Plasma Creatine Phosphokinase Research Articles

Plasma creatine phosphokinase level may predict successful treatment after a single injection of methotrexate for ectopic pregnancy

Our finding that creatine phosphokinase level was significantly higher in women successfully treated for ectopic pregnancy with only a single injection of methotrexate suggests that this indicator predicts this outcome.

Effect of short-term ornithine alpha-ketoglutarate pretreatment on intestinal ischemia-reperfusion in rats

To investigate the effects of preventive enteral administration of ornithine alpha-ketoglutarate (OKG) in an ischemia-reperfusion rat model. Sixty rats were randomized into five groups (G1-G5, n = 12). Each group was divided into two subgroups (n = 6) and treated with calcium carbonate (CaCa) or OKG by gavage. Thirty minutes later, the animals were anesthetized with xylazine 15mg + ketamine 1mg ip and subjected to laparotomy. G1-G3 rats served as controls. Rats in groups G4 and G5 were subjected to ischemia for 30 minutes. Ischemia was achieved by clamping the small intestine and its mesentery, delimiting a segment of bowel 5 cm long and 5 cm apart from the ileocecal valve. In addition, G5 rats underwent reperfusion for 30 minutes. Blood samples were collected at the end of the laparotomy (G1), after 30 minutes (G2, G4) and 60 minutes (G3, G5) to determine concentrations of metabolites (pyruvate, lactate), creatine phosphokinase (CPK), thiobarbituric acid reactive substances (TBARS) and glutathione (GSH). There was a significant decrease in tissue pyruvate and lactate and plasma CPK levels in OKG-treated rats at the end of reperfusion period. GSH levels did not change significantly in ischemia and reperfusion groups. However, TBARS levels increased significantly (p<0.05) in tissue samples in OKG-treated rats subjected to ischemia for 30 minutes. Short-term pretreatment with OKG before induction of I/R decreases tissue damage, increases pyruvate utilization for energy production in the Krebs cycle and does not attenuate the oxidative stress in this animal model.

Influence of Ionizing Radiation on Echis pyramidium Snake Venom: Biochemical and Immunological Aspects

The effect of a single LD50 dose of native Echis pyramidum venom (27.69μg/mouse) on the activities of certain serum enzymes levels: aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), urea, creatinine, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), creatine kinase isoenzyme (CK-MB) were studied. Samples from the serum were collected 4hr following LD50 venom dose intraperitonealy injected in male Swiss albino mice. The activities of these enzymes showed significant elevation compared to the non-envenomated group. In contrast, an equivalent dose of 1.5 kGy γ irradiated Echis pyramidum venom (27.69g/mouse) did not cause any significant increase compared to non-envenomated group. The effect of a dose that is equivalent to 1⁄2 LD50 (13.8 μg/50 μl) of native Echis pyramidum venom on plasma creatine phosphokinase (CPK) induced a significant increase of creatine phosphokinase (CPK) level compared to normal control (P<0.01). In contrast, an equivalent dose of 1.5 kGy γ irradiated Echis pyramidum venom showed non significant difference in creatine phosphokinase activity when compared to the normal control. Light microscopic examinations of gastrocenemius muscles of mice injected with native Echis pyramidum venom (1⁄2 LD50; 13.8μg/50μl) showed fragmentation, disorganization, loss of myofibrils in some of the muscle fibers, hemorrhage in-between the muscle fibers and mononuclear cellular infiltration. While light microscopic examinations of gastrocenemius muscles of mice injected with 1.5 kGy γ irradiated Echis pyramidum venom (13.8μg/50μl; a dose identical to that used from native venom) showed that most muscle fibers were of normal appearance except for small area of fragmentation and disorganized myofibrils and oedema of the intercellular connective tissue. Double immunodiffusion test revealed a similar reactivity for native, 1 kGy, 1.5 kGy and 3 kGy γ irradiated Echis pyramidum venoms against a commercial polyvalent Egyptian antivenin. The visible lines obtained in the immunodiffusion reactions were identical and joined smoothly at the corners, indicating that there was no change in their antigenic reactivity. These results demonstrate that the ability of the venom antigens to react with its corresponding antibodies was maintained in spite of being exposed to radiation doses of 1 kGy, 1.5 kGy and 3 kGy. Both antivenins raised against native or 1.5 kGy γ irradiated venoms recognized Echis pyramidum venom when submitted to protein blotting, but the anti 1.5 kGy γ irradiated venom show a higher intensity bands than the antivenin raised against native Echis pyramidum venom, in spite of having less neutralizing activity (native neutralize 50 LD50, 1.5 kGy γ irradiated neutralize 40 LD50), this indicates that antibodies were formed not only for toxic fraction but also for non toxic fraction. Irradiation of the whole Echis Pyramidium Venom with 1.5KGy reduced its lethality 12.5 times though keeping its immunogenicity. The 1.5KGy dose was shown to be the best radiation dose to promote detoxification without significantly affecting its immunogenicity. Thus results of this study confirm the conclusion that γ radiation is a suitable way to detoxify Echis Pyramidium Venom without affecting its immunogenicity provided that proper dose is used.

