Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated hearts from rabbits, hamsters, ferrets, gerbils, rats, mice and guinea pigs were used to investigate species differences in (i) stability during aerobic perfusion, (ii) susceptibility to ischemic injury and (iii) responsiveness to cardioplegic protection. During 120 minutes of continuous aerobic perfusion, the rate of functional deterioration differed between species. The rabbit was the most stable and the guinea pig the least: the mean +/- SEM of the left ventricular developed pressure falling, after 120 minutes of perfusion, to 82 +/- 4% and 60 +/- 6%, respectively. In studies with 30 minutes of ischemia and 60 minutes of reperfusion, the developed pressure recovered to 72 +/- 2, 71 +/- 2, 65 +/- 3, 64 +/- 2, 58 +/- 3, 50 +/- 8 and 50 +/- 2% of its pre-ischemic value in the rabbit, hamster, ferret, gerbil, rat, mouse and guinea pig, respectively. With 60 minutes of ischemia, the recovery of developed pressure in the guinea pig, rabbit, rat, mouse, hamster, ferret and gerbil was 5 +/- 1, 19 +/- 2, 22 +/- 3, 30 +/- 5, 55 +/- 4, 60 +/- 2 and 45 +/- 5%, respectively. Creatine kinase leakage and changes in tissue metabolite content generally reflected the degree of functional injury. In further studies, groups of 6 hearts were infused for 2 minutes with St. Thomas' Hospital Cardioplegic Solution, then subjected to 30 minutes of ischemia. Cardioplegia improved the recovery of developed pressure in the rabbit, hamster, gerbil, rat and mouse (from 72 +/- 2, 71 +/- 2, 64 +/- 2, 58 +/- 3 and 50 +/- 8% to 82 +/- 3, 103 +/- 3, 84 +/- 4, 77 +/- 2 and 78 +/- 5%, respectively; p less than 0.05 for each species). However, no protection was observed in the ferret and guinea pig (65 +/- 3 and 50 +/- 2% versus 66 +/- 3 and 47 +/- 6%, respectively; p = NS). With cardioplegia, tissue high-energy phosphates increased significantly in all species except the gerbil. Rat and guinea pig hearts were taken for time-response studies (ischemia for 15, 20, 30, 45, 50 and 60 minutes in the rat and 15, 30, 45 and 60 minutes in the guinea pig) with or without cardioplegia. In the rat, cardioplegia improved recovery over an ischemic time-window of 20-45 minutes, but in the guinea pig no improvement was detected. Creatine kinase leakage reflected the patterns of functional recovery. In contrast, high-energy phosphates were preserved better in both species after 30 minutes of ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Species differences in susceptibility to ischemic injury and responsiveness to myocardial protection. 210 1

Creatine kinase (CK; EC 2.7.3.2) has been used as an indicator of myocardial cellular damage. In this study we used a Krebs-Henseleit (KH) solution to reperfuse isolated rat hearts after 24 h of cold preservation and collected the KH reperfusate for assay of CK to assess cellular damage. We wanted to determine the stability of CK in the KH solution at different cold-storage temperatures and albumin concentrations. CK activity (mean +/- SEM) after one week of refrigeration (5 degrees C) was 93% +/- 1% of control values, whereas CK activity in nitrogen-frozen (-200 degrees C) samples was only 1.6% +/- 1% of control values, and that in samples frozen at moderately low temperatures (-10 degrees C) was 63% +/- 1% of control values. To enhance stability, we added albumin at several concentrations (49, 25, 12, and 6 g/L) to reperfusion collections in which CK had been previously determined. Specimens were frozen (-10 degrees C), then re-analyzed for CK weekly for three weeks. CK activity was maintained (100% +/- 5%) only in samples containing 25 g/L or more albumin. These data suggest that refrigeration (5 degrees C) for one week maintains normal CK activity in KH solution; however, if prolonged storage is necessary, a stabilizer such as albumin (greater than or equal to 25 g/L) will maintain analyte stability in frozen storage (-10 degrees C) for at least three weeks.
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PMID:Decreased storage stability of creatine kinase in a cardiac reperfusion solution. 233 90

