Rise In Creatine Kinase Activity Research Articles

INFLUENCE OF A LOW-LEVEL SEMICONDUCTOR GALLIUM ARSENATE LASER IN EXPERIMENTAL ENVENOMATION INDUCED BY <i>BOTHROPS ATROX</i> SNAKE VENOM

Bothrops atrox is responsible for the majority of snakebite accidents in Brazilian Amazon and its venom can cause prominent local tissue damage. Experimental groups consisted of five male mice, each administered either B. atrox Venom (VB), B. atrox Venom + Antivenom (VAV), B. atrox Venom + Laser (VL), B. atrox Venom + Antivenom + Laser (VAVL), or Sterile Saline Solution (SSS) alone. Paw oedema was induced by intradermal administration of 0.05 mg kg-1 of B. atrox venom and was expressed in mm of directly induced oedema. Mice were subcutaneously injected with 0.10 mg kg-1 of venom for evaluation nociceptive activity and the time (in seconds) spent in licking and biting responses of the injected paw were taken as an indicator of pain response. Inflammatory infiltration was determined by counting the number of leukocytes present in the gastrocnemius muscle after venom injection (0.10 mg kg-1). Myotoxicity was studied by determining the plasmatic rise of creatine kinase activity after venom injection (0.20 mg kg-1). For histological examination of myonecrosis, venom (0.10 mg kg-1) was administered intramuscularly. The site of venom injection was irradiated by GaAs laser and some animals received antivenom intraperitoneally. GaAs laser irradiation administered in conjunction with antivenom, reduced pain, oedema, inflammation and myonecrosis induced by B. atrox venom in mice. The combined antivenom and GaAs laser treatment was more effective than separately treatments. The results suggest that laser therapy may reduce the local effects induced by B. atrox venom when associated with antivenom.

Titin is not the weak link in the Z‐disk streaming induced by plyometric exercise

The purpose was to analyze the skeletal muscle changes induced by an acute bout of plyometric exercise (PlyEx) before and after a PlyEx training.Healthy untrained individuals (N=13) completed an acute bout of PlyEx (10×10 squat‐jumps, 1 min rest). Thereafter, 8 subjects completed 8 weeks of PlyEx, while 5 subjects were instructed to refrain from doing any jumping activity for 8 weeks. Seven days after the last training session all subjects repeated a second acute bout of PlyEx.The first acute bout of PlyEx induced a rise of creatine kinase activity (CK = 2421 ± 4978 U/l), Z‐line streaming mainly in fast twitch fibers, a stretch of the c‐terminus of titin (observed by immunogold) not limited to fast twitch fibers, and an increase in calpain‐3 autolysis. The second acute bout of PlyEx in the trained group did not induce: a rise of CK (110 ± 58 U/l), Z‐line streaming, or calpain‐3 activation; while in the control group only two subjects exhibited Z‐line streaming, although all subjects presented a stretch of titin.Eccentric explosive exercise induced a stretch of titin, which is not responsible for the weakness of the sarcomere and of the calpain‐3 activation involved in sarcomeric remodelling.Grant Funding Source: Claude Leon Foundation, National Research Foundation (NRF)

Non-invasive diagnosis of arterial patency after thrombolytic treatment and its relation to prognosis.

To validate a simple noninvasive method with serial creatine kinase measurements for diagnosis of early patency of the infarct related artery after thrombolytic treatment with streptokinase. To investigate the relation between early patency of the infarct related artery and prognosis. Patients under 76 years of age and seen within six hours of the start of prolonged chest pain and ST segment elevation were treated with streptokinase (1.5 x 10(6) U) intravenously over 30-60 minutes. Blood for measurement of total creatine kinase activity was taken at baseline and at 1, 2, 3, 4, 8, 12, 16, 20, and 24 hours after starting treatment. The rise in enzyme activity at each time from baseline was expressed as a proportion of the total rise from baseline to peak. Patients studied were in the following groups: (a) Sixty patients took part in a validation study with angiographic determination of patency of the infarct related coronary artery at 2.6 (0.3) hours (mean (SD)) after starting streptokinase. (b) A further 258 patients did not have early arteriography, but data were added to those from the 60 validation patients to find the relation between enzymatically determined early patency of the infarct related artery and 30 day mortality. (c) A further subset of 232 patients with first infarctions (including patients from groups (a) and (b) had angiocardiography at three weeks after infarction, and data were used to investigate the relation between early patency of the infarct related artery and left ventricular function. Normalised rate of rise of creatine kinase activity at three hours after starting streptokinase in relation to angiographic patency of the infarct related coronary artery at 2.5 hours; 30 day cardiac mortality; and left ventricular function at three weeks in survivors of first infarction. In the validation study, a rise in three hour creatine kinase activity of > 20% of peak occurred in 34/37 patients with initially patent infarct related coronary arteries (sensitivity 92%), and a rise to < 20% of peak occurred in 21/23 patients with initially occluded arteries (specificity 91%). In the prognostic study, 30 day mortality was 2.1% in the 191 patients with three hour creatine kinase > 20% of peak and 8.7% in the 127 patients with three hour creatine kinase < 20% of peak (p < 0.01). Angiocardiography in three week survivors of anterior infarction (n = 95) showed better left ventricular function when three hour creatine kinase was > or = 20% than when it was < 20% of peak (mean (SEM) end systolic volume 71 (5) v 96 (9) ml, p < 0.02; ejection fraction 56% (2%) v 51% (2%), NS). Non-invasive determination of early patency of the infarct related artery by the normalised rate of rise of creatine kinase activity at three hours seems to be reliable, and may be prognostically important and of value for use in clinical trials.

