Effect Of Creatine Phosphate Research Articles

Clinical Effect of Creatine Phosphate Combined with Vitamin C in the Treatment of Pediatric Viral Myocarditis and its Effect on Myocardial Enzyme and Troponin T

Clinical Effect of Creatine Phosphate Combined with Vitamin C in the Treatment of Pediatric Viral Myocarditis and its Effect on Myocardial Enzyme and Troponin T

Effect of creatine phosphate on myocardial injury induced by lung ischemia-reperfusion in rats

Objective To evaluate the effect of creatine phosphate on the myocardial injury induced by lung ischemia-reperfusion (I/R) in rats. Methods Twenty-four male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-350 g, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S), I/R group, and I/R+ creatine phosphate group (group CP). Lung I/R was induced by clamping the left hilum of lung for 0.5 h with a non-invasive microvascular clip followed by mechanical ventilation and 2.0 h of reperfusion.Creatine phosphate 6.6 mg·kg-1·min-1 were infused intravenously at 30 min before ischemia in group CP, while the equal volume of normal saline was administered in group I/R.At 2.0 h of reperfusion, blood samples were obtained from the right ventricle for determination of the serum concentration of cardiac troponin I (cTnI). Myocardial specimens were obtained from the apex for microscopic examination and for determination of the levels of myocardial superoxide dismutase (SOD), malondialdehyde (MDA), and myeloperoxidase (MPO). Results Compared with group S, the serum cTnI concentrations, MDA content, and MPO activity were significantly increased, and the SOD activity was significantly decreased in I/R and CP groups (P<0.05). Compared with group I/R, the serum cTnI concentrations, MDA content, and MPO activity were significantly decreased, and the SOD activity was significantly increased in group CP (P<0.05). Myocardial injury was significantly attenuated in group CP as compared with group I/R. Conclusion Creatine phosphate can attenuate the myocardial injury induced by lung I/R in rats, and the mechanism is related to decrease in damage caused by lipid peroxidation. Key words: Phosphocreatine; Lung; Reperfusion injury

The effect of creatine phosphate combined with salvia miltiorrhiza polyphenols acid salt in treatment of coro-nary heart disease with heart failure

Objective To explore the effect of creatine phosphate combined with salvia miltiorrhiza polyphe-nols acid salt in treatment of coronary heart disease heart failure. Methods 114 cases of patients with coronary heart disease heart failure were selected as research objectives, who were treated in our hospital from August 2012 to August 2014. And they were randomly divided into control group(55 cases)and research group(59 cases)according to the number table method. Routine therapy of heart failure were given in both groups and the research group were added creatine phosphate combined with salvia miltiorrhiza polyphenols acid salt. The clinical efficacy of two groups of patients were observed and compared. Results The total effective rate in research group was 96.61%(57／59), significantly higher than 85.45%(47／55)in control group, the difference was statistically significant(χ2＝4.427,P＝0.035). Before treatment, the left ventricular ejection fraction(LVEF), left ventricular end diastolic diameter (LVEDD),left ventricular end systolic diameter(LVESD)and 6min walking distance between two groups had no sig-nificant difference(P＞0.05). After treatment, the LVEDD and LVESD of research group were decreased and LVEF and 6 minutes walking distance of two groups were increased, the difference was statistically significant(P＜0.05), the LVEDD and LVESD of research group were lower than that of the control group and LVEF and 6 minutes walking distance were higher than that of control group, the difference was statistically significant(P＜0.05). No complications or side effects related to the treatment were found in both groups. Conclusion On the basis of routine therapy of heart failure, the effect of creatine phosphate sodium combined with salvia miltiorrhiza polyphenols acid salt in treat-ment of coronary heart disease heart failure can improve cardiac function of the patients with the indicators, and the clinical effect is obvious,and side effects is rarely observed. Key words: Coronary heart disease heart failure; Salvia miltiorrhiza polyphenols acid salt; Creatine phosphate

