compared with healthy sites. The PISF volume of the peri-implantitis sites was also significantly higher than of the healthy peri-implant sites. Although not statistically significant, a trend of increase was demonstrated in ICTP PISF samples sampled from peri-implantitis sites compared with healthy sites. A significant increase was noticed for OC PISF level in peri-implantitis sites compared with healthy ones. As well as peri-implant clinical measurements, volumetric changes at PISF may be counted as an important clinical parameter to distinguish the bone destruction sites from healthy sites around oral implants.

Effect of low-dose N-acetyl-cysteine infusion on tourniquet-induced ischaemia-reperfusion injury in arthroscopic knee surgery.

BACKGROUND: Temporary occlusion of blood flow is used during arthroscopic knee surgery in order to provide a bloodless surgical field. The resulting ischaemia-reperfusion causes lipid peroxidation, which contributes to tissue injury. The aim of the study was to investigate the effect of low-dose n-acetyl cysteine (NAC) infusion on oxidative stress by determining malondialdehyde (MDA) levels during arthroscopic knee surgery. METHODS: Thirty patients, ASA I - II, undergoing arthroscopic knee debridement under a tourniquet were divided into NAC and control groups. Anaesthesia was induced with propofol, fentanyl and vecuronium bromide and maintained with desflurane in an equal parts O(2)-N(2)O mixture. In the NAC group, an infusion of NAC, 5 mg kg(-1).h(-1), was started after intubation, and continued until extubation. An equal volume of saline was infused to the control group. Duration of ischaemia, anaesthesia time, total dose of NAC infused were also recorded. Venous blood and synovial membrane tissue samples were obtained 10 min after the onset of NAC infusion but before tourniquet inflation (t1), after 30 min of ischaemia (t2), and after 5 min of reperfusion following tourniquet release (t3). RESULTS: Plasma MDA levels were significantly lower in the NAC group on reperfusion. There were no differences between the groups in tissue MDA levels at ischaemia and reperfusion times. CONCLUSION: Low-dose n-acetyl cysteine infusion attenuates lipid peroxidation and ischaemia-reperfusion injury in arthroscopic knee surgery requiring tourniquet application.

A single dose of erythropoietin attenuates lipid peroxidation in experimental liver ischemia-reperfusion injury in the rat fetus.

OBJECTIVE: The aim of the study was investigate the effectiveness of recombinant human erythropoietin (r-Hu-EPO) in attenuating the severity of experimental liver ischemic injury in fetal rats. METHODS: The animals were divided randomly into four groups. In the control group, fetal whole liver tissue was taken immediately after laparotomy from pregnant animals. In the ischemia-reperfusion (I/R) group, tissue samples were taken immediately after I/R injury. In the vehicle group, 0.4 ml of human serum albumin solution and in the treatment group, r-Hu-EPO (5000 IU/kg) in 0.4 ml of human serum albumin solution were given intraperitoneally, 30 min before I/R injury, as a single dose. Thiobarbituric acid-reactive substances (TBARS) were estimated to demonstrate lipid peroxidation. RESULTS: Lipid peroxidation byproducts increased after I/R injury. Administration of r-Hu-EPO reduced TBARS after I/R injury. CONCLUSION: Further investigations are needed to understand the mechanism of the hepatoprotective effect of erythropoietin and the clinical importance of ischemic liver injury in the fetus.

The effects of etomidate, thiopental, and propofol in induction on hypoperfusion-reperfusion phenomenon during laparoscopic cholecystectomy.

