Sunday, January 26, 2020

Cerebral Autoregulation Mechanism | Report

Cerebral Autoregulation Mechanism | Report From: Biose Ifechukwude Joachim Introduction Cerebral autoregulation (CA) is the multifactorial vascular mechanism that maintains a constant cerebral blood supply in spite of fluctuations in the cerebral perfusion pressure (CPP) (Lassen, 1959; Tiecks et al., 1995). This mechanism thrives for CPP values within the range of 50-150 mmHg (Lassen, 1959; Paulson, Strandgaard and Edvinsson, 1990; Panerai, 1998) (Fig. 1). The vascular response involved in CA is rapid and so robust that hypertension (Eames et al., 2003; Serrador et al., 2005; Zhang et al., 2007) and aging (Eames et al., 2003; Fisher et al., 2008; Liu et al., 2013; Oudegeest-Sander et al., 2014) does not alter its physiological role. However, CA is compromised following pathologic conditions such as traumatic brain injury, intracerebral haemorrhage, stroke, hyper-perfusion syndrome, and subarachnoid haemorrhage (Diedler et al., 2009; Atkins et al., 2010; Budohoski et al., 2012; Saeed et al., 2013; Buczek et al., 2013). Fig. 1. Cerebral autoreglation in relation to vascular response. Within the upper and lower boundaries of the autoregulatory range (dotted lines), blood flow remains constant (blue line with beads). As Pressure falls below the lower limit, vascular smooth muscle relaxes to allow dilatation, while constriction of vessels (red circles) ensues to reduce blood flow as pressure approximates the upper limit. Adapted from Pires et al., 2013. Classification Based on factors affecting cerebral blood flow (CBF), CA can be classified into two categories, metabolic autoregulation (MA) and pressure autoregulation (PA). Mainly due to changes in brain tissue pH (Cotev and Severinghaus, 1969; Betz and Heuser, 1967; Raichle, Posner and Plum, 1970), MA is the principal regulatory mechanism of CBF according to metabolic demand. This implies that MA responds to local or global ischemia and hypoxia which increases pH by increasing CBF via vasodilatation (Ekstrom-Jodal et al., 1971; Raichle and Stone, 1971).While PA is the vascular response to maintain blood flow following changes in perfusion pressure, achieved by varying the degree of vasoconstriction or vasodilatation of the cerebral vasculature. Mechanism In adults and under normal conditions, provided CPP falls within the boundary of 50-150 mmHg, CBF is preserved at approximately 50 mL per 100 g of brain tissue per minute (McHenry et al., 1974; Strandgaard et al., 1976; Paulson, Strandgaard and Edvinsson, 1990). Outside this range of CPP, CA is impaired and CBF becomes directly dependent on mean arterial pressure (MacKenzie et al., 1976; Heistad and Kontos, 1979; Baumbach and Heistad, 1985; Paulson et al., 1990). More so, should CPP falls below the lower boundary of CA, blood flow reduces and ischemia sets in (Hossmann, 2006). The precise mechanism of CA is currently elusive; however, it is believed to be subject to the interaction of neurogenic, metabolic and myogenic factors (Czosnyka et al., 2009; Novak and Hajjar, 2010). Intrinsic innervation is touted to be directly involved in the mechanisms of CA (Goadsby and Edvinsson, 2002) and extrinsic pathway is implausible, since CA is unimpaired following sympathetic and parasympathetic denervation in experimental animals (Busija and Heistad, 1984). The perikarya within the subcortical region of the brain, precisely those from the nucleus basalis, locus ceruleus and raphe nucleus project to cortical microvessels for the control of local blood flow by release of neurotransmitters (ACH, norepinephrine and 5HT) (Hamel, 2006). These released neurotransmitter substances interact with the receptors on smooth muscle, endothelium, or astrocytes to cause constriction or dilation, thus regulating blood supply according to the metabolic demand (Iadecola, 2004; Hamel, 2006; Drake and Iadecola, 2007). Also, metabolic by-products released by the brain during CBF decrease are important for CA (Paulson, Strandgaar and Edvinsson, 1990). These substances, potassium, adenosine, and hydrogen ion triggers vasodilatation. Another important component of the CA mechanism is the myogenic response of the cerebrovascular smooth muscle in regulating vascular tone. Constriction of the cerebral vasculature due to smooth muscle contraction ensues during pressure