We evaluated the efficacy of intracoronary administration of verapamil hydrochloride in reducing myocardial injury during acute ischemia and reperfusion. Ischemia was induced by 30% and 45% reductions of circumflex arterial blood flow for successive 2-hour periods. A reperfusion period (1 hour and 45 minutes) followed ischemia upon deflation of a pneumatic occluder. Verapamil (30 micrograms/kg) was slowly injected into the circumflex artery as a bolus 15 minutes after each blood flow reduction step. To prevent verapamil-induced decreases in heart rate, ventricular pacing was established at 170 beats/min before a baseline period and maintained throughout the protocol. Creatine kinase activities (international units per milligram protein) measured in samples obtained from posterior papillary muscles were 15 +/- 1 (mean +/- SEM) and 10 +/- 2 for animals receiving verapamil or its saline vehicle, respectively (p less than 0.05). Quantitative morphometry was performed on left ventricular myocardium after staining with p-nitro blue tetrazolium. Intracoronary administration of verapamil reduced the extent of left ventricular infarction, as disclosed by positive tetrazolium staining of the tissue, from 34 +/- 4% of the left ventricle in vehicle-treated animals to 21 +/- 4% of the left ventricle in verapamil-treated animals (p less than 0.05). We conclude that intracoronary administration of verapamil reduced the extent of myocardial infarction acutely, independent of increases in blood flow through the circumflex coronary artery or decreases in heart rate. Administration of verapamil was not associated with decreases in ventricular afterload, the pressure-rate index, cardiac output, or the maximum rate of pressure development in the left ventricle. Verapamil treatment of animals subjected to ischemia was not associated with sustained elevations of left atrial pressure to values above those measured in animals receiving the vehicle.
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PMID:Effects of intracoronary verapamil administration in a sheep model of acute myocardial ischemia and reperfusion. 338 62

Diabetes mellitus is well known to increase the death rate after acute myocardial infarction in humans. The mechanisms of this adverse effect of diabetes, however, remain unknown. In the present study an animal model was developed in which the influence of diabetes on the survival rate after acute myocardial infarction could be studied in more detail. Male Wistar rats were rendered diabetic with streptozotocin (45 mg X kg-1 intravenously) and kept in the study if one week later their tail blood glucose concentration was between 13.9 and 22.2 mmol X litre-1 after a four hour fast. Ten weeks later they underwent acute left coronary artery ligation. In comparison with control rats (n = 30), diabetic rats (n = 32) had a higher mortality in the first 20 minutes after acute coronary artery ligation (78% vs 53%; p less than 0.05 by chi 2 test). Creatine kinase-MB isoenzyme activity tended to increase less in surviving diabetic rats than in their non-diabetic counterparts. Moreover, blood samples collected a few minutes before the surgical procedure showed that diabetic rats dying within the first 20 minutes (n = 25) had higher mean (SEM) plasma glucose concentrations (26.9(0.5) vs 23.4(1.2) mmol X litre-1; p less than 0.01) and lower mean(SEM) plasma insulin concentrations (20(1) vs 26(2) mU X litre-1; p less than 0.05) than those (n = 7) that survived that critical period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased mortality rate in diabetic rats submitted to acute experimental myocardial infarction. 370 52

Brief periods of ischemia have been suggested to protect against myocardial injury caused by a subsequent episode of prolonged ischemia and reperfusion. However, the protective effects of brief ischemic periods against myocardial dysfunction after prolonged myocardial ischemia are controversial. To examine whether the protective effects of brief ischemic episodes relate to the extent of prior ischemic events, isolated rat hearts were subjected to either no preischemia (group A); one 5-minute episode of preischemia and 10 minutes of reperfusion (group B); or two 1-minute episodes of ischemia, each followed by 5 minutes of reperfusion (group C). All hearts were then subjected to 15 minutes of total ischemia and 10 minutes of reperfusion. In group A, after 10 min of reperfusion coronary perfusion pressure (CPP) was 31% +/- 10% (mean +/- SEM) higher than the control value, peak force of cardiac contraction (FCC) was 64% +/- 5% lower, and heart rate was 18% +/- 3% lower. In group B, CPP increased 26% +/- 6%, FCC fell 58% +/- 7%, and heart rate decreased 22% +/- 8% (group B vs group A, P value not significant) after ischemia and reperfusion. In group C, CPP increased 23% +/- 7%, FCC decreased 57% +/- 8%, and heart rate fell 8% +/- 4% on reperfusion (group C vs groups A and B, P value not significant). Creatine kinase (CK) was measured in the hearts from different groups and was found to be similar. Release of the adenosine triphosphate (ATP) metabolites hypoxanthine, inosine, and adenosine was also not different in the coronary effluents of the three groups of hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of brief ischemic episodes to protect against myocardial dysfunction caused by ischemia and reperfusion in isolated rat hearts. 798 1