BACKGROUND: A hypoperfusion-reperfusion human model is observed during and soon after laparoscopic surgery. The aim of the study was to research the preventive effects of etomidate, thiopental, and propofol in induction on hypoperfusion- reperfusion phenomenon during laparoscopic cholecystectomy. METHODS: Thirty-six consecutive ASA I-II patients were randomized into three groups of 12 patients each. Anaesthesia was induced with etomidate in group 1, thiopental in group 2, and propofol in group 3. Venous blood samples were obtained at different time points for measurement of plasma malondialdehyde (MDA) levels. Arterial blood and gastric juice samples were obtained for the calculation of gastric intramucosal pH (pHi). Also changes in aminotransferases, alkaline phosphatase and total bilirubin levels were assessed. RESULTS: There was a significant decrease in pHi at 1 min before desufflation (BD) and 20 min after desufflation (AD) compared with before insufflation (BI) in all groups. Plasma level of MDA was significantly increased in group 1 at 1 min BD and 20 min AD compared with before induction of anaesthesia (baseline). Malondialdehyde levels were decreased significantly in group 3 and increased non-significantly in group 2 at the same time points. Also AST and ALT levels were significantly increased in both groups 1 and 2 at 24 h postoperatively. CONCLUSION: Propofol with antioxidant activity may offer many advantages by scavenging reactive oxygen species and their metabolites in case of anticipated hypoperfusion-reperfusion phenomenon, such as would occur in laparoscopic surgery.

Early effects of mild brain trauma on the cytoskeletal proteins neurofilament160 and MAP2, and the preventive effects of mexilitine.

OBJECTIVE: The aims were to investigate the early effects of graded, closed, mild head injury on neurofilament protein (NF160) and microtubule-associated protein-2 (MAP2) and to examine the levels of lipid peroxidation and the impact of mexilitine, inhibitor of lipid peroxidation, pretreatment on tissue damage. MATERIAL AND METHOD: One hundred and twenty-six rats were divided into groups as follows: Group 1 (n = 14) were controls; group 2 (n = 56) sustained trauma alone; and group 3 (n = 56) were pretreated with mexilitine (50 mg/kg). Groups 2 and 3 were subdivided into subgroups (n = 14 each), which were subjected to 100 g/cm2, 125 g/cm2, 150 g/cm2, and 175 g/cm2 trauma forces, respectively. Two hours after trauma, the frontal lobes from all groups were removed and processed for lipid peroxidation H&E staining, immunofluorescent labelling of neurofilaments and microtubules with anti-NF160 and anti-MAP2 antibodies. RESULTS: Compared to control findings, all the trauma-only animals showed increased lipid peroxidation levels and the elevations paralleled the amount of force applied. Administration of mexilitine significantly reduced the level of lipid peroxidation. In NF160 stainings, in group 2, the degree of impairment in axonal organization paralleled the different levels of force that were applied. Groups 3C and 3D (mexilitine pretreated) showed well-preserved axons and intact perikarya. In MAP2 stainings group 2 animals showed remarkably less MAP2 staining throughout the sections. There were no significant differences in MAP2 staining intensity or pattern among the group 2 subgroups. In contrast, in the sections from the group 3 animals, the level of MAP2 positivity was markedly preserved. CONCLUSION: In conclusion, our results show that the cytoskeletal proteins we investigated have different capacities for resisting injury, and that MAP2 is more vulnerable to injury than NF160. One of the reason for this cytoskeletal disruption may be increased lipid peroxidation. Inhibition of lipid peroxidation by pre-treatment with 50-mg/kg mexilitine significantly reduces the level of lipid peroxidation and may protect MAP2 and NF160 integrity in closed mild head injury. This protection is inversely proportional to the magnitude of the applied force.

Effect of erythropoietin on bcl-2 gene expression in rat cardiac myocytes after traumatic brain injury.

The purpose of this study was to investigate whether erythropoietin (EPO) has an effect on the expression of bcl-2 in rat cardiac myocytes following experimental isolated traumatic brain injury (TBI). Forty-eight Wistar-Albino female rats were randomly allocated into eight groups. Groups AC and BC were controls; groups AS and BS were sham-operated animals. Groups A1 and B1 underwent head trauma without treatment. Groups A2 and B2, head traumas plus EPO intraperitoneally (1000 IU/kg); groups A3 and B3, the vehicle groups, head traumas and intraperitoneal albumin (0.4 ml/rat). The method of weight drop was used to produce impact trauma at 24 hours after injury. Samples obtained from the left ventricle were assayed for lipid peroxidation and bcl-2 gene expression using real-time quantitative polymerase chain reactions. Lipid peroxidation in the heart tissue was determined by the concentration of thiobarbituric acid reactive substances (TBARs). The results showed that administration of EPO significantly reduced the increase in lipid peroxidation by-products after moderate or severe trauma. The bcl-2 expression was significantly higher in EPO (A2 and B2) compared to trauma groups (A1 and B1) suggesting a protective effect. These findings suggest that EPO may play an important role in the expression of bcl-2 and decrease in TBARs-the end product of lipid peroxidation in myocytes-after moderate or severe TBI.

