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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study muscle necrosis due to prolonged limb compression, we measured intramuscular pressure by inserting wick catheters into 10 volar forearms and 10 anterior tibial compartments of adult volunteers. We then placed the subjects in positions in which victims of drug overdose are commonly found. Intramuscular pressures in the area of direct compression on hard surfaces ranged from 26 to 240 mm Hg, and averaged 101 mm Hg. Most remarkable was a mean pressure of 180 mm Hg on compression of the forearm by the rib cage. These pressures are sufficient to cause muscle and capillary ischemia and necrosis by local obstruction of the circulation. This local injury by limb compression may produce edema sufficient to start compartment tamponade and consequent muscle-compartment and crush syndromes.
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PMID:Intramuscular pressures with limb compression. Clarification of the pathogenesis of the drug-induced muscle-compartment syndrome. 43 46

In a patient with progressive systemic sclerosis (PSS), osteolysis of the posterior portion of the rib cage developed in an insidious fashion, without symptoms or preceding trauma. Six previous examples of rib resorption in PSS are reviewed. The destructive mechanism is unknown but may be related to endarteritis and ischemia.
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PMID:Osteolysis of the ribs in progressive systemic sclerosis. 48 4

The aim of this study was to investigate the propensity to develop cardiac arrhythmias during an acute period of ischemia between normal and hypertrophied (by means of a swimming training regimen) rat hearts. We used the coronary artery ligation in vivo technique which induced the occurrence of cardiac arrhythmias in rats that was followed by the determination of the occluded zone size. This study was coupled to an in vitro study using a two-compartment tissue bath in which half of the ventricular preparation was exposed to normal conditions and the other to ischemic conditions (low pH, hypoxia, and hyperkalemia). We also measured the collagen content and the DNA/protein ratio of the hearts. Twenty-eight male Wistar rats submitted to an eight-week swimming training (SWT) and twenty-eight cage-confined matched rats were used for the studies. SWT resulted in a 14% decrease in mean body weight and an 8% increase in absolute heart weight. We also observed a resting bradycardia in the trained animals and blood pressure remained unchanged between the two groups. Collagen content was unchanged and DNA/protein ratio was lower in the left ventricle of trained animals. During a 30-min period of coronary artery ligation, SWT rats demonstrated fewer ischemia-induced arrhythmias as compared to controls. The size of the zone affected by the vasal occlusion was lower in trained animals. Electrophysiological data recorded in the two-compartment bath showed a marked prolongation of action potential duration and refractory period in the SWT rat hearts. During the 15-min period of in vitro ischemia there was a global alteration of all electrophysiological parameters which did not differ between the two groups. Our data support the hypothesis that resting bradycardia and decrease in ischemic zone size may be involved in the arrhythmogenic protection observed in hypertrophied hearts of swimming rats after an acute ligation of the left coronary artery. Our results also indicate that cardiac hypertrophy, as defined by quantitative changes in cardiac mass or by the electrophysiological alterations that are related to its development, is not necessarily associated with an increased risk for the occurrence of arrhythmias.
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PMID:Decreased susceptibility to arrhythmias in hypertrophied hearts of physically trained rats. 141 4

Ischemia and reperfusion in skeletal muscle is associated with increases in total vascular resistance (Rt) and the microvascular permeability to plasma proteins. To determine whether exercise training can attenuate ischemia and reperfusion-induced microvascular injury in skeletal muscle, intact (with skin) and skinned, maximally vasodilated (papaverine), isolated hindquarters of control (C) and exercise-trained (ET) rats were subjected to ischemia (intact 120 min; skinned 60 min) followed by 60 min of reperfusion. ET rats ran on a motorized treadmill at 32 m/min (8% grade), 2 h/day for 12 wk, whereas the C rats were cage confined. Before ischemia, ET hindquarters had higher isogravimetric flow, lower Rt, and similar solvent drag reflection coefficients (sigma f) compared with C. During reperfusion in intact hindquarters, flow was higher (P less than 0.05) and Rt tended to be lower (15 +/- 2 vs. 25 +/- 5 mmHg.ml-1.min.100 g; P less than 0.1) in ET compared with C; however, in skinned hindquarters flow and Rt (14 +/- 2 vs. 13 +/- 2 mmHg.ml-1.min.100 g) were not different between C and ET. During reperfusion, sigma f was reduced (P less than 0.05) in both intact (C 0.68 +/- 0.03; ET 0.68 +/- 0.02) and skinned (C 0.66 +/- 0.03; ET 0.68 +/- 0.03) hindquarters, indicative of an increased microvascular permeability to plasma proteins. These results indicate that exercise training did not attenuate the microvascular injury (increased Rt and decreased sigma f) associated with ischemia and reperfusion in rat skeletal muscle.
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PMID:Microvascular injury after ischemia and reperfusion in skeletal muscle of exercise-trained rats. 238 13