Effects of Bungarus candidus (Malayan krait) venom on general circulation and renal hemodynamics in experimental animals

Abstract Background: Many studies have reported the occurrence of lethal acute renal failure after snakebites. Bungarus candidus (Malayan krait) is a medically important venomous snake distributed widely throughout Southeast Asia. The best known features of systemic envenoming by B. candidus are neurotoxic. Objective: Obtain more information on effects of B. candidus venom on changes in systemic and renal hemodynamics in experimental animals. Methods: Twelve adult male New Zealand white rabbits were used to study the effect of B. candidus venom on general circulation and renal hemodynamics. An anesthetized animal was intravenously injected with B. candidus venom at a dosage of 50μg/kg bodyweight. All changes of parameters were observed after initial post venom injection and recorded at 30 min intervals until 150 minutes after envenomation. Results: After envenomation, cardiovascular responses showed a marked decrease in mean arterial pressure within two minutes, afterwards gradually returning closely to baseline values. There were stepwise decreases in heart rate and cardiac output, while total peripheral resistance was slightly increased. The renal hemodynamics significantly decreased by glomerular filtration rate, effective renal plasma flow and effective renal blood flow, while the filtration fraction significantly increased. Envenomed animals showed a reduction in renal fraction, while renal vascular resistance stepwise increased. The plasma potassium level tended to increase. Animals showed stepwise decreases in urinary excretion of Na+, K+ and Cl-. A marked decrease in plasma calcium level was apparent at 120 minutes, while plasma creatine phosphokinase and lactate dehydrogenase levels increased at 30-120 minutes. Conclusion: A significant drop in blood pressure was attributed to a sustained fall in cardiac output, which would be associated with a reduction in heart rate. Sustained hypotension would contribute to reduction of renal blood flow, which results in decreased GFR.

Age-related protective effect of deprenyl on changes in the levels of diagnostic marker enzymes and antioxidant defense enzymes activities in cerebellar tissue in Wistar rats

Antioxidants are free radical scavengers and protect living organisms against oxidative damage to tissues. Experimental evidence implicates oxygen-derived free radicals as important causative agents of aging and the present study was designed to evaluate the age-related effects of deprenyl on the antioxidant defense in the cerebellum of male Wistar rats. Experimental rats of three age groups (6, 12, and 18 months old) were administered with liquid deprenyl (2 mg/kg body weight/day for a period of 15 days i.p) and levels of diagnostic marker enzymes (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and creatine phosphokinase) in plasma, lipid peroxides, reduced glutathione and activities of glutathione-dependent antioxidant enzymes (glutathione peroxidase and glutathione-S-transferase) and antiperoxidative enzymes (catalase and superoxide dismutase) in the cerebellar tissue were determined. Intraperitonial administration of deprenyl (2 mg/kg body weight/day for a period of 15 days) significantly (p < 0.05) attenuated the age-related alterations noted in the levels of diagnostic marker enzymes plasma of experimental animals. Deprenyl also exerted an antioxidant effect against aging process by hindering lipid peroxidation to an extent. Moderate rise in the levels of reduced glutathione and activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes was also observed. The results of the present investigation indicated that the protective potential of deprenyl was probably due to the increase of the activity of the free radical scavenging enzymes or to a counteraction of free radicals by its antioxidant nature or to a strengthening of neuronal membrane by its membrane-stabilizing action. Histopathological observations also confirmed the protective effect of deprenyl against the age-related aberrations in rat cerebellum. These data on the effect of deprenyl on parameters of normal aging provides new additional information concerning the anti-aging potential of deprenyl.