The study of myocardial protective effect of creatine phosphate sodium in liver transplant patients

Objective: To study the cardioprotective effectof creatine phosphate sodium by measuring perioperative myocardial enzymes of allogeneic liver transplant patients. Methods: The 26 cases of orthotopic liver transplant patients were randomly divided into control group and creatine phosphate sodium group, 13 cases in each group. The creatine phosphate sodium group were given creatine phosphate sodium 30 mg/kg at the time of induction. The control group were given equal amount of N.S. All patients at six-phase of before surgery, after anesthesia,before anhepatic phase, anhepatic phase,new liver and the 12 hours after surgery extraction radial artery. The CK, CK-MB and cTnI activity was measured. Results: To compared with control group, creatine phosphate sodium group’s plasma CK, CK-MB and cTnI concentrations in before anhepatic phase, anhepatic phase, new liver and the 12 hours after surgery 4 phase are significantly lower ( p&lt;0.05). Conclusions: The creatine phosphate sodium has a protective effect on liver transplantation in patients with myocardial damage.

The study of myocardial protective effect of creatine phosphate sodium in liver transplant patients

Objective: To study the cardioprotective effectof creatine phosphate sodium by measuring perioperative myocardial enzymes of allogeneic liver transplant patients. Methods: The 26 cases of orthotopic liver transplant patients were randomly divided into control group and creatine phosphate sodium group, 13 cases in each group. The creatine phosphate sodium group were given creatine phosphate sodium 30 mg/kg at the time of induction. The control group were given equal amount of N.S. All patients at six-phase of before surgery, after anesthesia,before anhepatic phase, anhepatic phase,new liver and the 12 hours after surgery extraction radial artery. The CK, CK-MB and cTnI activity was measured. Results: To compared with control group, creatine phosphate sodium group’s plasma CK, CK-MB and cTnI concentrations in before anhepatic phase, anhepatic phase, new liver and the 12 hours after surgery 4 phase are significantly lower ( p&lt;0.05). Conclusions: The creatine phosphate sodium has a protective effect on liver transplantation in patients with myocardial damage.

Effect of creatine phosphate on perioperative myocardial injury caused by living donor fiver transplantation in adult patients

Objective To investigate the effect of creatine phosphate on perioperative myocardial injury caused by living donor liver transplantation(LDLT)in adult patients.Methods Forty ASA Ⅱ -Ⅳ patients(liver function Child-Pugh grade B or C)aged 45-62 yr weighing 47-91 kg undergoing LDLT were randomly divided into 2 groups(n = 20 each): control group(group C)and creatine phosphate group(group CP).In group CP,creatine phosphate 30 mg/kg was injected intravenously at skin incision followed by creatine phosphate infusion at 4 mg· kg- 1 · h- 1 until the end of surgery.In group C,equal volume of normal saline was infused instead of creatine phosphate.HR,MAP,CVP,PCWP,CO and SvO2 were recorded immediately before skin incision,at 5 and 30 min of anhepatic phase,at 5 and 30 min of neohepatic phase and at the end of operation.Blood samples were taken from central vein immediately before skin incision(baseline,T0),at 30 min of anhepatic phase(T1),at 30min of neohepatic phase(T2),at the end of operation(T3)and at 4 and 24 h after operation(T4,5)for determination of serum cardiac troponin I(cTnI)and creatine kinase MB(CK-MB)concentrations and lactate dehydrogenase(LDH)activity.Postoperative adverse events were recorded.Results The serum cTnI and CK-MB concentrations and LDH activity were significantly increased at T2-5 as compared with the baseline value at T0 in both groups(P ＜0.05 or 0.01).MAP and CO were significantly higher from 5 min of neohepatic phase to the end of operation,the serum cTnI and CK-MB concentrations and LDH activity were significantly lower at T2-5,and the incidence of ventricular arrhythmia was significantly lower in group CP than in group C(P ＜ 0.05 or 0.01).Conclusion Creatine phosphate can attenuate perioperative myocardial injury caused by LDLT in adult patients. Key words: Phosphocreatine; Liver transplantation; Myocardial reperfusion injury

Effects of creatine phosphate on Ca2+ regulation by the sarcoplasmic reticulum in mechanically skinned rat skeletal muscle fibres.