fluctuations at the upper boundary of the autoregulatory range of CPP, thus blood flow is not excessive (Fig. 1). Conversely, fluctuations at the lower limit of CPP is followed by vasodilatation (Fig.1) (Kontos, 1978,Busija and Heistad, 1984; Mellander, 1989; Osol et al., 2002). Furthermore, the direct contact between astrocytes and the parenchymal arterioles of the brain have been shown to play a role in CA (Rennels and Nelson, 1975; Cohen, Molinatti and Hamel, 1997; Iadecola, 2004; Hamel, 2006; Drake and Iadecola, 2007; Zlokovic, 2008). Most microvessels at the subcortical level have astrocytic end-feet at the interface between them and neurons (Kulik et al., 2008), thus, under the direct influence of the vasoactive factors released by astrocytes (Murphy et al., 1994). Interestingly, the type of cerebral vasculature may also contribute to CA in an unexpected manner, with respect to their response to blood flow changes. While basilar artery dilates in response to increased blood flow, MCA constricts Koller and Toth, (2012). Under Anaesthesia Anaesthesia puts the brain in a state of reduced neuronal activity, as a result CBF decreases in light of neurovascular coupling (Attwell et al., 2010). Also, in their studies in rats, Jones et al., (2002) reported that anaesthesia reduces the CCP levels below the lower limit of CA. More importantly, anaesthetics have significant impact on CA as they affect the vasculature of the brain, directly or indirectly. Under the influence of volatile anaesthetics, calcium entry via voltage gated Ca2+ channels on vascular smooth muscle cells is reduced significantly, causing the vasculature to dilate (Bosnjak et al. 1992), thereby, directly overriding CA. Also, anaesthetics cause profound respiratory depression in spontaneously breathing animals, consequently PaCO2 increased. Given that the vasculature of the brain is highly sensitive to changes in CO2, an increase value of PaCO2 stimulates cerebral vasodilatation (Kuschinsky, 1997; Willie et al., 2014); correspondingly CBF increases (Figure 2). These effects of anaesthetics lead ultimately to the failure of CA in mammals. However, certain anaesthetics for example Ethomidate, preserves CA (Wang et al., 2010). This is mainly due to their ability to keep PaCO2 nearly constant within the nomal range without artificial ventilation (Lacombe et al. 2005; Joutel et al., 2010). Fig. 2. Cerebral blood flow with respect to arterial pressure of CO2. CBF increases as PaCO2 level increases beyond the level of 25 mmHg. However, at 80 mmHg blood vessels are maximally dilated and CBF remains constant with a further increase in PaCO2 values. Adapted from Adapted from Hill and Gwinnutt, no date. Stroke During arterial occlusion, as in the case of ischaemic stroke, local cerebral perfusion pressure falls below the normal CA range while MAP does not change. With persistent occlusion, autoregulation fails (Reinhard et al., 2008; Reinhard et al., 2012; Immink et al., 2005; Atkins et al., 2010) and regional CBF further decreases. For this reason, blood pressure changes, high or low, results in poor outcome (Castillo et al, 2004; Aslanyan et al., 2003; Sandset et al., 2012). However, this is not entirely due to the failed autoregulatory capacity of the vessels during ischemia, but perhaps their normal vasodilatory capacity has reached a maximal limit (Petersen et al., 2015). The impaired autoregulatory response following acute stroke has been observed both in the affected and contralateral hemispheres (Cupini et al., 2001; Dawson et al., 2000; Dawson, Panerai and Potter, 2003; Fieschi et al., 1988; Gelmers, 1982; Lisk et al., 1993; Hakim et al., 1989). References Aslanyan S, Fazekas F, Weir CJ, Horner S and Lees KR (2003). GAIN International Steering Committee and Investigators: Effect of blood pressure during the acute period of ischemic stroke on stroke outcome: a tertiary analysis of the GAIN International Trial. Stroke. 34: 2420–2425. Atkins ER, Brodie FG, Rafelt SE, Panerai RB and Robinson TG (2010). Dynamic cerebral autoregulation is compromised acutely following mild ischaemic stroke but not transient ischaemic attack. Cerebrovasc. Dis. 29: 228–235. Attwell D, Buchan AM, Charpak S et al. (2010). Glial and neuronal control of brain blood flow. Nature. 468: 232–43. Baumbach GL and Heistad DD (1989). Remodeling of cerebral arterioles in chronic hypertension. Hypertension. 