Aspirin does not improve early arterial patency after streptokinase treatment for acute myocardial infarction.

To investigate the hypothesis that the magnitude of the life saving effect of aspirin in the second international study of infarct survival (ISIS-2) trial cannot be explained solely by prevention of late reocclusion of the infarct related artery. The aim of this study was to discover whether or not aspirin in combination with streptokinase had an adjuvant thrombolytic effect. Aspirin (150 mg) or placebo was given at the start of streptokinase infusion to 200 patients seen within six hours of the start of prolonged ischaemic cardiac pain and ST segment elevation. All patients received active aspirin at three hours. Patency of the infarct related artery was assessed non-invasively by the normalised rise of creatine kinase activity at three hours after starting streptokinase in these 200 patients and in a further 52 patients who had already taken aspirin within one week of the start of infarction. Rise in creatine kinase activity from baseline to > or = 20% or < 20% of the peak rise of activity in blood taken at three hours after starting infusion of streptokinase. This correlates with patency or occlusion of the infarct related coronary artery at about 2.5 hours after starting streptokinase. Assessed in this way, patency of the infarct related artery was 60% in patients given aspirin, 63% in those given placebo, and 62% in patients who had already taken aspirin within one week of infarction. The magnitude of the life saving effect of aspirin remains unexplained. Further investigation is needed into the mechanism of action of antiplatelet treatment in relation to thrombolytic treatment.

Ouabain-induced tachyarrhythmias and cell damage in isolated perfused guinea-pig hearts: I. Protection by propranolol

An arrhythmogenic concentration of ouabain (1.37 × 10 −6 m) was added to the media perfusing guinea-pig Langendorff hearts after a 60 min period for establishment of a steady-state. Within 15 min following the addition of ouabain, a significant though transient increase in ventricular cyclic-AMP occurred. The first appearance of electrocardiographic abnormalities occurred at a mean time of +22.6 (±5.1) min following ouabain, a fall in ATP, coronary flow and myocardial oxygen consumption (MVO 2) at +28 min, tachycardia at +33.9 (±6.7) min, and asystole (due to fibrillation) at 42.2 (±2.6) min. When ATP levels, coronary flow and MVO 2 declined, they remained depressed for the duration of the experiments. While these changes were occurring following ouabain, creatine kinase (CK) activity in the coronary effluent began a progressive increase at +45 min, as did lactate dehydrogenase (LDH) at +60 min, indicative of cellular damage. Electron microscopic analysis of tissues exposed to ouabain for 1 h revealed changes in the mitochondria (e.g. swelling, fragmentation or loss of cristae and loss of calcium granules) similar to those seen in anoxia and ischemia. The prior administration of propranolol (3.38 × 10 −6 m) attenuated the rise in creatine kinase activity, and abolished all other effects elicited by ouabain. Neither increasing coronary flow, alpha-adrenergic blockade with phentolamine (1 × 10 −6 m) nor “washing” preparations with drug-free media for 1 h affected the results observed with ouabain. On the basis of these results, we conclude that arrhythmogenic doses of ouabain activate the formation of cyclic-AMP, lending support to the hypothesis that increased levels of the nucleotide may act as a triggering event for the subsequent development of arrhythmias. The sequence of events obtained suggests that arrhythmogenic doses of ouabain produce an oxygen deficit similar to that observed in ischemia, as evidenced by the fall in coronary flow, MVO 2 and ATP, the rise in released LDH and CK, and changes in mitochondrial ultrastructure. This deficit, at least in part, appears to be responsible for the development and maintenance of arrhythmias induced by the concentration of ouabain used in this model.

Glycosaminoglycan metabolism following acute myocardial infarction and the effects of intravenous hyaluronidase therapy

A series of thirteen patients with acute myocardial infarction was studied. In the 12 patients heparinised on admission, there was a fall in serum hyaluronidase activity, free amino sugar and uronic acid levels. This contrasted with a rise in creatine kinase activity. In a single unheparinised patient, the hyaluronidase level rose. This suggests that necrotic cardiac tissue releases hyaluronidase. Any beneficial effects of the local release of hyaluronidase may be minimized by heparin therapy. Study of patients on a trial of intravenous bovine testicular hyaluronidase following acute myocardial infarction could detect no rise in hyaluronidase levels. This confirms previous reports that human serum inhibits bovine testicular hyaluronidase.

Brain isoenzyme of creatine kinase. III. Active and inactive forms in dystrophic muscle of vitamin E-dificient rabbit.

Rabbits were fed a vitamin E-deficient diet for 7 weeks. Control rabbits, paired for weight, were pair-fed an identical diet supplemented with vitamin E. After 3 weeks the expermental animals showed a rise in serum creatin kinase activity which was attributable to the muscle isoenzyme (MM). No rise in creatine kinase activity or appearance of MM was noted in the serum of the control rabbits. Total creatine kinase activity and MM activity were reduced in the gastrocnemii of the experimental animals while the activities of the brain (BB) and hybird (MB) isoenzymes were increased. The specific activity of BB based on immunochemically determined BB protein was not different from normal in either the experimental or control group. Activation of pre-existing inactive BB is probably not the explanation for increased BB activity in the gastroncnemii of the experimental group.