The purposes of this study were to determine whether exercise training induces increases in skeletal muscle antioxidant enzymes and to further characterize the relationship between oxidative capacity and antioxidant enzyme levels in skeletal muscle. Male Sprague-Dawley rats were exercise trained (ET) on a treadmill 2 h/day at 32 m/min (8% incline) 5 days/wk or were cage confined (sedentary control, S) for 12 wk. In both S and ET rats, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities were directly correlated with the percentages of oxidative fibers in the six skeletal muscle samples studied. Muscles of ET rats had increased oxidative capacity and increased GPX activity compared with the same muscles of S rats. However, SOD activities were not different between ET and S rats, but CAT activities were lower in skeletal muscles of ET rats than in S rats. Exposure to 60 min of ischemia and 60 min of reperfusion (I/R) resulted in decreased GPX and increased CAT activities but had little or no effect on SOD activities in muscles from both S and ET rats. The I/R-induced increase in CAT activity was greater in muscles of ET than in muscles of S rats. Xanthine oxidase (XO), xanthine dehydrogenase (XD), and XO + XD activities after I/R were not related to muscle oxidative capacity and were similar in muscles of ET and S rats. It is concluded that although antioxidant enzyme activities are related to skeletal muscle oxidative capacity, the effects of exercise training on antioxidant enzymes in skeletal muscle cannot be predicted by measured changes in oxidative capacity.
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PMID:Skeletal muscle oxidative capacity, antioxidant enzymes, and exercise training. 238 14

Whether exercise protects the myocardium from arrhythmias during ischemia (ISC) or alters electrophysiology is controversial. We used microelectrode techniques in isolated cardiac fibers from exercise-trained (ET: 8-10 wk daily exercise) and sedentary (SED: 8-10 wk cage-rest) dogs to examine the effect of exercise on cellular electrophysiology during simulated ISC. We superfused fibers first with normal Tyrode's, then "ischemic Tyrode's" ([K+]o = 10 mM, pH = 6.7, pO2 < 25 mm Hg), and then again with normal Tyrode's. In automatic fibers, maximum diastolic potential in normal Tyrode's was -98 +/- 1 mV (ET, N = 22) and -97 +/- 1 mV (SED, N = 23); rates were 20 +/- 2 and 18 +/- 3 bpm for ET and SED, respectively. All fibers depolarized to -61 +/- 2 mV with ISC. Abnormal rhythms (abnormal automaticity with or without delayed afterdepolarizations) during ISC alone were seen in 0% of ET and 33% of SED; during ISC with alpha-adrenergic stimulation with 5 x 10(-8) M phenylephrine the incidence was 25% of ET and 0% of SED; during ISC with isoproterenol it was 75% for ET (P < 0.05 vs control) and 38% for SED. Transmembrane potentials in paced subendocardial fibers were similar for ET and SED during control, ISC, and reperfusion. Exercise did not alter cellular electrophysiology but did influence ectopic rhythms seen with beta-stimulation during ISC.
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PMID:Cardiac adrenergic responses and electrophysiology during ischemia: effect of exercise. 756 86