13: 968–972. Betz E and Heuser D (1967). Cerebral cortical blood flow during changes of acid-base equilibrium the brain. J. Appl. Physiol. 23: 726-733. Bosnjak ZJ, Aggarwal A, Turner LA, Kampine JM and Kampine JP (1992). Differential effects of halothane, enflurane, and isofluurane on Ca2 + transients and papillary muscle tension in guinea pigs. Anesthesiology. 76: 123–131 Buczek J, Karlin ´ski M, Kobayashi A, BiaÅ‚ek P and CzÅ‚onkowska A (2013). Hyperperfusion syndrome after carotid endarterectomy and carotid stenting. Cerebrovasc. Dis. 35: 531–7. Budohoski KP, Czosnyka M, Smielewski P, Kasprowicz M, Helmy A, Bulters D et al. (2012). Impairment of cerebral autoregulation predicts delayed cerebral ischemia after subarachnoid hemorrhage: a prospective observational study. Stroke. 43: 3230–3237. Busija DW and Heistad DD (1984). Factors involved in the physiological regulation of the cerebral circulation. Rev. Physiol. Biochem. Parmacol. 101: 161–211. Castillo J, Leira R, Garcà ­a MM, Serena J, Blanco M and Dà ¡valos A (2004). Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 35: 520–526. Cohen Z, Molinatti G and Hamel E (1997). Astroglial and vascular interactions of noradrenaline terminals in the rat cerebral cortex. J. Cereb. Blood Flow Metab. 17: 894–904. Cotev S and Severinghaus JW (1969). Role of cerebrospinal fluid pH in management of respiratory problems. Anesth. Analg. 48: 42-47. Cupini LM, Diomedi M, Placidi F, Silvestrini M and Giacomini P (2001). Cerebrovascular reactivity and subcortical infarctions. Arch. Neurol. 58: 577–581. Czosnyka M, Brady K, Reinhard M, Smielewski P and Steiner LA (2009). Monitoring of cerebrovascular autoregulation: facts, myths, and missing links. Neurocritical Care. 10: 373–86. Dawson SL, Blake MJ, Panerai RB and Potter JF (2000). Dynamic but not static cerebral autoregulation is impaired in acute ischaemic stroke. Cerebrovasc. Dis.10:126–132. Dawson SL, Panerai RB and Potter JF (2003). Serial changes in static and dynamic cerebral autoregulation after acute ischaemic stroke. Cerebrovasc. Dis. 16:69–75. 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Immink RV, van Montfrans GA, Stam J, Karemaker JM, Diamant M and van Lieshout JJ (2005). Dynamic cerebral autoregulation in acute lacunar and middle cerebral artery territory ischemic stroke. Stroke. 36: 2595–2600. Jones SC, Radinsky CR, Furlan AJ et al. (2002). Variability in the magnitude of the cerebral blood flow response and the shape of the cerebral blood flow pressure autoregulation curve during hypotension in normal rats [corrected]. Anesthesiology. 97: 488–96. Joutel A, Monet-Lepretre M, Gosele C, Baron-Menguy C, Hammes A, Schmidt S, Lemaire-Carrette B, Domenga V, Schedl A, Lacombe P and Hubner N (2010). Cerebrovascular dysfunction and microcirculation rarefaction precede white matter lesions in a mouse genetic model of cerebral ischemic small vessel disease. J. Clin. Invest. 120: 433–445. Koller A and Toth P (2012). Contribution of flow-dependent vasomotor mechanisms to the autoregulation of cerebral blood flow. J. Vasc. Res. 49: 375–389. Kontos HA, Wei EP, Navari RM, Levasseur JE, Rosenblum WI and Patterson JL, Jr (1978). Responses of cerebral arteries and arterioles to acute hypotension and hypertension. Am. J. Physiol. 234: H371–H383. Kulik T, Kusano Y, Aronhime S, Sandler AL and Winn HR (2008). Regulation of cerebral vasculature in normal and ischemic brain. Neuropharmacology. 55: 281–288. Kuschinsky W (1997). Neuronal-vascular coupling. A unifying hypothesis. Adv. Exp. Med. Biol. 413: 167–176. Lacombe P, Oligo C, Domenga V, Tournier-Lasserve E and Joutel A (2005). Impaired cerebral vasoreactivity in a transgenic mouse model of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy arteriopathy. Stroke. 36: 1053–1058. Lassen NA (1959).Cerebral blood flow and oxygen consumption in man. Physiol. Rev. 39: 183–238. Lassen NA (1974). Control of cerebral circulation in health and disease. Circ. Res. 34: 749–760. Lisk DR, Grotta JC, Lamki LM, Tran HD, Taylor JW, Molony DA and Barron BJ (1993). Should hypertension be treated after acute stroke? A randomized controlled trial using single photon emission computed tomography. Arch. Neurol. 