Cell damage within the sinusoidal lining of human liver grafts during transplantation is an early event that is critical in ischemia-reperfusion injury and probably plays a key role in primary liver dysfunction after transplantation. No simple biochemical marker for sinusoidal injury is currently available. Because creatine kinase activity has been described in heart endothelial cells, we hypothesized that release of this enzyme might serve as an index of sinusoidal injury. To test this hypothesis, we used several in vivo and in vitro experimental models. Occlusion of the rat hepatic pedicle in situ for 60 min (normothermic ischemia) induced a significant increase in serum creatine kinase levels relative to those in laparotomized controls (2,530 +/- 530 vs. 389 +/- 64 IU/L, mean +/- SEM; p < 0.005). In the isolated perfused rat liver, 60-min ischemia induced early (< or = 3 min) creatine kinase and AST release (0.87 +/- 0.14 vs. 0.08 +/- 0.01 IU/min/gm liver, respectively). A similar phenomenon was observed after 24-hr or 48-hr hypothermic conservation in University of Wisconsin solution. Electrophoretic analysis and immunoinhibition studies showed that creatine kinase activity comprised creatine kinase-BB (approximately 50%) and mitochondrial creatine kinase. Trypan blue infusion showed a loss of viability in sinusoidal cells, whereas hepatocytes were relatively spared. Finally, murine sinusoidal cells were isolated, cultured and then lysed by a freeze-thaw cycle and sonication. Creatine kinase activity was found in endothelial cells (creatine kinase-BB), Kupffer cells (creatine kinase-BB) and Ito cells (creatine kinase-MM). Creatine kinase-BB was not found in hepatocytes, but mitochondrial creatine kinase was detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Creatine kinase-BB: a marker of liver sinusoidal damage in ischemia-reperfusion. 827 65

In an experimental animal exercise model we tested whether daily administration of prednisone prevents the development of mechanically induced muscle fibre damage. Six-week-old rats were treated with different doses of prednisone ranging from 1 to 50 mg/kg body weight per day or with placebo, for 8 days. On day 6 of treatment the rats were forced to run for 2 h on a level treadmill. Two days after exercise morphological damage in the soleus muscles was quantified using light microscopy and a semi-automatic image analysis system. Creatine kinase (CK) activity was measured before exercise (day 5) and directly after exercise (day 6). The expression of dystrophin in a placebo group and in a group that received 5 mg prednisone/kg body weight per day with and without performing exercise was studied with Western blotting. The effect of prednisone on fibre type distribution was determined with an antibody against fast myosin and the effect of prednisone on the proliferative activity of muscle satellite cells was studied using bromodeoxyuridine (BrdU) immunohistochemistry. Exercise-induced muscle fibre damage varied in a dose-dependent way. In the placebo group the mean (SEM) damaged muscle fibre area was 4% (1%). The groups that received low doses of prednisone, 1 or 2.5 mg/kg per day, showed a similar level of muscle damage. However, with 5 mg prednisone/kg per day the amount of muscle fibre damage [mean (SEM)] was significantly reduced to 1.4% (0.5%) (P <or= 0.05, Student's t-test). High doses of prednisone had no protective effect. Directly after exercise the CK activity was increased two-fold, except in the group that received 50 mg prednisone/kg body weight per day. No changes in the amount of dystrophin were found after densitometric analysis of the Western blots. Prednisone did not affect the fibre distribution or the labelling index of satellite cells. We conclude that prednisone, given in an appropriate dose, protects muscle fibres against the development of mechanically induced damage, possibly by stabilizing the muscle fibre membranes. This action may explain the beneficial effect of prednisone observed in Duchenne muscular dystrophy patients.
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PMID:Prednisone can protect against exercise-induced muscle damage. 874 Oct 82

