Abstract Murine chronic cerebral hypoperfusion (CCH) results in white matter (WM) injury and behavioral deficits. Pericytes influence blood-brain barrier (BBB) integrity and cerebral blood flow. Under hypoxic conditions, perictyes detach from perivascular locations, increasing vessel permeability and neuronal injury. This study characterizes the time course of BBB dysfunction and pericyte coverage following murine experimental CCH secondary to bilateral carotid artery stenosis (BCAS). Mice underwent BCAS or sham operation. On post-procedure days 1, 3, 7 and 30, corpus callosum BBB permeability was characterized using Evans blue (EB) extravasation and IgG staining and pericyte coverage was calculated. The BCAS cohort demonstrated increased EB extravasation on postoperative days 1 (p=.03) and 3 (p=.01) when compared to sham mice. Further, EB extravasation was significantly greater (p=.03) at day 3 than at day 30 in BCAS mice. Positive IgG staining was seen at post-procedure day 3 in the BCAS group. BCAS mice demonstrated a nadir in pericyte coverage on post-operative day 3 (p50%) was reported to be 7% in women and 9% in men3. Clinical carotid endarterectomy studies of cerebral hypoperfusion, demonstrate a nearly 25% incidence of subtle cognitive decline in the absence of overt neurologic change or radiographic evidence of stroke4. Neurodegenerative diseases such as Alzheimer’s disease and vascular dementia have become increasingly more common as the population ages5-8.
Ischemic stroke is the blockage of blood vessels in the brain as a result of blood clots (thrombi), causing the portions of the brain nourished by the vessel and its tributaries to be starved of nutrients, poisoned, and to eventually die (“Symptoms
When an artery in the brain is block (ie; TIA) open collateral vessels can allow blood to
Three main maps can be reconstructed from CTP data: cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT). Interpretation of the CTP maps is crucial in reversing functional damage and choosing the ideal treatment plan. Ischaemic brain tissue can be visualised in each map as regions of hypoperfusion within the brain tissue (Birenbaum et al., 2011; El-Koussy et al., 2014). Because CTP is a dynamic quantitative imaging technique, the percentage of brain damage can be calculated by measuring the mean values at the location of the same damaged tissue in the three maps. Moreover, the values for the damaged tissue are compared with those for normal tissue in the other, unaffected hemisphere. Finally, CBF is calculated by dividing CBV by MTT (Dorn et al.,
The sepsis induced by fecal peritonitis leads to the development of edema around the microvessels of frontal cortex in a rat model of sepsis. The results suggest that the edema observed around the microvessels can have a role in the pathogenesis of the SAE probably by affecting the exchange of oxygen and nutrients with carbon dioxide and waste products between the blood and brain parenchyma (73). Perimicrovascular edema together with intact tight junctions has previously been reported in a pig model of sepsis (74). Further studies are warranted not only for understanding the development of perimicrovascular edema associated with peritoneal sepsis in this model, but also for setting targets for the design of novel drugs to treat perivascular edema and
Neonatal cerebral hypoxia-ischemia (HI) remains a major cause of death and neurological disability. Neural stem cells (NSCs) shows great promise in restoring HI-associated neurological tissue damage and hypothermia is reported to be beneficial for HI recovery in animal studies. We aimed to investigate whether mild hypothermia after neonatal cerebral hypoxia-ischemia (HI) could enhance the therapeutic effect of NSCs transplantation with a neonatal HI mouse model. Postnatal day 7 mice underwent right common carotid artery ligation followed by 1.5 h of hypoxia. After HI, these mice underwent different treatments with hypothermia, NSCs transplantation, or both. Animals were sacrificed at 24, 48, 72 h and 1, 2, 4 week after the HI. The numbers of apoptotic cells, survived, and differentiated grafted cells were counted. The levels of caspase-3 and NF-κB protein were analyzed. And the restoration of sensorimotor and behavioral functions of HI mice was assessed. We found caspase-3-dependent apoptosis and inflammation were significantly lower in the NSCs+hypothermia group. Meanwhile, transplanted cells survived and differentiated better in the NSCs+hypothermia group, and animals of this group exhibited enhanced functional recovery in sensorimotor and behavioral tests. These observations suggest that mild hypothermia enhances the therapeutic effect of NSCs in HI mice through protecting grafted cells, suppressing apoptosis, and attenuating NF-κB signaling.