50:855–862. Liu J, Zhu YS, Hill C, Armstrong K, Tarumi T, Hodics T, Hynan LS and Zhang R (2013). Cerebral autoregulation of blood velocity and volumetric flow during steady-state changes in arterial pressure. Hypertension 62: 973– 979. MacKenzie ET, Strandgaard S and Graham DI et al. (1976). Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier. Circ. Res. 39:33-41. McHenry LC, Jr., West JW, Cooper ES, Goldberg HI and Jaffe ME (1974).Cerebral autoregulation in man. Stroke. 5: 695-706. Mellander S (1989). Functional aspects of myogenic vascular control. J. Hypertens. 7(4): S21–S30. Murphy S, Rich G, Orgren KI, Moore SA and Faraci FM (1994). Astrocyte-derived lipoxygenase product evokes endothelium-dependent relaxation of the basilar artery. J. Neurosci. Res. 38: 314–318. Novak V and Hajjar I (2010). The relationship between blood pressure and cognitive function. Nature Reviews Cardiology. 7: 686–98. Osol G, Brekke JF, McElroy-Yaggy K and Gokina NI (2002). Myogenic tone, reactivity, and forced dilatation: a three-phase model of in vitro arterial myogenic behavior. Am. J. Physiol. Heart Circ. Physiol. 283: H2260– H2267. Oudegeest-Sander MH, van Beek AH, Abbink K, Olde Rikkert MG, Hopman MT and Claassen JA (2014). Assessment of dynamic cerebral autoregulation and cerebrovascular CO2 reactivity in ageing by measurements of cerebral blood flow and cortical oxygenation. Exp Physiol. 99: 586–598. Panerai RB (1998). Assessment of cerebral pressure autoregulation in humans—a review of measurement methods. Physiol. Meas. 19: 305–338. Paulson OB, Strandgaard S and Edvinsson L (1990). Cerebral autoregulation. Cerebrovasc. 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Capillary innervation in the mammalian central nervous system: an electron microscope demonstration (1). Am. J. Anat. 144: 233–241. Saeed NP, Panerai RB and Robinson TG (2013). The carotid artery as an alternative site to the middle cerebral artery for reproducible estimates of autoregulation index. Ultrasound Med. Biol. 39: 735–741. Sandset EC, Murray GD, Bath PM, Kjeldsen SE and Berge E (2012). Scandinavian Candesartan Acute Stroke Trial (SCAST) Study Group: Relation between change in blood pressure in acute stroke and risk of early adverse events and poor outcome. Stroke. 43: 2108–2114. Serrador JM, Sorond FA, Vyas M, Gagnon M, Iloputaife ID and Lipsitz LA (2005). Cerebral pressure-flow relations in hypertensive elderly humans: transfer gain in different frequency domains. J. Appl. Physiol. 98: 151–159. Strandgaard S (1976). Autoregulation of cerebral blood flow in hypertensive patients. 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Saturday, January 18, 2020

Staying Informed: Old News

There was a time when news information was disseminated by a select few who had access to the relevant reports, files, and statistics.   When this was the case, the world gathered around a radio, shared a newspaper, or turned on the television—one that had fewer than ten channels).   This â€Å"news† was often like a leftover meal in terms of value: by the time it was released, the world had moved forward, and something new was hot. Progress was made, and television news programs began to delve deeper into stories; reporters suddenly began delivering â€Å"breaking† news reports, and the information was at least lukewarm when the public got its hands it.   It was the era of reporters like Paul Harvey who took what the world knew, dug more deeply, and presented â€Å"the rest of the story† (Radio Legend Paul Harvey Biography, 2003). Today, a cell phone can alert its owner of breaking news stories from around the world; reporters deliver broadcasts live from battlefields; and the internet has made it possible to receive information almost instantly.   Most consumers now get their news online, via one of hundreds of television channels, or through a variety of print media.   