1. The effect of creatine phosphate (PCr) on sarcoplasmic reticulum (SR) Ca2+ regulation was studied in mechanically skinned skeletal muscle fibres from rat extensor digitorium longus (EDL). Preparations were perfused with solutions mimicking the intracellular milieu and the [Ca2+] within the muscle was monitored continuously using fura-2. 2. Brief application of 40 mM caffeine caused a transient increase in [Ca2+] due to SR Ca2+ release, and an associated tension response. Withdrawal of PCr resulted in (i) a slow transient release of Ca2+ from the SR (ii) a marked prolongation of the descending phase of the caffeine-induced fluorescence ratio transient and (iii) a decrease in the Ca2+ transient amplitude to 69.2 +/- 2.7 % (n = 16) of control responses. 3. Prolongation of the caffeine-induced Ca2+ transient also occurred following application of the SR Ca2+ pump inhibitor cyclopiazonic acid (CPA). This suggests that (i) the descending phase of the caffeine-induced Ca2+ transient is dependent on the rate of Ca2+ uptake by the SR and (ii) prolongation associated with PCr withdrawal may also reflect a decrease in the net Ca2+ uptake rate. 4. The effects of PCr withdrawal were mimicked by addition of the creatine kinase (CK) inhibitor 2,4-dinitro-1-fluorobenzene (DNFB). Hence, reducing the [PCr] may influence SR Ca2+ regulation by limiting local ATP regeneration by endogenous CK. After treatment with DNFB, PCr withdrawal had no effect on the Ca2+ transient, confirming that PCr does not have an additional direct effect on the SR. 5. The Ca2+ efflux associated with PCr withdrawal was insensitive to ryanodine or Ruthenium Red, but was effectively abolished by pretreatment with the SR Ca2+ pump inhibitor cyclopiazonic acid (CPA). This suggests that the Ca2+ efflux associated with PCr withdrawal is independent of the SR Ca2+ channel, but may involve reversal or inhibition of the Ca2+ ATPase. 6. These data suggest that Ca2+ regulation by the SR is strongly dependent on the supply of ATP via endogenous CK. Depletion of PCr may contribute to impaired SR Ca2+ regulation known to occur in intact skeletal muscle under conditions of fatigue.

Beneficial effect of creatine phosphate (cp) in cardiac surgery: biochemical evidence

Beneficial effect of creatine phosphate (cp) in cardiac surgery: biochemical evidence

Improved Myocardial Protection by Creatine Phosphate in Cardioplegic Solution. An In Vivo Study in the Pig During Normothermic Ischemia

The effect of creatine phosphate in potassium cardioplegia was studied in a pig heart model in vivo. Fifteen pigs divided into two groups were placed on cardiopulmonary bypass and subjected to 1 hour of cardioplegic arrest at normothermia. In group I (control), in which a potassium cardioplegic solution was used, only two out of eight animals could successfully be weaned from bypass. In group II, on the other hand, in which creatine phosphate (10 mmol/l) was added to the cardioplegic solution, six out of seven animals could be weaned from bypass and the heart performance assessed by volume loading. Group II also exhibited better maintenance of high-energy phosphates during ischemia, with significantly higher adenylate charge potential, than group I. In all animals weaned from bypass--two in group I and six in group II--the ventricular performance was decreased compared with that before induction of ischemia. The results indicate that creatine phosphate could be an effective constituent in potassium cardioplegia.

