It is clear that creatine plays a reservoir of high energy phosphate bond as creatine phosphate and maintains ATP levels in skeletal muscle and nervous tissues. Creatine and creatine kinase activity are required to utilize creatine phosphate as high energy phosphate. The contents of creatine in testis of rats were determined by the method of Van Pilsum and compared with other organs for the study of the physiological role of creatine in testis. Creatine content of tests was 39.82+/-3.36 ug/g wet tissue compared with skeletal muscle, 52.92+/-10.25 ug/g wet tissue. It was relatively high compared with brain (15.45+/-6.49 ug/g wet tissue), heart (20.0+/-2.91 ug/g wet tissue), kidney (29.55+/-2.52 ug/g wet tissue) and liver (12.68+/-1.94 ug/g wet tissue). Creatinine content of testes (45.84+/-4.08 ug/g wet tissue) was very high, compared with skeletal muscle (24.14+/-7.73 ug/g wet tissue), heart .(23.71+/-4.73 ug/g wet tissue), brain (17.24+/-1.19 ug/g wet tissue), kidney (14.92+/-3.45 ug/g set tissue), and liver (9.59 +/-1.26 ug/g wet tissue). I suppose that creatine in testis of rats may be a part of potent system for generation of ATP from ADP hydrolyzing creatine phosphate.
Adenosine Diphosphate ; Adenosine Triphosphate ; Animals ; Brain ; Creatine Kinase ; Creatine* ; Creatinine ; Heart ; Kidney ; Liver ; Muscle, Skeletal ; Phosphocreatine ; Rats* ; Testis

Serum creatine phosphokinase(CPK) levels were measured serially in 20 adults with closed tibial shaft fractures, CPK activity increased significantly after fracture(p < 0.01). High energy and delayed healing fractures had significantly higher levels of CPK than low energy and normally healing fractures, respectively. Thus, CPK determinations could be used to assess the severity of trauma and possible prognosis of the healing in tibial shaft fractures.
Adult ; Creatine Kinase ; Creatine ; Humans ; Prognosis

No abstract available.
Creatine Kinase* ; Electrophoresis*

Creatine Kinase ; Humans

During a 3 month period in 1984, 12 patients undergoing scheduled valvular replacement were Studied by CK and CK-MB isoenzyme to evaluate the myocardial damage during open heart operation. Total creatine kinase value was 58.3+/-25.6 u/L at control, 59.8+/-23.5 u/L at prebypass period, 85.5+/-49.6 U/L at during bypass period, 20.2+/-87.6 at postbypass period respectively. It began to rise in prebypass period and showed higtest level in postbypass period. CK-MB value was low in most cases below 20 U/L but in 2 patients postbypass period showed high level which above 40U/L. Initial isoenzyme activity was detected in 2 patients prior to anesthesia, in 2patients prior to bypass, in 5 patients during bypass, and in all others after termination of bypass. Considering above data we concluded that anesthetic management during prebypass period and myocardial preservation during bypass period required more proper and aggressive management despite of good operation results.
Anesthesia ; Creatine Kinase* ; Creatine* ; Heart ; Heart Valve Diseases* ; Humans

This study was conducted to evaluate the postnatal changes of serum creatine kinase (CK) and its isoenzymes in normal and asphyxiated newborns. In normal newborns total CK, CK-MM and CK-MB reached a plateau between 2 and 24 hr after birth whereas the serum CK-BB remained stable after birth. CK-MM, CK-MB and CK-BB respectivily composed 90~94%, 5~7% and 1~5% of total CK during study period. In asphyxiated newborns total CK, CK-MM and CK-MB reached maximal value at 12 hr after birth whereas CK-BB decreased after birth. There were no significant differences between normal and asphyxiated newborns in total CK, CK-MM and CK-MB during study period (up to 24 hrs after birth). But CK-BB of asphyxiated newborn was elevated significantly (p<0.05) within 6 hrs after birth compared to normal newborns. There were no significant differences of CK and its isoenzymes between patients evaluated by 5 min Apgar scores(0~3, 4~6 and 7~10) or degree of HIE (HIE stage 0~I, II and III). According to these results, the serum CK-BB is elevated in asphyxiated newborns during 1st 6hrs after birth but has no predictive values of the extent of cerebral damage.
Creatine Kinase* ; Creatine* ; Humans ; Infant, Newborn* ; Isoenzymes ; Parturition