Ultrastructural effect of sildenafil citrate on corpus cavernosum and other genital organs in female rats.

AIM: To determine the ultrastructural effects of sildenafil on the female genital organs. METHODS: Twenty female cycling Wistar albino rats weighing 250+/-20 g were randomly divided into two groups of 10 each. Rats of one group were gavaged with 0.5 mg.kg(-1).d(-1) of sildenafil 3 days in a week for 4 weeks and the other served as the controls. After cessation of treatment animals were sacrificed by cervical dislocation under methoxyflurane anaesthesia. The clitoris, vagina, uterus and bartholin glands were taken at the estrous and were fixed with 10% formalin solution for light microscopy and 2.5% glutaraldehyde and osmic acid for electron microscopy. RESULTS: Under the light microscope, the fibrocollageous tissue was found increased, the capillaries enlarged and the connecting tissue elements increased in the corpus cavernosum in the treated group. On electron microscopy, increased connective tissue, fibroblasts with notched nucleus, shorten immature collagen fibers without striation were seen. Abundant foldings and penetration with collagen bundles were observed in the basal membrane. Large connection complexes, especially gap junctions among the wide capillary endothelial cells were observed. CONCLUSION: There are evident histological changes due to sildenafil citrate in female rat corpus cavernosum. The clitoris and bartholin glands were the most effected organs. While the histopathological changes of clitoral tissue could be expected, an increase in the mass of bartholin gland was surprising.

Propofol attenuates myocardial lipid peroxidation during coronary artery bypass grafting surgery.

BACKGROUND: Propofol can scavenge free radicals because it has a chemical structure similar to antioxidants. METHODS: We examined if free radical scavenging occurs with propofol during CABG operations. We studied 24 patients undergoing CABG surgery for triple vessel disease, randomized into two groups. After induction of anaesthesia with fentanyl 10 micrograms kg-1 and midazolam 0.1 mg kg-1, patients in the fentanyl group (n = 14) received fentanyl infusion 10-30 micrograms kg-1 h-1 and patients in the propofol group (n = 10) received propofol infusion 3-6 mg kg-1 h-1 for maintenance of anaesthesia. Atrial tissue biopsies were taken during cannulation for bypass, 45 min after cross-clamp insertion, 5 min after unclamping, and in the decannulation period. Lipid peroxidation was assessed by measurement of thiobarbituric acid reactive substances (TBARS) in the atrial tissue samples. RESULTS: Lipid peroxidation in the propofol group was less than in the fentanyl group (P < 0.05) in all sampling periods. Lipid peroxidation in the fentanyl group increased significantly during cardiopulmonary bypass (CPB) (P < 0.05), but no increase was found in the propofol group (P > 0.05). CONCLUSION: In clinical doses, propofol strongly attenuates lipid peroxidation during CABG surgery.

Serum lipid peroxidation levels in small-for-gestational-age babies.

The levels of lipid peroxidation in sera of asymmetric small-for-gestational-age (SGA) babies at the second hour of life were investigated. Lipid peroxidation levels, measured as malondialdehyde (MDA), were 3.3 +/- 1.1 and 3.9 +/- 1.2 mmol/L in SGA and appropriate-for-gestational age (AGA) groups, respectively. The difference was not significant (p>0.05). This result may indicate that free radical scavengers are sufficient in SGA babies.

C-Reactive protein as a risk factor for left ventricular thrombus in patients with acute myocardial infarction.

