Plasma Creatine Phosphokinase Levels Research Articles

Curcumin and Nanocurcumin Oral Supplementation Improve Muscle Healing in a Rat Model of Surgical Muscle Laceration.

To compare the effects of curcumin and nanocurcumin oral supplementation on the muscle healing rate of an animal model of surgical muscle laceration. Thirty-two male adult rats were randomly divided into sham, control, curcumin, and nanocurcumin groups. Partial transection of the gastrocnemius muscle was made in the right limb of the control and treatment groups. The sham and control groups received normal saline, curcumin group received 500 mg/kg of curcumin and nanocurcumin group received 100 mg curcumin-loaded nanomicelles orally every day. They euthanized two weeks later and the specimens were stained by hematoxylin-eosin (H&E) and Masson's trichrome methods. Aspartate transaminase (AST) and creatine phosphokinase(CPK) were measured in blood samples. The percentage of collagen fibers in the nanocurcumin group was significantly lesser than the control and curcumin groups (p<0.001). Muscle fiber regeneration in the treatment groups was significantly higher than the control group (p<0.001). The blood vessels of the nanocurcumin group were significantly more than other groups (p<0.001). Plasma AST had a significant difference in the control group compared to the sham and nanocurcumin groups (p=0.026). The plasma CPK level of the control group was also significantly higher than other groups (p<0.001). In conclusion, although oral curcumin supplementation has little effects because of its poor bioavailability, embedding it in nanoparticles could enhance its systemic effects in promoting the muscle healing process.

No Association between Hyponatremia and Rhabdomyolysis in Rats

BackgroundRhabdomyolysis is an uncommon complication of hyponatremia, reported previously only in case reports and small retrospective studies, and its underlying mechanism is controversial. Some studies support the hypothesis that the rapid correction of hyponatremia is responsible for rhabdomyolysis, whereas others emphasize the severity of the hyponatremia as a predisposing factor for rhabdomyolysis. ObjectivesTo test the association between hyponatremia and rhabdomyolysis and to demonstrate a causal association. MethodsHyponatremia was induced by administration of water and desmopressin acetate in rats during 3 days, followed by its rapid correction, using animal models established for the evaluation of central pontine myelinolysis. The plasma creatine phosphokinase levels, a marker for rhabdomyolysis, were monitored, and hematoxylin and eosin sections of the quadriceps and gastrocnemius muscles were evaluated for signs of rhabdomyolysis. ResultsThe induction of hyponatremia and its correction were accompanied by the previously reported neurological sequelae, including signs of central pontine myelinolysis. However, no increase in plasma creatine phosphokinase levels was found, and histopathological examination of the quadriceps and gastrocnemius muscles revealed no sign of rhabdomyolysis. ConclusionsThe present study, which is the first to test the association between hyponatremia and rhabdomyolysis in an animal model, does not support any causal association between hyponatremia and rhabdomyolysis. Thus, other factors might be necessary for an association between hyponatremia and rhabdomyolysis, such as genetic factors or convulsions that are known to be associated with both hyponatremia and rhabdomyolysis. Further research in this important physiologic and clinical question is needed.

Catechins Suppress Muscle Inflammation and Hasten Performance Recovery after Exercise

Catechins, abundant in green tea, exhibit many biological actions for potential clinical applications. Our purpose was to explore the potential benefits of catechin ingestion on recovery of physical performance after downhill running. Institute of Cancer Research mice were used to examine the effects of prior catechin ingestion (0.5% w/w in diet for 3 wk) on 1) wheel-running activity, 2) running endurance, 3) muscle force, and 4) muscle oxidative stress and inflammation after downhill running (16 m·min for 5 min, 18 m·min for 5 min, 20 m·min for 10 min, and 22 m·min for 130 min). Voluntary wheel-running activity and the contractile force of the isolated soleus muscle decreased (P < 0.05) after downhill running. Notably, catechin ingestion significantly alleviated the running-induced decrease in voluntary wheel-running activity by 35%; the catechin-treated mice maintained endurance running capacity (214 ± 9 vs 189 ± 10 min, P < 0.05). Furthermore, catechins alleviated (P < 0.05) the decrease in tetanic force evident in the soleus muscle after downhill running. Catechins suppressed the running-induced increases in plasma creatine phosphokinase levels by 52%; this was also true of the carbonylated protein content of the soleus muscle by 17% (P < 0.05), malondialdehyde levels by 32% in the gastrocnemius muscle, and myeloperoxidase activity of the gastrocnemius by 22% (P < 0.05). The levels of tumor necrosis factor-α, interleukin-1β, and monocyte chemoattractant protein-1 in the gastrocnemius muscle were significantly lower (P < 0.05) by 33%, 29%, and 35%, respectively, in treated mice; the expression levels of mRNAs encoding these fell in parallel. Our results suggest that long-term intake of catechins, perhaps through their antioxidant properties, attenuates downhill running-induced muscle damage by suppressing muscle oxidative stress and inflammation, hastening recovery of physical performance in mice.