Effect of creatine phosphate on ATP and CP contents of rat heart and blood after I.V. administration

Effect of creatine phosphate on ATP and CP contents of rat heart and blood after I.V. administration

Effect of creatine phosphate on ATP and CP contents of rat heart and blood after I.V. administration

Effect of creatine phosphate on ATP and CP contents of rat heart and blood after I.V. administration

Effect of creatine phosphate on action potential duration and contractility of the frog myocardium in hypoxia

Effect of creatine phosphate on action potential duration and contractility of the frog myocardium in hypoxia

Effect of creatine phosphate on the slow inward calcium current, action potential, and the contractile force of frog atrium and ventricle

The effects of creatine phosphate on frog heart muscle contraction have been studied further. It has been shown that after inhibition of mitochondrial oxidative phosphorylation by sodium cyanide the frog heart ventricle contraction can be maintained at a high level by addition of creatine phosphate. The effect of creatine phosphate on the contractile force and action potential is similar for frog heart ventricle and atrium. It has been directly demonstrated by using the voltage-clamp technique that creatine phosphate controls the slow inward calcium current through the surface membrane of frog atrium cells.

Studies of energy transport in heart cells: The effect of creatine phosphate on the frog ventricular contractile force and action potential duration

The effect of creatine phosphate on the contractile force and action-potential duration has been investigated using contracting frog ventricular preparation perfused with Ringer's solution. Creatine phosphate in concentrations of 10 m m and 20 m m enhanced both the force of contraction and action-potential duration, which returned to their normal value after the washout of creatine phosphate excess from the heart muscle. Significantly increased creatine-phosphate concentration in the perfusate (70 m m) initially caused an increase in both the force of contraction and action-potential duration followed by a spontaneous decrease of the contractile force which was increased again within the first minutes of creatine phosphate washout. However, during perfusion with creatine phosphate (70 m m) action-potential duration increased monotonically. These data are taken to indicate the existence of two different sites of creatine phosphate action in heart cells: on myofibrils and on the surface membrane of the cell. Changes in action-potential duration may be observed also after prolonged perfusion of heart strips with normal Ringer's solution and during subsequent perfusion with creatine solution. Perfusion of frog heart strips for 8 hr does not damage the ultrastructure of heart cells and does not lead to the depletion of their glycogen content. It has been shown that 1-fluoro 2 4-dinitrobenzene, often used for creatine phosphokinase inibition in intact tissue, inhibits both the force of contraction and action potential. The experimental results obtained support the concept of energy transport via creatine-phosphate pathway in heart cells and demonstrate the important role of creatine phosphate in regulation of heart muscle contraction.

Isometric force development, isotonic shortening, and elasticity measurements from Ca2+-activated ventricular muscle of the guinea pig.

Isometric tension and isotonic shortening were measured at constant levels of calcium activation of varying magnitude in mechanically disrupted EGTA-treated ventricular bundles from guinea pigs. The results were as follows: (a) The effect of creatine phosphate (CP) on peak tension and rate of shortening saturated at a CP concentration more than 10 mM; below that level tension was increased and shortening velocity decreased. We interpreted this to mean that CP above 10 mM was sufficient to buffer MgATP(2-) intracellularly. (b) The activated bundles exhibited an exponential stress-strain relationship and the series elastic properties did not vary appreciably with degree of activation or creatine phosphate level. (c) At a muscle length 20 percent beyond just taut, peak tension increased with Ca(2+) concentration over the range slightly below 10(-6) to slightly above 10(-4)M. (d) By releasing the muscle length-active tension curves were constructed. Force declined to 20 percent peak tension with a decrease in muscle length (after the recoil) of only 11 percent at 10(-4)M Ca(2+) and 6 percent at 4x10(-6)M Ca(2+). (e) The rate of shortening after a release was greater at lower loads. At identical loads (relative to maximum force at a given Ca(2+) level), velocity at a given time after the release was less at lower Ca(2+) concentrations; at 10 M(-5), velocity was 72 percent of that at 10(-4)M, and at 4x10(-6)M, active shortening was usually delayed and was 40 percent of the velocity at 10(-4) M. Thus, under the conditions of these experiments, both velocity and peak tension depend on the level of Ca(2+) activation over a similar range of Ca(2+) concentration.