Unfortunately, the days of print media and even local reporting seem to be dying, and while their loss may not even create a ripple, what they have to offer the consumer is irreplaceable. It is true that the average printed report cannot provide the live-action, emotionally packed footage of a series of photographs or a streaming video, but words do matter, and while one’s brain struggles to capture the intricacies of backgrounds, sounds, and images that flash in front of the eyes in photographs and videos, the thought-process of the viewer is overwhelmed by the visual imagery. MSNBC online featured a written report and a series of videos and slide shows on October 16, 2006 that captured the story surrounding the earthquake in Hawaii the previous day. When compared, the headline video and headline print report reveal some very interesting trends in the ways in which the news is disseminated. The headlining video report â€Å"Powerful Earthquakes Shake Hawaii† is two and one-half minutes long and features a variety of images that show damage to a local woman’s home, the picture of a landslide caught by a photographer, various tourists being inconvenienced, file footage of volcanic eruption, the Hawaiian coastline, people buying gas, and shoppers at a grocery store. These pictures are accompanied by interview sound bites or voiced-over by reporter Howard Dashefsky, but the entire report is devoid of real information.   What might one expect as the aftermath of an earthquake on a populated island that is also a tourist attraction?   If I had guessed at the â€Å"aftermath,† I would have imagined almost everything I saw in Dashefsky’s report.   Although the images were fascinating and even engaging at times, I left the report with virtually no residual caring and no remnant thoughts: nothing of value had been added to my brain. The headline print report begins with â€Å"officials fanned out across Hawaii early Monday to inspect bridges and roads following the strongest earthquake to rattle the islands in more than two decades, a 6.6-magnitude quake that caused blackouts and landslides, but no immediate reports of fatalities† (Associated Press).   In the opening paragraph of the print report, I found out what happened; I felt sorrow and relief; and I was driven to consider the after-effects of the earthquake in ways not even broached by the video report.   It took me less than one minute to read the print report, but in that minute I learned about what had happened, where it had happened, that no tsunami was expected, what was being done, what would be done—the list is almost endless. Those who watch the video report will stand around water coolers discussing benign elements of the event.   The will recall the semi-ravaged home of one resident and the fight to get gas and groceries; moreover, they will congratulate themselves on not having wasted their own money on a spoiled Hawaiian vacation.   This is the kind of thinking that is being fostered in the United States: superficial, image-based, self-centered, and desensitized. Those who take (less) time to actually read about the earthquake will stand around the water cooler discussing factual details.   They will likely be amazed by the good fortune of such a historically large earthquake resulting in no fatalities; they will wonder if the roads and bridges where they live would be damaged after such an event; they may ponder how long the state of disaster will remain in effect; they will think about how happy they are not to be there on vacation, but it will most likely not be the first thing on which they comment.   This is the kind of thinker that is in danger of dying in the United States: one who craves facts and the chance to critique them while expanding his/her knowledge base. The ability to receive immediate information is a boon to the news consumer; however, the availability of instant images, facts, and reports must be combined with words that are as stimulating, powerful, and informative as the visual clues—or a numbing of the mind and the senses is bound to occur.   Reports that are piping hot can be delivered to the public as a combination of the best of what can be seen, what can be heard, and what can be read.   Like a dinner filled with the necessary food groups, communication needs to combine its sources and resources for the most palatable and healthiest results. References Associated Press, The.   (October 16, 2006).   Hawaii checks bridges, roads after quake: Landslides and power outages but no reports of deaths.   MSNBC.   Retrieved October 16, 2006, from http://www.msnbc.msn.com/id/15286294/. Dashefsky, H.   (October 16, 2006).   Powerful earthquakes shake Hawaii.   MSNBC Video.   Retrieved October 16, 2006, from http://video.msn.com. Radio Legend Paul Harvey Biography.   (2003).   Paul Harvey: The Voice of the New Millennium.   paulharvey.com: ABC Radio Networks.   Retrieved October 16, 2006, from http://www.paulharvey.com/bio.shtml.