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.

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.

Nutritional supplementation of the leucine metabolite β-hydroxy-β-methylbutyrate (hmb) during resistance training

The effects of supplementation of the leucine metabolite β-hydroxy-β-methylbutyrate (HMB) were examined in a resistance training study. Thirty-nine men and 36 women between the ages of 20–40 y were randomized to either a placebo (P) supplemented or HMB supplemented (3.0 g HMB/d) group in two gender cohorts. All subjects trained three times per week for 4 wk. In the HMB group, plasma creatine phosphokinase levels tended to be suppressed compared to the placebo group following the 4 wk of resistance training (HMB:174.4 ± 26.8 to 173.5 ± 17.0 U/L; P:155.0 ± 20.8 to 195.2 ± 23.5 U/L). There were no significant differences in strength gains based on prior training status or gender with HMB supplementation. The HMB group had a greater increase in upper body strength than the placebo group (HMB:7.5 ± 0.6 kg; P:5.2 ± 0.6 kg; P = 0.008). The HMB groups increased fat-free weight by 1.4 ± 0.2 kg and decreased percent fat by 1.1% ± 0.2% while the placebo groups increased fat-free weight by 0.9 ± 0.2 kg and decreased percent fat by 0.5% ± 0.2% (fat-free weight P = 0.08, percent fat P = 0.08, HMB compared to placebo). In summary, this is the first short-term study to investigate the roles of gender and training status on the effects of HMB supplementation on strength and body composition. This study showed, regardless of gender or training status, HMB may increase upper body strength and minimize muscle damage when combined with an exercise program.

Malignant Hyperthermia During Sevoflurane Administration

Malignant Hyperthermia During Sevoflurane Administration

Pathophysiology of superoxide radical as potential mediator of reperfusion injury in pig heart.

The role of oxygen-derived free radicals in myocardial reperfusion injury was studied using the isolated in situ pig heart model. The free radical scavengers, superoxide dismutase (SOD) and catalase, protected the ischemic pig heart subjected to one hour of normothermic regional ischemia followed by one hour of global hypothermic arrest and one hour normothermic reperfusion. A significant increase in thiobarbituric acid reactive material and oxidized glutathione appeared in the perfusate demonstrating free radical-mediated lipid peroxidation during reperfusion, and this was prevented by the addition of SOD plus catalase. The values of three important antioxidative enzymes, SOD, catalase, and glutathione peroxidase, showed reduced activities after 2 hours of ischemia. These values did not change significantly after 60 minutes of reperfusion following the 2 hours ischemic insult. The concentrations of high-energy phosphate compounds including creatine phosphate (CP), adenosine triphosphate (ATP), and total adenine nucleotide were reduced significantly during ischemia and reperfusion in hearts which were not protected by SOD and catalase. The plasma creatine phosphokinase levels were lowered appreciably as a result of SOD and catalase treatment. It may be concluded from these experiments that oxygen-derived free radicals are present during reperfusion and SOD and catalase play a significant role in the protection of ischemic myocardium from reperfusion injury.

Plasma mexiletine concentrations following combined oral and intramuscular administration.

Mexiletine in doses of 50, 100 and 400 mg was administered by intramuscular injection to a healthy subject and the resulting plasma concentrations were compared with those after 100 mg given intravenously. The bioavailability of mexiletine given by this route is complete and the kinetics are linear with dose. Plasma mexiletine concentrations resulting from 200 mg given orally with either two 4-ml intramuscular injections each containing 100 mg (Mexitil--for intravenous use) or one 2-ml intramuscular injection of an experimental preparation containing 200 mg were compared in 3 and 6 normal subjects respectively. Plasma levels within the therapeutic range of 0.75-2 microgram/ml were attained at mean times of 28.7 and 42.5 min respectively. Apart from raised plasma creatine phosphokinase levels (as would be expected following an intramuscular injection) the tolerability of intramuscular mexiletine injections was satisfactory. Further studies in patients will be required to determine whether the combined oral and intramuscular administration of mexiletine is of value in acute myocardial infarction.