BACKGROUND: Elevated C-reactive protein (CRP) has been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI). It has been suggested that CRP may be involved in initiation process of coagulation; however, the role of CRP level in the formation of left ventricular (LV) thrombus has not been studied. HYPOTHESIS: This study investigated whether CRP is a risk factor for LV thrombus in patients with AMI. METHODS: Clinical, echocardiographic, and biochemical data were analyzed in 141 consecutive patients (aged 57 +/- 13 years; 33 women) with first anterior AMI. Two-dimensional and Doppler echocardiographic examinations were performed on Days 1, 3, 7, 15, and 30. Blood samples were obtained every day during hospitalization. Serum CRP concentrations were measured by an ultrasensitive immunonephelometry method. RESULTS: Left ventricular thrombus was detected in 33 (23.4%) patients. Univariate analysis showed that patients with LV thrombus had a higher peak creatine kinase (CK) level (2,879 +/- 742 vs. 1,693 +/- 1,210 I/U, p = 0.001), higher peak CRP level (14.9 +/- 7.1 vs. 9.2 +/- 6.8 mg/dl, p = 0.001), higher wall motion score index (1.8 +/- 0.2 vs. 1.5 +/- 0.3, p = 0.002), higher apical wall motion score index (2.35 +/- 0.72 vs. 2.07 +/- 0.70, p = 0.001), larger end-diastolic volume (145.2 +/- 43.7 vs. 116.5 +/- 44.2 ml, p = 0.002), larger end-systolic volume (85.4 +/- 37.2 vs. 62.9 +/- 31.6 ml, p = 0.003), and lower ejection fraction (42.1 +/- 12 vs. 47.3 +/- 13, p = 0.04). In multivariate analyses, only peak CK level (p = 0.0001), LV apical wall motion score index (p = 0.001), and CRP levels (p = 0.001) were independent predictors of LV thrombus formation. CONCLUSIONS: These results suggest that CRP is a risk factor for LV thrombus in patients with AMI.

Nimodipine attenuates lipid peroxidation during the acute phase of head trauma in rats.

Oxygen free radical-mediated lipid peroxidation is one of the major mechanisms of secondary damage in traumatic brain injury. We assessed the effects of nimodipine on lipid peroxidation 1 h after head trauma in rats. Nimodipine (1.5 microg/kg IV bolus injection) was given immediately after head trauma by either the carotid artery or the jugular vein. Placebo treated rats received saline by the same routes. Control rats received head trauma only. Sham-operated rats were the group without head trauma. Malondialdehyde (MDA), which is the end product of lipid peroxidation, was measured as an indicator of oxygen free radical formation in the brain tissue. The mean values for MDA in sham operated rats were 92.4 +/- 4.9 nanomoles/gram wet weight (nmol/gww) of brain tissue. In the control group, MDA content of the brain tissue was 120.8 +/- 9.4 nmol/gww. In placebo treated rats, the results were similar. In the groups receiving nimodipine via carotid artery or jugular vein, the mean values were 101.1 +/- 6.9 and 106.5 +/- 6.0 nmol/gww, respectively. These results indicate that nimodipine caused a significant decrease in lipid peroxidation when given in the acute phase of head trauma in rats. This occurred regardless of the route of injection.

Myoglobin-catalyzed tyrosine nitration: no need for peroxynitrite.

The nitration of tyrosine residues in protein to yield 3-nitrotyrosine derivatives has been suggested to represent a specific footprint for peroxynitrite formation in vivo. However, recent studies suggest that certain hemoproteins such as peroxidases catalyze the H(2)O(2)-dependent nitration of tyrosine to yield 3-nitrotyrosine in a peroxynitrite-independent reaction. Because 3-nitrotyrosine has been shown to be present in the postischemic myocardium, we wished to assess the ability of myoglobin to catalyze the nitration of tyrosine in vitro. We found that myoglobin catalyzed the oxidation of nitrite and promoted the nitration of tyrosine. Both nitrite oxidation and tyrosine nitration were H(2)O(2)-dependent and required the formation of ferryl (Fe(+4)) myoglobin. In addition, nitrite oxidation and tyrosine nitration were pH-dependent with a pH optimum of approximately 6.0. Taken together, these data suggest that the acidic pH and low oxygen tension produced during myocardial ischemia will facilitate myoglobin-catalyzed, peroxyntrite-independent formation of 3-nitrotyrosine.

Analysis of factors that may affect the enzymatic profile of gingival crevicular fluid: sampling technique, sequential sampling and mode of data presentation.

