Exemplos de uso de Global ischemia em Inglês e suas traduções para o Português
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Global ischemia from the hypotension?
After stabilization, hearts were subjected to global ischemia for 30 minutes followed by reperfusion for 45 minutes.
Global ischemia was induced by interrupting the perfusate flow and maintaining the balloon deflated.
Regarding the limitations of this study,we used global ischemia, which has been commonly used in the Langendorff-perfused heart model.
IDRA-21 does not produce neurotoxicity under normal conditions,although it may worsen neuronal damage following global ischemia after stroke or seizures.
In conclusion, 20 min of global ischemia is probably the best period for the study of mild to moderate myocardial contractile dysfunction, at a level that can be alleviated or exacerbated by the drugs tested.
A reduction in its flow, due to spasm,can result in drastic consequences such as global ischemia of the left coronary territory.
In this study, in a partial hind limb amputation model submitted to global ischemia, it was tested the protective effect of allopurinol, heparin, tirofiban or vitamin c during secondary ischemia after venous congestion.
Spontaneous increases in body temperature have been reported after experimental focal and global ischemia and may be a consequence of brain damage.
Over the last decade, data from many studies support the idea that estrogens provide neuroprotective effects in a variety of neurodegenerative diseases,including cerebral global ischemia.
Myocardial protection: protective effects to delay irreversible cell injury caused by global ischemia as well as to limit the extent of the reperfusion injury;
These results, together with those of this study,suggest that the transition from mild/moderate to severe tissue damage occurs after 20 min of global ischemia.
After a stabilization period of 25 min,the hearts were submitted to different periods of global ischemia 20, 25 or 30 min by stopping the perfusion flow.
In a model of transient global ischemia, which occluded the middle cerebral artery in adult rats during 90 minutes, 50% xenon administered over 3 hours, starting 15 minutes after the insult, significantly reduced the neuronal damage in the striatum cortex.
After 20 minutes of stabilization, the hearts of the animals in all groups were exposed to 30 minutes of global ischemia, followed by 60 minutes of reperfusion.
This study showed that, in the isolated rat heart model,twenty minutes of global ischemia results in mild/moderate contractile dysfunction, while longer periods of ischemia can lead to severe contractile dysfunction.
In the C-IR and H-IR groups, after 20 min of stabilization,the hearts were subjected to 30 min of global ischemia, followed by 120 min of reperfusion.
The time-course of cardiovascular changes induced by global ischemia 20, 25 and 30 min in the isolated rat heart model showed that when the hearts were exposed to 20 min of ischemia, the functional recovery was reduced in the early phase of reperfusion, but not at the end of reperfusion 30 min, suggesting that the degree of tissue damage was mild to moderate.
Methods: isolated rat hearts were submitted to ipc(3 cycles of 5 min ischemia and5 min reperfusion) before global ischemia(30 min) followed by reperfusion 60 min.
The ischemia group GII consisted of six hearts undergone 20 minutes of global ischemia after the stabilization period and all parameters were measured during reperfusion, as previously described.
The regional normothermic ischemia in OPCAB, the temporary interruption of coronary flow approached,seems to cause less myocardial injury compared to hypothermic global ischemia induced by cardioplegic arrest 20.
Soon after the end of ischemia andafter a period of regional ischemia followed by global ischemia in which groups were treated, the reperfusion of the isolated heart was started in passive mode.
The maintenance of the model was over 240 minutes 90 minutes of reperfusion after the isolated heart remained under regional ischemia 30 minutes followed by global ischemia 90 minutes, which demonstrates the feasibility of the model.
During reperfusion- after 30 minutes of regional ischemia followed by 90 minutes of global ischemia- the Control group and the St Thomas group showed a median of 5 defibrillations.
The preconditioning Group GIII consisted of six hearts udergone five minutes of global ischemia, followed by five minutes of reperfusion prior to 20-minutes ischemia. .
In the period of reperfusion, after 30 minutes of regional ischemia, followed by 90 minutes of global ischemia, the Control Group and the group St Thomas presented average of five defibrillations.
These findings are in consistency with previous functional and metabolic data from Wang et al andPalmer et al who reported that mild post-ischemic dysfunction occurred when short periods of global ischemia 15-20 min were employed, but observed a severe myocardial dysfunction with persistent increase of creatine kinase after 25 min of ischemia, suggesting irreversible myocardial injury.
Administration of both agents for three days before ischemia provided seven days of neuroprotection in an animal model of global cerebral ischemia.
Cardiorespiratory arrest CRA is the most frequent cause of global brain ischemia.
The mechanism responsible for delayed infarction after transient global cerebral ischemia is not clearly described.