Subdiaphragmatic vagotomy promotes nociceptive sensitivity of deep tissue in rats

To verify whether vagal dysfunction is associated with chronic pain, we evaluated the effects of subdiaphragmatic vagotomy (vgx) on the sensitivity toward noxious stimuli in rats. Vgx rats showed sustained hyperalgesia in the gastrocnemius muscle without tissue damage (no increase in vgx-induced plasma creatine phosphokinase or lactose dehydrogenase levels) accompanied by hypersensitivity to colonic distension. We found a dramatic increase in the levels of metabotropic glutamate receptor 5, protein kinase C (PKC) γ and phosphorylated-PKCγ within the spinal cord dorsal horn in vgx rats, which suggests that vgx may evoke sensory nerve plasticity. Morphine produced a dose-dependent increase in the withdrawal threshold in both vgx and sham-operated rats, but the effect of a lower dose in vgx rats was weaker than that in sham-operated rats. Muscle hyperalgesia in vgx rats was also attenuated by gabapentin and amitriptyline, but was not affected by diclofenac, dexamethasone or diazepam. These findings indicate that subdiaphragmatic vagal dysfunction caused chronic muscle hyperalgesia accompanied by visceral pain and both gabapentin and amitriptyline were effective for subdiaphragmatic vagotomy-induced pain, which are partially similar to fibromyalgia syndrome. Furthermore, this chronic muscle pain may result from nociceptive neuroplasticity of the spinal cord dorsal horn.

Sulforaphane treatment protects skeletal muscle against damage induced by exhaustive exercise in rats

Sulforaphane (SF), one of the most important isothiocyanates in the human diet, present in cruciferous vegetables, is known to have chemopreventive activities in different tissues. No data are available on its effects in the prevention of skeletal muscle damage. In this study, we investigated the potential protective effects of SF treatment on muscle damage and oxidative stress induced by an acute bout of exhaustive exercise in rats. Male Wistar rats were treated with SF (25 mg/kg body wt ip) for 3 days before undergoing an acute exhaustive exercise protocol in a treadmill (+7% slope and 24 m/min). Acute exercise resulted in a significant increase in plasma lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) activities. It also resulted in a significant increase in thiobarbituric acid-reactive substances, in a significant decrease in tissue total antioxidant capacity, and in a significant decrease in NAD(P)H:quinone oxidoreductase 1 (NQO1) expression and activity in vastus lateralis muscle. SF treatment significantly increased muscle NQO1, glutathione-S-transferase, and glutathione reductase expression and activity, with no effect on glutathione peroxidase and thioredoxin reductase. The observed SF-induced upregulation of phase II enzymes was accompanied by a significant increase in nuclear erythroid 2 p45-related factor 2 expression and correlated with a significant increase in total antioxidant capacity and a decrease in plasma LDH and CPK activities. Our data demonstrate that SF acts as an indirect antioxidant in skeletal muscle and could play a critical role in the modulation of the muscle redox environment, leading to the prevention of exhaustive exercise-induced muscle damage.