The purpose of this work was to study if enriched housing conditions and fetal neocortical transplantation could enhance the functional outcome after focal brain ischemia in adult rats. The right middle cerebral artery (MCA) was ligated in 34 inbred, spontaneously hypertensive male rats, which were then randomly divided into three groups. Groups A and B were transferred to an enriched environment, i.e., a large cage with opportunities for various activities but not forcing the rats to do any particular tasks; group C was kept in standard laboratory cages. Three weeks after the MCA occlusion blocks of fetal neocortical tissue (Embryonic Day 17) were transplanted to the infarct cavity in groups B and C. Rats in group A (n = 11) and group B (n = 11) performed equally well and significantly better than rats in group C (n = 10) when placed on an inclined plane and when traversing a rotating pole 6 and 9 weeks after the MCA occlusion and in a leg placement test at 9, but not 6 and 12 weeks. Skilled forelimb function did not differ between the groups. Infarct size and thalamic atrophy did not differ between the groups and graft size was similar in group B and C. There was no correlation between infarct size and motor function in any of the tests in rats housed in an enriched environment. Since the environment can significantly alter functional outcome without reducing infarct size we suggest that more attention should be given to the role of the laboratory environment and to long term behavioral outcome in experimental stroke.
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PMID:Influence of an enriched environment and cortical grafting on functional outcome in brain infarcts of adult rats. 760 Dec 67

Seven conscious dogs documented to be at high risk by the occurrence of ventricular fibrillation (VF) during acute myocardial ischemia were randomly assigned to 6 weeks of either daily exercise training or cage rest followed by exercise training. After 6 weeks of daily treadmill training, heart rate variability, a marker of vagal tone, increased by 74% (P < .001); baroreflex sensitivity, a marker of the capability to reflexly augment vagal activity, increased by 69% (P < .01); the repetitive extrasystole threshold, a marker of ventricular electrical stability, increased by 44% (P < .05). After exercise training, the incidence of ventricular fibrillation during acute myocardial ischemia decreased by 100%, as all animals survived. Neither passage of time nor heart rate level during ischemia contributed to the outcome. The most likely mechanism to explain the striking change in risk status is the shift in autonomic balance characterized by increased cardiac vagal activity, which was previously shown to have an antifibrillatory effect. These results suggest that exercise training in healthy individuals may decrease their likelihood of developing lethal arrhythmias during acute myocardial ischemia.
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PMID:Exercise training confers anticipatory protection from sudden death during acute myocardial ischemia. 808 69

Rats housed in an enriched environment allowing both social interaction and physical activity improve more than rats housed in standard laboratory cages after focal brain ischemia. To determine the relative importance of social and physical activity, rats that sustained ligation of the middle cerebral artery were kept in an enriched environment with opportunities for various activities (group A), housed together in the same size of cage as group A but with no activity-stimulating equipment (group B), or housed in individual cages with a running wheel (group C). There was no significant difference in infarct size between the groups. Limb placement, climbing, balance on an inclined plane, and ability to traverse a beam and a rotating pole were repeatedly tested 2-13 weeks after the operation. During the entire postoperative period, group A performed significantly better than group C in all tests and better than group B on the rotating pole. With time they also performed significantly better than group B in limb placement, climbing, and on the inclined plane. Group B performed significantly better than group C on the inclined plane and in climbing at all times, and by 13 weeks also in the limb placement test and on the beam. Thus, social interaction was superior to wheel-running but an enriched environment allowing free physical activity combined with social interaction resulted in the best performance.
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PMID:Environment, social interaction, and physical activity as determinants of functional outcome after cerebral infarction in the rat. 865 35

After permanent ligation of the middle cerebral artery the motor function of rats housed in an enriched environment, i.e. cages with opportunities for various activities but not forcing the rats to do any particular task, is significantly better than in rats housed in individual cages. Rats kept in an enriched environment before and after MCA ligation improved sooner and slightly more than those placed in the enriched environment after ischemia but with no lasting significant difference except for climbing. Preliminary studies suggest that social stimulation is more important than physical activity. Rats with fetal neocortical grafts implanted into the infarct cavity performed better if exposed to enriched environment than grafted control rats housed in standard laboratory cages with 5 rats in each cage. However, they did not perform better than non-grafted rats housed in the same enriched environment. The infarct size did not differ between rats housed in an enriched environment and control rats. There was no correlation between infarct size and performance in rats exposed to an enriched environment. The improved motor function suggest that a rich environment may stimulate mechanisms that enhance brain plasticity.
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PMID:Environmental influence on outcome after experiment brain infarction. 878 Jul 99


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