Friday, January 10, 2020

House and Apartment: Similarities and Differences Essay

A home is a place that makes us feel secure and comfortable. So, it should be a place that is the most suitable place for us to rest after did many activities at the day. However, as the time goes by, there has been built an apartment which is has the same function as a house, that is a place to live in. Unlike a house, an apartment usually located at the center of city which is give an extra benefit for business utility. â€Å"Your apartment is your home, and you should be able to enjoy it to the fullest† (Ron Leshnower, 2010). Nonetheless, some people think that living in house would give the maximum comfortibility. There are 2 similarities between a house and an apartment. First of all, both of them would make you spend the same living cost. When you decide to live with luxurious life style, wherever you live, you would stay to live with that kind of habit. Second of all, whether it is a house or an apartment, it has a big role as a place to live in. In the other hand, there are 3 differences between living in a house and apartment. Firstly, living in a house would spend more money rather than an apartment. If you think that someday you would buy a house, first thing that you need to purchase is a land. A land is primary requirement to build a house. Thus, it should be really expensive especially if it is close by the city. And next, you need to buy the raw materials and hire someone to build a house. However, if you decide to buy an apartment, all you need to do is be ready for the money. â€Å"It is cheaper then living in a traditional house and paying different kinds of fees I am not familiar with.† (IELTS Essay Task 2: Apartment Or House, paragraph 2, http://www.goodatesl.com/ielts/writing-ielts/ielts-writing-task-2/ielts-essay-task-2-apartment-or-house.html, 2010). Secondly, living in apartment would give you feel secure and that is real. â€Å"Most apartment buildings offer 24 hour security and security cameras throughout the facility to ensure that tenants do not have to worry about their persons or property being victims of terrorism or theft† (Apartment Living in Jakarta, paragraph 7, http://www.expat.or.id/info/apartmentlivinginjakarta.html). Compare with a house, you need to make sure you lock all doors and windows before you go to sleep and check everything before you go to somewhere. Thirdly, living in a house would never give you a full satisfaction. For example, if you want more, you need to spend more.

Thursday, January 2, 2020

My Experience With Science And Mathematics Essay - 1402 Words

My mother was determined for all her children to graduate high school so we moved often to various counties in the St. Louis area because she knew quality education was based on place. I was now in my junior year and this was my sixth high school that my siblings and I attended. This school was unlike the others. We were surrounded by middle and upper class families that looked like us. This was definitely a new experience. I walked into the corridor of this brand new school and the brightness made me feel alive. My obsession with science and mathematics took hold. I immersed myself in this new community, taking part in various clubs, learning, inventing and experimenting. I walked into my guidance counselor’s office as I did many times that year. But this time it was different because a visitor was waiting for me. This towering man introduced himself as Dr. Keener Tippin and he explained to me he was there to recruit me for a program that would allow me to spend a summer on campus taking college courses and engage in scientific research. I never considered college as an option. A door opened. I became a teacher to honor my mother with her determined spirit and commitment for all her children to have a quality education no matter the financial burden of as a single parent of five. I became a teacher because of luck, someone I never knew, opened a door. Access to career opportunities should not be based on place or the roll of a die. I moved to Boston withShow MoreRelatedMy Field Of Computer Science874 Words   |  4 Pagesfascinated by the field of computer science, and that led to me pursuing a degree in Computer Science from North Carolina State University (NCSU). While at NCSU I had the chance to work under a computer science professor and learn a great deal from him. 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However, what would life and philosophy be like if we did not have a basis of pure mathematics and/or mathematical truths to rely on? Descartes’ based