Carbohydrate and Protein Hydrolysate Coingestion’s Improvement of Late-Exercise Time-Trial Performance

This study examined whether a carbohydrate + casein hydrolysate (CHO+ProH) beverage improved time-trial performance vs. a CHO beverage delivering approximately 60 g CHO/hr. Markers of muscle disruption and recovery were also assessed. Thirteen male cyclists (VO2peak = 60.8 +/- 1.6 ml . kg-1 . min-1) completed 2 computer-simulated 60-km time trials consisting of 3 laps of a 20-km course concluding with a 5-km climb (approximately 5% grade). Participants consumed 200 ml of CHO (6%) or CHO+ProH beverage (6% + 1.8% protein hydrolysate) every 5 km and 500 ml of beverage immediately postexercise. Beverage treatments were administered using a randomly counterbalanced, double-blind design. Plasma creatine phosphokinase (CK) and muscle-soreness ratings were assessed immediately before and 24 hr after cycling. Mean 60-km times were 134.4 +/- 4.6 and 135.0 +/- 4.0 min for CHO+ProH and CHO beverages, respectively. All time differences between treatments occurred during the final lap, with protein hydrolysate ingestion explaining a significant (p < .05) proportion of between-trials differences over the final 20 km (44.3 +/- 1.6, 45.0 +/- 1.6 min) and final 5 km (16.5 +/- 0.6, 16.9 +/- 0.6 min). Plasma CK levels and muscle-soreness ratings increased significantly after the CHO trial (161 +/- 53, 399 +/- 175 U/L; 15.8 +/- 5.1, 37.6 +/- 5.7 mm) but not the CHO+ProH trial (115 +/- 21, 262 +/- 88 U/L; 20.9 +/- 5.3, 32.2 +/- 7.1 mm). Late-exercise time-trial performance was enhanced with CHO+ProH beverage ingestion compared with a beverage containing CHO provided at maximal exogenous oxidation rates during exercise. CHO+ProH ingestion also prevented increases in plasma CK and muscle soreness after exercise.

Combined selenium and vitamin C deficiency causes cell death in guinea pig skeletal muscle

Combined antioxidant deficiencies of selenium and vitamin E or vitamin E and vitamin C in guinea pigs result in clinical illness. We hypothesized that combined selenium and vitamin C deficiency would have clinical consequences because in vitro interactions of these antioxidant nutrients have been reported. Because guinea pigs are dependent on dietary vitamin C, weanling male guinea pigs were fed selenium-deficient or control diet for 15 weeks before imposing vitamin C deficiency. Four dietary groups were formed and studied 3 weeks later: controls, vitamin C deficient, selenium deficient, and doubly deficient. Deficiencies were confirmed by determinations of glutathione peroxidase activity and vitamin C concentration in liver and skeletal muscle. Plasma creatine phosphokinase activity and liver, kidney, heart, and quadriceps histopathology were determined. Doubly deficient animals had moderately severe skeletal muscle cell death as judged by histopathology and plasma creatine phosphokinase activity of 6630 +/- 4400 IU/L (control, 70 + or - 5; vitamin C deficient, 95 + or - 110; selenium deficient, 280 + or - 250). Liver, kidney, and heart histology was normal in all groups. Muscle alpha-tocopherol levels were not depressed in the doubly deficient group, but muscle F2 isoprostane concentrations were elevated in them and correlated with markers of cell death. We conclude that combining selenium and vitamin C deficiencies in the guinea pig causes cell death in skeletal muscle that is more severe than the injury caused by selenium deficiency. The elevation of muscle F2 isoprostanes is compatible with the cell death being caused by oxidative stress.

