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Related to Cerebral ischemia: transient ischemic attack, cerebral infarction


Localized tissue anemia as a result of obstruction of the blood supply or to vasoconstriction.



a local deficiency of blood; insufficient blood in an organ or tissue because of the narrowing or complete occlusion of the lumen of an afferent artery.

Transitory ischemia (like hyperemia) may result from physiological regulation of the blood supply, such as in reflex spasm of an artery caused by a mental factor (fright); the influence of pain, cold, chemical substances (epinephrine, ergotin), and biological stimuli (bacteria, toxins); the obstruction of an artery by a thrombus or embolus; constriction of the lumen of a blood vessel in connection with an atherosclerotic or inflammatory process in the wall; or compression of an artery by a tumor, scar, or foreign body. The aftereffects of ischemia depend on the degree of disruption of the blood flow, the rate of development and duration of the ischemia, the sensitivity of the tissue to oxygen deficiency, and the general condition of the body. Ischemia may end in complete restoration of the structure and function of the affected organ or tissue, but it also may lead to necrosis (infarct). The central nervous system and heart muscle are particularly sensitive to ischemia.


References in periodicals archive ?
15) reported that the oral intake of Clostridium butyricum for 14 days significantly improved neurobehavioral function in a mouse model of global cerebral ischemia.
Among endogenous antioxidant enzymes, SOD1 is one of the most important antioxidant enzymes against oxidative stress, and the importance of SOD1 in cerebral ischemia has been emphasized by extensive experiments, for example, SOD1 displays neuroprotective action in animal models of cerebral ischemia.
The sham-operated animals were subjected to all experimental manipulations, including surgery, except that they did not have cerebral ischemia nor received vehicle or FO administration.
Study of animals with cerebral ischemia showed that the average score of neurological deficit was 8.
In summary, the present study demonstrated that STVNA can reduce the damage induced by focal cerebral ischemia and was still effective even if the treatment was delayed up to 4 hours after recirculation in temporary focal ischemia or up to 4 hours after artery occlusion in permanent ischemia.
On the way to protect cells from cerebral ischemia, molecular chaperones or stress proteins and some antiapoptotic members of the BCL2 family of apoptosis regulatory proteins can protect mitochondrial function, reducing oxidative stress [16-18].
In cases of severe cerebral ischemia and infarction, intensive care unit monitoring is indicated until the patients condition stabilizes.
Cerebral ischemia was initiated by transient middle cerebral artery occlusion in Sprague-Dawley rats [3].
As the occlusion of major intracranial vessels occurs, there is therefore the installation of a chronic state of cerebral ischemia.
Comparison between the Two Groups: In the observation group two patients suffered from transient cerebral ischemia during the perioperative period which was mainly attributed to the placement of distal protection device.