Perfusion CT Imaging of Brain is a quick and convenient method of assessing perfusion disturbances in acute stroke patients. Three-color image maps with quantitative results related to patient regional cerebral blood volume (rCBV), mean transit time (MRTT) and regional cerebral blood flow (rCBF) are generated that displays stroke much earlier than the conventional CT images. Areas of less severe CBF reduction, with preserved CBV value represent “ischemic penumbra”, a term describing tissue at high risk for infarction but not yet irreversibly infracted. The larger the ischemic penumbra relative to the core, the more likely the patient would benefit from early thrombolytic therapy. If both CBV and CBF are already reduced dramatically, the
A cerebrovascular accident more commonly known as a stroke or brain attack is the term used to describe the sudden death of brain cells in a localized area due to inadequate blood flow. In order to woke the brain needs a constant supply of oxygen and nutrients. This supply is carried to the brain
This paper will discuss the effects perfusion has on the body as well as the multiple body systems that are effected from poor perfusion. We will be looking at the relationships between profusion as it relates to ischemic stroke, myocardial infarction, and tuberculosis. This paper will use online journal entries from EPSCO as well as off line entries from Lewis to help us find a better understanding into the related topics at hand. Lastly I will discuss stroke in depth as it pertains to my clinical experience and explain the strong link profusion has on ischemic stroke and the measures used to retain brain tissue. We will look at research done by Agarwal, Smriti (2015) that looks at the effectiveness and time saving procedures researched by his team when detecting stroke as well as research done by Dong, Hongli (2015) that shows a strong correlation between vitamin b12 and folic acid and the prevention of an ischemic event.
When our brains are deprived of oxygen it is called cerebral anoxia.Our brain needs approximately 3.3 ml of oxygen per 100 g of brain tissue per minute,Usually our bodies respond to lowered blood oxygen by redirecting the blood flow the brain and increasing your cerebral blood flow.Sometimes blood flow will increase up to twice its normal flow but no more.If the blood flow or increased blood flow is sufficient enough to supply the brain the oxygen it needs then no symptoms will occur,however if the blood flow cannot be increased or if doubled blood flow does to correct it,symptoms of cerebral
In order to assess participants’ neuropathologic status, researchers examined participants’ number of cortical brain plaques, tangles, and the amount of stroke (infarct) damage they had. The number
Hence, in the present study, the elevated expression of ED-2 in both dorsal and ventral hippocampus accounts for the incidence of alternate activation of macrophages and microglia activation up to the 12th week PDC. A recent study on AD has also shown that the ED-2 positive cells were present in higher density around the compromised blood vessels (Pey et al., 2014) might be indicating the BBB breakdown. This information supports the functional aspect of ED-2 expression in the resolution phase of inflammation (Polfliet et al., 2006) due to infiltration of inflammatory molecules following BBB damage (Perry, 2004). In our previous study (Nagayach et al., 2014a) we reported the astrocytic fragmentation a possible sign for the compromised functioning of the blood brain barrier (Huber et al., 2006) and oxidative stress (Mastrocola et al., 2005) in the brain following diabetes. Considerably, the recorded intense expression of ED-2 was might be a consequence of BBB damage. In addition to this, it might also be possible that the observed intense expression of ED-2 in the diabetic hippocampus (both dorsal and ventral) was aggravated by the activated microglia to further facilitate its role in initiating the cascade of events of the immune system. Similarly, the presence of ED-2
The purpose of this study is to understand what happens with the blood vessels in the brain when notch signaling is deleted in pericytes.
Stroke risk has become one of the biggest public health problems and is currently the second leading cause of deaths in the United States and Worldwide (Barnett, et al. 2003). There are many different types of Stroke which can be big or small based on the arteries it has been affected. Stroke happens when the blood supply is blocked by plaques to the brain causing it to burst. This occurring is considered as the most common with an approximate of eighty percent in death cases. On the other hand, there are about twenty percent of this risk occurred in the results of bleeding inside the brain. In another words, the arteries are affected and crushed around all the tissues of the brain (Rudd, et al. 2004). The mortality rate of Stroke
The over the counter medication once known only for its ability of easing aches and pains or fighting off fever and inflammation is proving itself to be quite the miracle drug. Aspirin has become part of the protocol for stroke victims as a preventative measure due to its neuro-protective benefits. Stroke can cause lesions in cerebral white matter, which may result in cognitive impairments such as deficits in learning and memory. White matter lesions (WML) have also been linked to increasing the risk of post-stroke dementia. Cerebral white matter damage has been widely overlooked. Comprised of oligodendrocytes that form the insulating myelin in the CNS, white matter is evidentially just as vulnerable to ischemia as gray matter.
The blood brain barrier protects brain cells from harmful substances, as well as, pathogens, by preventing passage of many substances from blood into brain tissue.