Influence of thromboxane inhibition on the severity of myocardial ischemia in cats

The effects of thromboxane (Tx) inhibition or arachidonic acid (AA) infusion were studied in anesthetized cats during acute myocardial ischemia (MI). AA (7.2 mg kg-1 h-1) or imidazole (25 mg kg-1 h-1) infusions were initiated 30 min after occlusion of the left anterior descending coronary artery. Assessment of the degree of protection of the ischemic myocardium was made by measurement of S-T segment elevation, plasma and myocardial creatine phosphokinase (CPK) activities, and myocardial amino-nitrogen content. Assessment of Tx inhibition was performed by radioimmunoassay. Administration of imidazole inhibited the sevenfold increase in plasma thromboxane B2 (TxB2) levels occurring in MI (p less than 0.001 at 2-5 h), markedly decreased S-T segment elevations at 2-k h (p less than 0.025), significantly prevented the elevation in plasma CPK (p less than 0.05, at 4 and 5 h), the increase in TxB2 post-MI, significantly decreased (p less than 0.025) S-T segment evaluations at 2-5 h, caused a decrease in plasmaCPK levels (p less than 0.05 at 5 h), but did not prevent loss of myocardial CPK or amino-nitrogen. In summary, the administration of imidazole resulted in significant protection of the myocardium in all indices of ischemic damage measured, while AA infusion resulted in only a partial protection. The mechanism of the imidazole protection of ischemic myocardial tissue appears to be via inhibition of Tx synthesis althoug we cannot exclude a hemodynamic or cytoprotective mechanism. These results suggest that specific inhibition of Tx formation is beneficial during acute MI.

Response of stress-susceptible and stress-resistant Hampshire pigs to electrical stress. I. Physiological and biochemical effects.

Stress susceptible (SS) and stress resistant (SR) purebred Hampshire swine, weighing approximately 100 kg, were utilized to study the effects of electrical stress on plasma creatine phosphokinase (CPK), blood pH, plasma lactic dehydrogenase (LDH), plasma glucocorticoids, rectal temperature, heart rate and respiration rate. Blood samples were obtained from jugular cannulas 15 min and 5 min pre-stress, and subsequently at 0, 5, 10, 15, 30, 60 and 120 min post-stress. The electrical stress (.05 amperes and 30 volts) was administered intermittantly (2 sec on and 1 sec off) directly on the skin at the point of the poll between the ears and on the medial side of the fore leg above the point of the elbow for a total stress time of 4 min over a 6-min period. Each pig was stressed three times with 3 days rest between stimulations. Post-stress responses (P<.01) were obtained over time for all the variables measured except respiration rate. Plasma CPK levels were greater (P<.01) for SS pigs at all the pre-stress and post-stress bleeding times. Thus, CPK may have value in differentiating between SS and SR pigs under standardized environmental (stress) conditions. The SS pigs had marked post-stress decrease (P<.01) in blood pH compared to SR pigs, although pre-stress blood pH was similar for both groups of pigs. Pre-stress plasma LDH levels were similar for the SS and SR pigs while several post-stress levels were greater for the SS pigs. Plasma glucocorticoid levels were similar for the SS and SR pigs at all the pre-and post-stress bleeding times. The SS pigs had a higher (P<.05) overall mean rectal temperature compared to the SR pigs. Both the SS and the SR pigs had elevated post-stress rectal temperatures. The heart rate of the SS pigs was higher at 0 min post-stress compared to the SR pigs while both groups were similar at the other times. Respiration rates were similar for both groups.

Plasma CPK levels in monozygotic and dizygotic twins discordant for schizophrenia

Plasma creatine phosphokinase (CPK) activity was determined in single samples of 9 monozygotic and 14 dizygotic twin pairs chosen from an earlier study on the basis of their having been discordant for clinical schizophrenia. The correlations within the MZ pairs was 0.89, and within the DZ pairs was 0.40. The results support a conclusion of genetic control of plasma CPK activity. The mean levels of activity were not abnormal, however.

