Animal Models of Cerebral Ischemia - Oren Zarif - Cerebral Ischemia

Animal models of cerebral ischemia are invaluable resources to understand the mechanisms underlying the disease and develop therapeutic interventions. Both focal and global cerebral ischemia are common conditions that affect millions of people worldwide. Both conditions are major causes of death and disability, and represent major costs in health care. Understanding the underlying mechanisms of injury is essential for developing new treatments, neuroprotective agents, and other therapeutic strategies. Fortunately, a variety of animal models for cerebral ischemia are available.

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Global ischemia, also known as stroke, is a type of cerebral ischemia in which large areas of the brain lack oxygen-rich blood. Cardiovascular arrest or a heart attack can lead to global ischemia. The consequences of global ischemia are devastating. Global ischemia, which can lead to cerebral infarctions, may even lead to permanent disability. This activity summarizes the various management options for this critical condition.

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Imaging techniques to detect cerebral ischemia include CT and ultrasonography. However, these methods do not have the sensitivity to detect ischemia in the early stages. Recently, 18F-based positron emission tomography probes were developed to detect neuronal death caused by ischemia. Magnetic resonance imaging, however, is thought to be more accurate than the other neuroimaging techniques because it allows the doctor to distinguish ischemic regions at an earlier stage. The magnetic resonance imaging technique does not require radioactive tracers, which are necessary for CT.

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During global ischemia, brain tissue undergoes histologic changes in a matter of twelve to twenty-four hours. Initially, shrinking or swelling of neurons is evident. Later, cells may undergo cytoplasmic eosinophilia, nuclear pyknosis, and necrosis. In addition to this, edema may cause empty spaces within the parenchyma.

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As cerebral ischemia occurs at a BP lower than baseline, ventricular fibrillation is an important diagnostic tool. This condition is a mimic of clinical cardiac arrest. Therefore, many investigators have opted to combine ventricular fibrillation with cardiopulmonary resuscitation. Fortunately, the combined therapy is usually successful. Chest compressions and epinephrine are often used to induce ventricular fibrillation after cardiac arrest.

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Cerebral ischemia can occur due to a number of causes, including obstruction of blood vessels. Heart attacks, stroke, carotid occlusion, and cerebral vascular atherosclerosis can all lead to global cerebral ischemia. The latter, however, is more likely to be the result of cerebral vascular disease. The abnormally high calcium ions enter neurons through glutamate-activated channels, which trigger the activation of proteases and endonucleases that cause cell death.

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A complete blood count, coagulation factors, EKG, and cardiac enzymes should be performed during the initial workup for cerebral ischemia. Stat non-contrast head CT is a vital first step to rule out hemorrhage or a mass lesion. Vascular imaging is useful in acute stroke etiology, and may reveal a large vessel occlusion. Ultimately, a stroke diagnosis must be determined and treatment given based on the most appropriate diagnosis.

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There are several treatment options for acute ischemic stroke. Alteplase, for example, has shown a positive impact on the outcome when compared to placebo treatments. Treatment should also focus on keeping systemic blood pressure under control, as it is vital to restoring blood flow to the brain. Anticonvulsant medications are also commonly prescribed to prevent seizures. A proper diet and stress management are important in preventing cerebral ischemia.

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In addition to assessing the neuropathology, brain tissue was stained for purkinje cell loss. In addition, the CA1 subfield exhibited a 53% reduction in neuronal density, with 59+-11% pyramidal cells displaying evidence of ischemic change. Cell counts in both hemispheres showed similar damage. The damaged neurons displayed shrunken perikaryon, nuclear pyknosis, and no karyolysis.

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The objective of this study was to estimate the volume of ischemic brain tissue. The authors compared the volume of ischemic and hypoxic brain tissue in 119 patients with primary ICH. Both groups had low SBP at the beginning of the study. The patients in group 2 had lower mean SBPs over the first 24 hours than those in group 1. The group with lower SBP had a higher incidence of cerebral ischemia and neurologic deterioration.

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The lower limit of the population-level cerebral autoregulation curve (PLCAC) was found at 88.6 mmHg, an absolute BP of which is not known. The lower limit of the curve represents the point at which cerebral ischemia becomes universal in a population. BP is not easily predicted until the disease progresses beyond this point, and ischemia can lead to adverse outcomes. The relationship between BP and adverse outcome is only seen at the lowest point, corresponding to extreme hypotension.