No abstract available.
Child* ; Creatine Kinase* ; Creatine* ; Epilepsy* ; Humans ; Liver* ; Prospective Studies*

No abstract available.
Creatine Kinase ; Hypothyroidism* ; Muscular Diseases

BACKGROUND: It is well known that both thiopental sodium and propofol reduce the cerebral metabolic rate. The author investigated whether these drugs have similar effects on neurobiochemical compounds by using 1H-NMR, which enables noninvasive in vivo measurements of brain biochemistry. METHODS: Six healthy white New Zealand rabbits (2.5-3.0 kg) were studied. A marginal ear vein was punctured for continuous intravenous infusion. Spontaneous breathing was maintained during the anesthesia. Neurobiochemical compounds such as N- acetylaspartate (NAA), choline-containing compounds (Cho), creatine plus phosphocreatine (Cr), myoinositol (MI), and lactate were examined at 30, 45 and 60 min during intravenous anesthesia induced with thiopental sodium (n = 3) and propofol (n = 3). RESULTS: The signals of NAA, Cho, Cr and MI were unchanged during thiopental anesthesia, but the NAA signal was reduced at 45 and 60 min, and that of Cr was reduced from 30 min until the end of the propofol anesthesia. The Cho signal was increased at 45 and 60 min during propofol anesthesia. Thiopental sodium signal were detected through the study, but propofol was detected only at 30 min. On comparing metabolic ratios in the two groups, the ratio of NAA/Cr was reduced and those of Cho/Cr and MI/Cr were higher in propofol group than in the thiopental sodium group. CONCLUSIONS: Our results suggest that thiopental sodium has a cerebral protective function. Howerver, further study is needed upon the cerebral protective function of propofol anesthesia. Propofol is more useful for total intravenous anesthesia than thiopental sodium.
Anesthesia ; Anesthesia, Intravenous* ; Biochemistry ; Brain* ; Creatine ; Ear ; Infusions, Intravenous ; Inositol ; Lactic Acid ; Magnetic Resonance Spectroscopy* ; Phosphocreatine ; Propofol* ; Protons* ; Rabbits ; Respiration ; Thiopental* ; Veins

Serum metabonomic profiles of the model of focal cerebral ischemia reperfusion is established with the suture-occluded method by Longa to study the effect of ginsenosides. In this study, 48 rats were randomly divided into six groups: sham-operated group, pathological model group, positive drug group(6 mg·kg~(-1)·d~(-1)) and high, medium, low-dose ginsenosides groups(200, 100, 50 mg·kg~(-1)·d~(-1)). They are given intragastric administration respectively with same amount of 0.5% CMC-Na,nimodipine and ginsenoside for 5 days. At 2 h after the final administration, the model was established with the suture-occluded method, and free radical-scavenging activity changes of ginsenoside were observed by maillard reaction, and Longa was possible used as a renoprotective agent-occluded method. At the end of 24 h after the reperfusion, the hemolymph of rats in each group was collected, and the ~1H-NMR spectrum was collected after being treated by certain methods, and analyzed by principal component analysis(PCA). Compared with sham-operated group, pathological model group showed significant increases in the levels of lactate, glutamate, taurine, choline, glucose and methionine, but decreases in the levels of 3-hydroxybutyrate and phosphocreatine/creatine in serum. After treatment with ginsenosides, lipid, 3-hydroxybutyrate and phosphocreatine/creatine were increased in the serum of ginsenosides group rats, but with decreases in lactate and glutamate. The results showed that ginsenosides could regulate metabolic disorders in rats with focal cerebral ischemia reperfusion, and promote a recovery in the process of metabolism. It's helpful to promote the metabolic changes in rats with focal cerebral ischemia reperfusion via ~1H-NMR, and lay a foundation to develop ginsenosides as a new drug to treat ischemic cerebral paralysis.
3-Hydroxybutyric Acid ; Animals ; Brain Ischemia/metabolism* ; Creatine ; Ginsenosides/pharmacology* ; Hemolymph ; Metabolome ; Phosphocreatine ; Proton Magnetic Resonance Spectroscopy ; Random Allocation ; Rats ; Reperfusion Injury/metabolism*