Effects of adenovirus transfected with IKB on multiple organ dysfunction syndrome induced with oleic acid and lipopolysaccharide in rats

Objective To investigate the effects of adenovirus transfected with IκB (Ad-IκB) on multiple organ dysfunction syndrome (MODS) induced with oleie acid and lipopolysaccharide (L P S) in rats. Methods Fifty pathogen-free SD rats of both sexes weighing 100-120 g were randomly divided into 3 groups: group Ⅰ control (C,n = 10); group Ⅱ MODS (M, n = 20) and group Ⅲ Ad-IκB + MODS (T, n = 20). The animals were anesthetized with intraperitoneal (IP) chloral hydrate 0.3-0.4 ml/100 g. MODS was induced with iv oleic acid 0.25 ml/kg and iv LPS 3.5 mg/kg at an interval of 4 h in group M and T. In group T (Ⅲ) Ad-h:B was given iv simultaneously with LPS. Blood samples were taken from abdominal aorta at 1 and 7 days after LPS or IκB transfected administration for determination of plasma creatine phosphokinase, glutamic pyruvie transaminase (GPT), total bilirubin and blood creatinine and blood gas analysis. The animals were then sacrificed and the liver and lungs were removed at 1 and 7 days after blood samples were obtained for determination of expression of NF-κB p65 in lung and liver tissue using immuno-histochemical staining and Western blotting, Immuno-histochemical staining was scored (0 = no positive cells, 4 = 81%-100% positive cells). Results Creatinine, GPT, total bilirubin and creatine phosphokinase were significantly higher in group M than in group C and IκB transfected significantly attenuated the MODS-induced increase. PaO2 at day 7 was significantly lower in group M and T than in group C and was signilicantly higher in group T than in group M. The expression of NF-κB p65 protein was significantly higher in group M than in group C and was significantly decreased by IκB transfected in group T. The immuno-histochemical staining scores were highest in group M and lowest in group C. Conclusion Ad- boB treatment can inhibit the activation of NF-κB and synthesis of inflammatory factors, resulting in amelioration of MODS induced with oleic acid and LPS. Key words: Transfection; Multiple organ dysfunction syndrome; Oleic acid; Endotoxins; NF-κB

Changes in serum cartilage oligomeric matrix protein (COMP), plasma CPK and plasma hs-CRP in relation to running distance in a marathon (42.195 km) and an ultra-marathon (200 km) race

Marathon running is frequently associated with numerous cellular changes, but little information is available on the effects of exercise-mediated prolonged impact-stress on cartilage integrity. This study was undertaken to evaluate muscle and cartilage damage with different running distances. Twenty male marathoners and ultra-marathoners participated in the study. Serum COMP and plasma CPK and hs-CRP were measured as markers of cartilage and muscle damage and inflammation. Serum COMP was increased 1.6-fold at 10 km during a marathon race and declined to the pre-race level after 2 days recovery. In contrast, serum COMP was increased 1.9-fold after a 200-km race and maintained until day 3 of recovery, only returning to the pre-race level on day 6. Plasma CPK was increased at 10 km of the marathon race and up to threefold at the end of the race. This was further increased on day 1, only returning to pre-race level on day 6. Plasma CPK was increased 35-fold at the end of the 200-km race and remained increased until day 5. There was no change in plasma hs-CRP during the marathon race, but this was increased 3.4-fold by day 1, returning to the pre-race level on day 4. Plasma hs-CRP increased 40-fold by the end of the 200-km race and was still increased on day 6 of recovery. Therefore, longer distance running may induce more impact-stress both on muscle and cartilage. Further, the required time for recovery may vary with running distance and the tissue type, e.g. cartilage or skeletal muscle as in this case.

Possible Mechanisms Underlying Statin-Induced Skeletal Muscle Toxicity in L6 Fibroblasts and in Rats

