Cerebral Autoregulation Mechanism | Report

Cerebral Autoregulation Mechanism ReportFrom Biose Ifechukwude JoachimIntroductionCerebral autoregulation (CA) is the multifactorial vascular mechanism that maintains a constant intellectual extraction bring out in spite of fluctuations in the noetic perfusion mechanical press (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 solvent involved in CA is speedy 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 straits injury, intracerebral haemorrhage, stroke, hyper-perfusion syndrome, and subarachnoid haemorrhage (Diedler et al., 2009 Atkins et al., 2010 Budohoski et al., 20 12 Saeed et al., 2013 Buczek et al., 2013).Fig. 1. Cerebral autoreglation in relation to vascular response. Within the upper and dismount boundaries of the autoregulatory range (dotted controversys), blood be given remains constant (blue line with beads). As Pressure fall below the lower limit, vascular smooth muscle relaxes to allow dilatation, while constriction of vessels (red circles) ensues to reduce blood flow as drive approximates the upper limit. Adapted from Pires et al., 2013.ClassificationBased on factors affecting cerebral blood flow (CBF), CA can be classified into both categories, metabolic autoregulation (MA) and pressure autoregulation (PA).Mainly collect 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 augments pH by increasing CBF via vasod ilatation (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.MechanismIn adults and under normal conditions, provided CPP falls within the boundary of 50-150 mmHg, CBF is preserved at around 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 straight dependent on beggarly 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 before long elusive however, it is believed to be subject to the interaction of neurogenic, metabolic and myogenic facto rs (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 befuddle 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 Edvin sson, 1990). These substances, potassium, adenosine, and henry 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 transmit to CA in an unexpected manner, with respect to their response to blood flow changes. While basilar arterial blood vessel refines in response to increased blood flow, MCA constricts Koller and Toth, (2012).nether AnaesthesiaAnaesthesia puts the brain in a state of reduced nervous 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 (Bosn jak 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 primarily 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.StrokeDuring 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 effect (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 piercing 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., 19 89).ReferencesAslanyan S, Fazekas F, Weir CJ, Horner S and Lees KR (2003). GAIN external Steering committal and Investigators Effect of blood pressure during the perspicacious period of ischemic stroke on stroke outcome a tertiary analysis of the GAIN International Trial. Stroke. 34 24202425.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 228235.Attwell D, Buchan AM, Charpak S et al. (2010). Glial and neuronal control of brain blood flow. Nature. 468 23243.Baumbach GL and Heistad DD (1989). Re shapeing of cerebral arterioles in chronic hypertension. Hypertension. 13 968972.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 123131Buczek J, Karlinski M, Kobayashi A, Biaek P and Czonkowska A (2013). Hyperperfusion syndrome after carotid endarterectomy and carotid stenting. Cerebrovasc. Dis. 35 5317.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 data-based study. Stroke. 43 32303237.Busija DW and Heistad DD (1984). Factors involved in the physiological regulation of the cerebral circulation. Rev. Physiol. Biochem. Parmacol. 101 161211.Castillo J, Leira R, Garca MM, Serena J, Blanco M and Dvalos A (2004). Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 35 520526.Cohen Z, Molinatti G and Hamel E (1997). Astroglial and vascular interactions of noradrenaline terminals in th e rat cerebral cortex. J. Cereb. Blood Flow Metab. 17 894904.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 577581.Czosnyka M, Brady K, Reinhard M, Smielewski P and Steiner LA (2009). Monitoring of cerebrovascular autoregulation facts, myths, and missing links. Neurocritical Care. 10 37386.Dawson SL, Blake MJ, Panerai RB and Potter JF (2000). Dynamic but not electrostatic cerebral autoregulation is impaired in acute ischaemic stroke. Cerebrovasc. Dis.10126132.Dawson SL, Panerai RB and Potter JF (2003). Serial changes in static and dynamic cerebral autoregulation after acute ischaemic stroke. Cerebrovasc. Dis. 166975.Diedler J, Sykora M, Rupp A et al. (2009). Impaired cerebral vasomotor activity in spontaneous intracerebral hemorrhage. Stroke. 40 8159.Drake CT and Iadecola C (2007). The role of neuronal signalling in controlling cerebral blood flow. Brain Lang. 102 141152.Ekstrom-Jodal B, Haggendal E, Linder LE and Nilsson NJ (1971). Cerebral blood flow autoregulation at high arterial pressures and unlike levels of coke dioxide tension in dogs. Eur. Neurol. 66-10.Fieschi C, Argentino C, Toni D and Pozzilli C (1988). Calcium antagonists in ischemic stroke. J. Cardiovasc. Pharmacol. 