Observations on plasma creatine phosphokinase activity in dogs.

Plasma creatine phosphokinase (PCPK) activity was determined in 14 clinically normal adult pedigree dogs of various breeds with an activated enzyme assay medium. PCPK levels were not significantly influenced by the time of sampling, body mass or eating, but there was a significant correlation (P is less than 0.05) between PCPK levels and moderate physical activity. The mean enzyme activity was 22.9 iu/litre at 30 degrees C. The PCPK levels are 10 times greater than those obtained by other authors with the non-activated enzyme assay method.

Plasma creatine phosphokinase levels in rats following lysergic acid diethylamide.

Lysergic acid diethylamide (LSD) injected intraperitoneally or intramuscularly did not increase rat plasma creatine phosphokinase (CPK) activity. LSD did not produce an increase in serum CPK activity in rats kept in a 2 degrees C environment for 2 hrs. LSD also did not potentiate, in rats, the increase in plasma CPK activity produced by restraint at 2 degrees C or 24 degrees C. It is likely that the increases in serum CPK activity previously reported to occur in people who became psychotic following LSD ingestion are a consequence of the psychotic state itself rather than a direct effect of LSD.

Release of creatine phosphokinase from muscle—I: Effect of polymyxin B, compound [formula omitted], and serotonin

Polymyxin B and compound 48 80 produce marked increases in the plasma levels of type III (skeletal muscle) creatine phosphokinase (CPK) in the Sprague-Dawley rat. Two other mast cell disrupters, dextran and ovomucoid, which also produce anaphylactoid shock, as well as the mast cell disrupters d-tubocurarine, diphenhydramine and tripellenamine, do not affect plasma CPK (PCPK) levels. The mast cell constituents histamine and heparin do not increase PCPK levels, although significant increases were noted following high doses of exogenous serotonin (5-HT). The effect of 5-HT on PCPK levels was inhibited by methysergide but that of polymyxin B was not. The neuromuscular blockade produced by polymyxin B was considered to have little if any role in the increase in PCPK levels, since neither succinylcholine or d-tubocurarine increases PCPK levels. Preventing the hypothermia secondary to polymyxin B or 5-HT did not block the increase in PCPK levels following treatment with these agents. Incubation of isolated extensor digitorum longus muscle in vitro in the presence of polymyxin B and compound 48 80 increases the rate of efflux of CPK from the muscle. It is postulated that polymyxin B and compound 48 80 have a toxic effect on muscle, one manifestation of which could be increased efflux of CPK from muscle.

Chlorpromazine-induced hypothermia and increased plasma creatine phosphokinase activity

The rate of efflux of creatine phosphokinase (CPK) from rat extensor digitorum longus muscle in vitro was significantly less at 22° than at 30°. Chlorpromazine (Cpz) at 10 −3 M and 10 −4 M, but not at 10 −5 M increased the efflux of CPK in vitro. In vivo, Cpz produced levels of CPK in plasma which were significantly correlated with the hypothermia that developed after the drug was administered ( R = −0.958, P < 0.001). When the hypothermia subsequent to Cpz administration was blocked by keeping rats at 31° or by administering the drug to cold acclimated rats, no increase in plasma CPK levels developed. Cpz, 25 mg/kg, produced a greater fall in body temperature and a greater increase in plasma CPK activity in rats kept at 2° than in rats kept at 22°. Cpz, given intramuscularly (i.m.) or intraperitoneally (i.p.) to rats kept at 22° produced equivalent increases in plasma CPK activity although the hypothermia following i.m. administration was slightly greater. Ganglionic blockade did not inhibit the increase in plasma CPK levels. Adrenalectomized rats did not differ from intact rats in the extent of increase in plasma CPK levels for a given degree of hypothermia. It is suggested that the increased plasma levels of CPK in vivo following Cpz in rats is due to the hypothermia produced by this drug rather than a direct toxic effect. In man, where IM Cpz does not produce hypothermia, the increased levels of CPK in plasma are probably due to the toxic effects of the drug, or its vehicle, on muscle.

Plasma creatine phosphokinase levels in hypomagnesaemic tetany in calves.

Plasma creatine phosphokinase levels in hypomagnesaemic tetany in calves.