3-Hydroxy-3-methylglutaryl CoA reductase inhibitors (statins) are safe and well-tolerated therapeutic drugs. However, they occasionally induce myotoxicity such as myopathy and rhabdomyolysis. Here, we investigated the mechanism of statin-induced myotoxicity in L6 fibroblasts and in rats in vivo. L6 fibroblasts were differentiated and then treated with pravastatin, simvastatin, or fluvastatin for 72 h. Hydrophobic simvastatin and fluvastatin decreased cell viability in a dose-dependent manner via apoptosis characterized by typical nuclear fragmentation and condensation and caspase-3 activation. Both hydrophobic statins transferred RhoA localization from the cell membrane to the cytosol. These changes induced by both hydrophobic statins were completely abolished by the co-application of geranylgeranylpyrophosphate (GGPP). Y27632, a Rho-kinase inhibitor, mimicked the hydrophobic statin-induced apoptosis. Hydrophilic pravastatin did not affect the viability of the cells. Fluvastatin was continuously infused (2.08 mg/kg at an infusion rate of 0.5 mL/h) into the right internal jugular vein of the rats in vivo for 72 h. Fluvastatin infusion significantly elevated the plasma CPK level and transferred RhoA localization in the skeletal muscle from the cell membrane to the cytosol. In conclusion, RhoA dysfunction due to loss of lipid modification with GGPP is involved in the mechanisms of statin-induced skeletal muscle toxicity.

Effect of Enzyme Addition on the Nutritive Value of High Oleic Acid Sunflower Seeds in Chicken Diets

Two experiments were conducted to evaluate the effects of enzyme addition in chicken diets containing high oleic acid sunflower seeds (HOASS). In the first experiment (4 to 21 d of age), enzyme addition (lipase, phospholipase, and a combination of these) was used at the inclusion level of 1 g/kg in diets containing HOASS (250 g/kg) compared with a control corn-soybean diet. Weight gain, feed consumption, relative liver weight, fat digestibility, and amylase, lipase, serum lactate dehydrogenase (LDH), and creatine phosphokinase (CPK) activities were reduced, and feed conversion, relative duodenum, jejunum, ileum, and ceca lengths, plasma uric acid, cholesterol, and glucose concentrations were increased in the unsupplemented HOASS diet compared with the control diet. The addition of enzymes to the HOASS diet increased weight gain, feed consumption, relative pancreas and liver weights, fat digestibility, amylase and lipase activities, plasma uric acid, calcium, serum LDH and CPK, and total protein concentration and reduced feed conversion, relative spleen weight, relative duodenum, jejunum, ileum, and ceca lengths, plasma cholesterol, and glucose compared with the unsupplemented HOASS diet. In the second experiment (0 to 21 d of age), the same enzymes (0.5 g/kg each) were included in diets containing 150 g/kg of HOASS compared with a conventional sunflower meal diet (150 g/kg). The HOASS diet did not affect performance but reduced relative pancreas and abdominal fat weights and relative duodenum and ceca lengths, and increased crude fat, CP, and essential and nonessential amino acid digestibilities (except Ser, which was reduced) compared with the control diet. The addition of enzymes in the HOASS diet increased weight gain, feed consumption, and relative pancreas weight and reduced feed conversion, CP, and essential and nonessential amino acid digestibilities compared with the unsupplemented HOASS diet. In conclusion, the addition of 250 g of HOASS/kg in the diets caused a negative effect on performance, digestive organ sizes, fat and protein digestibilities, and pancreatic enzymes and modified blood parameters. However, the inclusion of HOASS at 150 g/kg improved some of these parameters and amino acid digestibilities. The enzyme addition counteracted some of these effects.