To evaluate the possible effect of sampling technique and sequential sampling on gingival crevicular fluid (GCF) volume and myeloperoxidase (MPO) activity, 14 patients presenting at least two symmetrical maxillary sites with mild/moderate periodontitis were selected. Two sites in each individual were sequentially sampled using either the deep-intracrevicular or orifice technique. Spectrophotometrically determined MPO levels were presented either as total MPO activity or MPO concentration. Although the clinical periodontal status of the 20 sampling sites were similar, the deep-intracrevicular technique regularly provided larger GCF volumes. With both techniques, the last samples contained the highest GCF volume. During sequential orifice sampling, GCF volume was relatively more stable. In general, a depletion of MPO activity was observed with sequential sampling performed with either of the techniques. Depletion of MPO did not replenish to baseline levels at the end of the 10-min sequential sampling. Although MPO activity showed a general reduction during sequential orifice sampling with both modes of data presentation, total MPO activity and MPO concentration did not match with the deep-intracrevicular technique. Due to the potential of affecting GCF volume/composition, the selection of sampling technique seems to be a critical methodological decision in GCF-profile studies, primarily during sequential sampling. In GCF-profile studies, mode of data presentation should also be considered.

Free radical changes in rat muscle tissue after exercise.

Intense exercise accompanied by a manifold increase in oxygen utilization over resting conditions has been shown to elevate the probability of the appearance of free radicals. One of the effects of free radicals appears to be the peroxidation of cell membrane lipids resulting in malondialdehyde formation, which is detrimental to cell function. A common method for the measurement of malondialdehyde involves a reaction with thiobarbituric acid. The aim of this study was to evaluate the influence of exercise on concentrations of thiobarbituric acid-reactive substances (TBARS) in the gastrocnemius and soleus muscles of rats. Thirty male rats were used in this study. Soleus and gastrocnemius muscle biopsies were performed and TBARS levels were studied in these two muscles. The rats were randomly assigned to three groups of ten each. Group A was the control group and did not perform exercise. In group B, gastrocnemius and soleus muscle biopsies were performed immediately after exercise, and in group C muscle biopsies were performed on the 2nd postexercise day. The exercise resulted in a significant increase in TBARS in the gastrocnemius muscle. In the soleus, TBARS also increased, but this was not statistically significant. In conclusion, exercise-induced free radical changes may depend on the muscle type studied.

Serum lipoprotein(a) and its relation to left ventricular thrombus in patients with acute myocardial infarction.

It is well known that the incidence of left ventricular (LV) thrombosis is high in patients with acute myocardial infarction (AMI). Due to the high degree of structural homology with plasminogen, lipoprotein(a) may produce thrombogenic effects by modulating the fibrinolytic system. However, the role of Lp(a) level in the formation of LV thrombus has not been studied. This study sought to determine whether Lp(a) is a risk factor for LV thrombus in patients with AMI. We have analyzed clinical, echocardiographic and biochemical data in 102 consecutive patients (aged 58+/-12 years, 92 men / 10 women) with first anterior AMI. Two-dimensional examination was performed on days 1, 3, 7, 15, and 30. Blood samples were obtained within 12 h after the onset of symptoms and before beginning the therapy. Plasma levels of fibrinogen and Lp(a) were measured using enzyme-linked immunosorbent assay and immunonephelometric methods, respectively. LV thrombus was detected in 20 (20.3%) patients. No significant difference was found for admission Lp(a) levels between patients with or without thrombus (30.5+/-17.2 vs 32.3+/-22.4 mg/dl, p = 0.7). Univariate analysis showed that patients with LV thrombus had a higher wall motion score index (1.8+/-0.3 vs 1.4+/-0.3, p = 0.002), a higher peak creatine kinase level (2945+/-898 vs 1805+/-1336, I / U p = 0.004), a larger end-diastolic volume (139.7+/-38.6 vs 114.1+/-41.8 ml, p = 0.04), a larger end-systolic volume (83.1+/-34.3 vs 59.2+/-30.6 ml, p = 0.02 ), and a lower ejection fraction (38+/-12 vs 47+/-11, p = 0.04). In multivariate analyses, only peak creatine kinase level (p = 0.04) and LV wall motion score index (p = 0.002) were independent predictors of left ventricular thrombus formation. These results suggest that Lp (a) is not a risk factor for LV thrombus in patients with AMI. Our data demonstrate that the best predictors of LV thrombus formation after AMI are a high peak creatine kinase level and a high LV wall motion score index.