Changes in the concentrations of thiobarbituric acid-reactive substances (TBARS), an index of lipid peroxidation in liver, heart and soleus muscle, were studied in trained (T) and untrained (U) rats throughout a period of 48-72 h following running until exhaustion. Creatine kinase (CK) concentration in serum was also determined. The running time till exhaustion in group T was significantly longer than in group U [174.5 (SEM 9.8) vs 92.7 (SEM 8.3) min, P < 0.01]. In group U TBARS concentration in investigated tissues increased significantly (P < 0.01) after exercise with the peak values observed 3 h after running. The postexercise increase in the TBARS concentration persisted longer in the soleus muscle (48 h) than in the liver or heart (3 h). A postexercise increase of TBARS was observed in group T only in the liver. The influence of training on the TBARS content depended on the kind of tissue. The TBARS concentrations in the liver at rest and immediately after the exercise were lower in group U than in group T. In contrast, TBARS concentrations in the heart and soleus muscle were higher in group U than in group T. The exercise resulted, in both groups, in a rise of serum CK concentration, peak values being observed 3 h following the exercise. Postexercise concentrations of CK were considerably lower in group T than in group U [3 h postexercise: 1740 (SEM 170) vs 2750 (SEM 231) U.l-1 P < 0.01]. A positive correlation (r = 0.66, P < 0.05) between TBARS content in muscle and serum CK concentration was found only in group U. The results obtained indicated that the generation of lipid peroxidation products in the soleus muscle was intensified for a relatively long time after the exercise. Endurance training decreased the susceptibility of tissues to the action of free radicals. However, this influence of training was more pronounced in the heart and soleus muscle than in the liver.
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PMID:Changes in concentrations of tissue free radical marker and serum creatine kinase during the post-exercise period in rats. 895 95

We investigated the effects of a single bout of aerobic and resistance exercise of similar relative intensity and duration on resting energy expenditure (REE) and substrate utilisation. Ten young healthy males volunteered [age 22 (1.8) years, weight 76 (7.9) kg, height 176 (4.1) cm, percentage body fat 10.5 (4.0)%; mean (SEM)]. They randomly underwent three conditions in which they either lifted weights for 60 min at 70-75% of 1-RM (WL), ran for 60 min at 70-75% of maximal oxygen intake (R) or did not exercise (C). REE and substrate utilisation, determined via respiratory exchange ratio ( R), were measured prior to exercise, and 10, 24, 48 and 72 h post-exercise. It was revealed that REE was significantly elevated ( P<0.05) 10 and 24 h after the end of WL [2,124 (78) and 2,081 (76) kcal, respectively] compared to pre-exercise [1,972 (82) kcal]. REE was also significantly increased ( P<0.05) 10 and 48 h after the completion of R [2,150 (73) and 1,995 (74) kcal, respectively] compared to pre-exercise data [1,862 (70) kcal]. R was lower 10 and 24 h following either WL or R [0.813 (0.043); 0.843 (0.040) and 0.818 (0.021); 0.832 (0.021), respectively] compared to baseline measurements [0.870 (0.025) and 0.876 (0.04), respectively]. Creatine kinase was significantly elevated ( P<0.05) 24 h after both WL and R, whereas delayed onset muscle soreness became significantly elevated ( P<0.05) 24 h after only WL. There were no significant changes for any treatment in thyroid hormones (T(3) and T(4)). These results suggest that a single bout of either WL or R exercise, characterised by the same relative intensity and duration, increase REE and fat oxidation for at least 24 h post-exercise.
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PMID:The effects of a single bout of exercise on resting energy expenditure and respiratory exchange ratio. 1520 61