Silymarin prevents adriamycin-induced cardiotoxicity and nephrotoxicity in rats

Adriamycin is a potent anticancer agent, its clinical use is limited for its marked cardiotoxicity and nephrotoxicity. The present study aimed to investigate the possible protective role of the natural antioxidant silymarin on ADR-induced heart and kidney toxicity. Studies were performed on four groups of rats. 1 – control group, 2 – silymarin group (50 mg/kg), 3 – adriamycin group (10 mg/kg), 4 – adriamycin + silymarin group. On the third day after ADR injection, plasma was separated for determination of LDH, CPK, cholesterol and total lipids. 30 days after ADR injection, plasma was separated for determination of creatinine and urea levels. Frozen heart specimens (72 h) and frozen kidney specimens (30 days) were used for estimation of lipid peroxides and GSH contents. Histopathological examinations of heart and kidney sections were also done. Pretreatment of ADR-treated rats with silymarin resulted in a significant decrease in the plasma CPK, LDH, creatinine and urea. On the other hand silymarin pretreatment did not change ADR-induced hyperlipidemia. Silymarin pretreatment significantly decreased the myocardial MDA contents. In addition, silymarin pretreatment normalized renal tissue contents of MDA and GSH. Histopathological examination of heart and kidney sections revealed that ADR caused only mild myocardial injury in silymarin pretreated rats. Also, silymarin pretreatment inhibited ADR-induced renal tubular damage in rats. These results have suggested that, silymarin ameliorated ADR-induced cardiotoxicity and protected against ADR-induced nephrotoxicity in male albino rats. The mechanisms of silymarin induced protection against ADR-induced toxicities were proved to be due to inhibition of lipid peroxidation and protection against GSH depletion.

Bicarbonate supplementation as a preventive way in statins-induced muscle damage

The aim of this study was to evaluate the bicarbonate-induced improvement of statins, cerivastatin, simvastatin acid and lovastatin acid -induced apoptosis using rat myoblast cell line (L6) as a model of in vitro skeletal muscle and of cerivastatin-induced muscle damage in vivo study. Statin-induced reduction of cell viability and apoptosis was measured by 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide (MTT) assay and caspase assay. In vivo, we evaluated plasma creatine phosphokinase (CPK) level in cerivastatin-treated rat. Bicarbonate prevented cerivastatin-, simvastatin- acid and lovastatin acid -induced reduction of cell viability, morphological change and caspase activation in L6 cells. Moreover, in the in vivo study, bicarbonate prevented cerivastatin-induced increase in CPK concentrations. These results from in vitro and in vivo studies support that bicarbonate supplementation prevented statin-induced muscle damage.

Sport-related hyperhomocysteinaemia: a putative marker of muscular demand to be noted for cardiovascular risk

Objective:Regular physical activity is associated with a reduction of cardiovascular morbidity and mortality; however, evidence of unfortunate cardiovascular events accompanying elite sport involvement continues to accumulate. To date, no information...

Effects of transport, lairage and stunning on the concentrations of some blood constituents in horses destined for slaughter

The aim of the present study was to determine, in horses destined to slaughter, the effects of transport, lairage and stunning on some blood constituents related to stress. Twenty one horses culled from a race track due to poor athletic performance, transported weekly to a nearby slaughterhouse were used. Each horse was canulated through venipuncture of the right jugular vein with a central venous catheter which remained permanently until after the exsanguination. Through the catheter, blood samples were taken at 6 sampling times: one hour before loading of the horses, immediately after loading, at the end of the journey, immediately after unloading, after lairage, in the stunning box before stunning and during exsanguination. Blood samples were analyzed for the following variables: plasma lactate concentration, plasma creatine phosphokinase activity (CK), plasma glucose concentration, plasma cortisol concentration and packed cell volume (PCV). Time in the stunning box, number of stunning attempts, presence of return to consciousness signs and time between stunning and sticking were also recorded. The results for pre-mortem variables were: mean time in the stunning box 9 min 48 sec, 85.7% of the horses fell at the first stunning attempt, 57.2% of the horses showed signs of returning to consciousness after stunning and the most frequent interval between stunning and sticking was 1.01 to 2 min. Mean values for the blood variables showed a significant rise (P < 0.05) in the concentrations of lactate, glucose and cortisol, as well as CK activity and PCV during transport. The highest values for these blood constituents were seen before stunning and during exsanguination, except for cortisol concentration, which showed the highest values during the transport process.