12(6) 8385.Fisher JP, Ogoh S, Young CN, Raven PB and Fadel PJ (2008). Regulation of spirit cerebral artery blood velocity during dynamic exercise in humans influence of aging. J. Appl. Physiol. 105 266273.Goadsby PJ and Edvinsson L (2002). Neurovascular control of the cerebral circulation, Lippincott Williams Wilkins, Philadelphia, Pa, USA.Gelmers HJ (1982). Effect of nimodipine (Bay e 9736) on postischaemic cerebrovascular reactivity, as revealed by measuring regional cerebral blood flow (rCBF). Acta Neurochir. (Wien). 63 283290.Hakim AM, Evans AC, Berger L , Kuwabara H, Worsley K, Marchal G, Biel C, Pokrupa R, Diksic M and Meyer E (1989). The effect of nimodipine on the evolution of human cerebral infarction studied by PET. J. Cereb. Blood Flow Metab. 9 523534.Hamel E (2006). Perivascular nerves and the regulation of cerebrovascular tone. J. Appl. Physiol. 100 10591064.Heistad DD and Kontos HA (1979). In Handbook of Physiology The Cardiovascular System III, Berne RM, Sperelakis N (Eds.). Bethesda, MD American Physiological Society.137182.Hossmann KA (2006). Pathophysiology and therapy of experimental stroke. Cell Mol. Neurobiol. 26 1057-1083.Iadecola C (2004). Neurovascular regulation in the normal brain and in Alzheimers disease. Nature Reviews Neuroscience. 5(5) 347360.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 25952600.Jones SC, Radinsky CR, Furlan AJ et al. (2002). Variabil ity 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 48896.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 transmissible model of cerebral ischemic small vessel disease. J. Clin. Invest. 120 433445.Koller A and Toth P (2012). Contribution of flow-dependent vasomotor mechanisms to the autoregulation of cerebral blood flow. J. Vasc. Res. 49 375389.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 H371H383.Kulik T, Kusano Y, Aronhime S, Sandler AL and Winn HR (2008). Regulation of cerebral vasculature in normal an d ischemic brain. Neuropharmacology. 55 281288.Kuschinsky W (1997). Neuronal-vascular coupling. A unifying hypothesis. Adv. Exp. Med. Biol. 413 167176.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 10531058.Lassen NA (1959).Cerebral blood flow and oxygen consumption in man. Physiol. Rev. 39 183238.Lassen NA (1974). Control of cerebral circulation in health and disease. Circ. Res. 34 749760.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. 50855862.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-st ate 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. 3933-41.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) S21S30.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 314318.Novak V and Hajjar I (2010). The relationship between blood pressure and cognitive function. Nature Reviews Cardiology. 7 68698.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. Physi ol. 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 586598.Panerai RB (1998). Assessment of cerebral pressure autoregulation in humansa review of measurement methods. Physiol. Meas. 19 305338.Paulson OB, Strandgaard S and Edvinsson L (1990). Cerebral autoregulation. Cerebrovasc. Brain Metab. Rev. 2 161-192.Petersen NH, Ortega-Gutierrez S, Reccius A, Masurkar A, Huang A and Marshall RS (2015). Dynamic Cerebral Autoregulation Is Transiently Impaired for One Week after Large-Vessel Acute ischemic Stroke. Cerebrovasc. Dis. 39 144150.Pires PW, Dams Ramos CM, Matin N and Dorrance AM (2013). The effects of hypertension on the cerebral circulation. Am. J. Physiol. Heart. Circ. Physiol. 304 15981614,Raichle ME and Stone HL (1971). Cerebral blood flow autoregul ation and graded hypercapnia. Eur. Neurol. 6 1-5.Reinhard M, Wihler C, Roth M, Harloff A, Niesen WD, Timmer J et al. (2008). Cerebral autoregulation dynamics in acute ischemic stroke after rtPA thrombolysis. Cerebrovasc. Dis. 26 147155.Reinhard M, Rutsch S, Lambeck J, Wihler C, Czosnyka M, Weiller C et al. (2012). Dynamic cerebral autoregulation associates with infarct size and outcome after ischemic stroke. ActaNeurol. Scand.125 156162.Rennels M and Nelson E (1975). Capillary innervation in the mammalian central nervous system an electron microscope demonstration (1). Am. J. Anat. 144 233241.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 735741.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 hazar d of early adverse events and poor outcome. Stroke. 43 21082114.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 151159.Strandgaard S (1976). Autoregulation of cerebral blood flow in hypertensive patients. The modifying influence of prolonged antihypertensive treatment on the tolerance to acute, drug-induced hypotension. Circulation. 53 720-727Tiecks FP, Lam AM, Aaslid R and Newell DW (1995). Comparison of static and dynamicCerebral autoregulation measurements. Stroke. 26 10141019.Wang Z, Schuler B, Vogel O, Arras M and Vogel J (2010). What is the optimal anesthetic protocol for measurements of cerebral autoregulation in spontaneously breathing mice? Exp. Brain Res. 207 249258.Willie CK, Tzeng YC, Fisher JA and Ainslie PN (2014). Integrative regulation of human brain blood flow. J. Physiol. 592 841859.Zhang R, Witkowski S, F u Q, Claassen JA and Levine BD (2007). Cerebral hemodynamics after short- and long-term reduction in blood pressure in mild and moderate hypertension. Hypertension. 49 11491155.Zlokovic BV (2008). The blood-brain barrier in health and chronic neurodegenerative disorders. Neuron. 57 178201.