Effects of oral l-carnitine supplementation in racing Greyhounds

Abstractl-Carnitine supplementation can stimulate erythropoiesis, reduce exercise-induced plasma lactate concentrations and decrease post-exercise muscle damage. Next to horses, Greyhounds represent the premier animal racing species and perform short-duration, very high-intensity exercise that has the potential to incur substantial muscle damage. Under resting and standard racing conditions (5/16 mile), we tested the novel hypotheses that l-carnitine supplementation in Greyhounds would: (1) elevate haematocrit at rest and immediately post-exercise; (2) reduce peak post-exercise plasma lactate; and (3) reduce indices of muscle damage (plasma creatine phosphokinase, CPK and aspartate aminotransferase, AST). Six conditioned Greyhounds (30.1 ± 1.6 kg) underwent a randomized placebo-controlled crossover study to determine the effects of 6 weeks of l-carnitine supplementation (100 mg kg− 1 of body weight/day) at rest and following a maximal speed 5/16 mile race. In accordance with our hypotheses, l-carnitine elevated resting and immediately post-race haematocrit (control, 60.1 ± 1.7, l-carnitine, 63.6 ± 1.7; P &lt; 0.05) and reduced peak post-race plasma CPK and AST concentrations (both P &lt; 0.05). Those dogs with the highest peak post-exercise plasma CPK concentrations under placebo conditions evidenced the greatest reduction with l-carnitine supplementation (r = 0.99, P &lt; 0.01). However, contrary to our hypotheses, l-carnitine did not change peak post-exercise plasma lactate concentrations (control, 27.0 ± 2.1, l-carnitine, 27.7 ± 1.3; P&gt;0.05). We conclude that l-carnitine supplementation increases the potential for oxygen transport and reduces plasma indicators of muscle damage, CPK and AST in racing Greyhounds.

Synergistic effects of squalene and polyunsaturated fatty acid concentrate on lipid peroxidation and antioxidant status in isoprenaline-induced myocardial infarction in rats

We have studied the synergistic effects of squalene and polyunsaturated fatty acids (PUFA concentrate) on isoprenaline-induced infarction in rats with respect to changes in the levels of plasma diagnostic marker enzymes and myocardial antioxidant defense system. Intraperitoneal injection of isoprenaline caused a significant elevation in the levels of diagnostic marker enzymes; alanine aminotranferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) in plasma of experimental rats. There was a significant rise in the level of lipid peroxidation with concomitant decline in the level of reduced glutathione (GSH) and in the activities of glutathione-dependent antioxidant enzymes; glutathione peroxidase (GPX) and glutathione-Stransferase (GST), and antiperoxidative enzymes; superoxide dismutase (SOD) and catalase (CAT) in heart tissue. Combined supplementation of squalene and PUFA concentrate significantly prevented the isoprenaline-induced elevations in the levels of diagnostic marker enzymes in plasma of experimental groups of rats. A tendency to counteract the isoprenaline induced lipid peroxidation was also noticed. Their combined administration maintained the level of GSH and the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes at near normalcy. The results of the present study indicated that the combined administration of squalene and PUFA concentrate exerted significantly better cardio-protection against isoprenaline-intoxication as compared to that of per second supplementation.

Effects of lipoprotein lipase and statins on cholesterol uptake into heart and skeletal muscle

Regulation of cholesterol metabolism in cultured cells and in the liver is dependent on actions of the LDL receptor. However, nonhepatic tissues have multiple pathways of cholesterol uptake. One possible pathway is mediated by LPL, an enzyme that primarily hydrolyzes plasma triglyceride into fatty acids. In this study, LDL uptake and tissue cholesterol levels in heart and skeletal muscle of wild-type and transgenic mice with alterations in LPL expression were assessed. Overexpression of a myocyte-anchored form of LPL in heart muscle led to increased uptake of LDL and greater heart cholesterol levels. Loss of LDL receptors did not alter LDL uptake into heart or skeletal muscle. To induce LDL receptors, mice were treated with simvastatin. Statin treatment increased LDL receptor expression and LDL uptake by liver and skeletal muscle but not heart muscle. Plasma creatinine phosphokinase as well as muscle mitochondria, cholesterol, and lipid droplet levels were increased in statin-treated mice overexpressing LPL in skeletal muscle. Thus, pathways affecting cholesterol balance in heart and skeletal muscle differ.