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Neurophysiology: Age-related changes
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Geriatric Neuroanesthesia, 2019
Dinu Chandran, Smriti Badhwar, Manpreet Kaur
Experimentally, changes in transmural pressure correlate positively with changes in smooth muscle action potentials and membrane potentials, which result in smooth muscle activation (26,39). Studies have shown that this smooth muscle activation is blocked by removal of calcium ions and addition of ethylene glycol tetra-acetic acid (40). Essentially, the stretching of vascular smooth muscles activates stretch-sensitive ion channels, which in turn initiate membrane depolarization through nonselective cation channels, resulting in the influx of calcium through voltage-gated calcium channels, and consequently, smooth muscle contraction (40,41). Some investigators believe that the myogenic mechanism sets the limits of autoregulation, whereas the metabolic mediators are responsible for cerebral autoregulation itself.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
The kidneys have effective mechanisms for maintaining the constancy of renal blood flow and GFR over an arterial pressure range between 70 and 170 mmHg, a process called autoregulation. This helps to maintain a normal excretion of metabolic waste products, such as urea and creatinine, that depend on GFR for their excretion. Autoregulation is an intrinsic property of the kidney; therefore, transplanted kidneys will autoregulate. There are two main theories to explain how renal autoregulation of blood flow occurs: tubuloglomerular feedback and the myogenic mechanism.
Neurophysiology in neurotrauma
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Anesthesia for Neurotrauma, 2018
Experimentally, changes in transmural pressure correlate positively with changes in smooth muscle action potentials and membrane potentials that result in smooth muscle activation.31,33 Studies have shown that this smooth muscle activation is blocked by removing calcium ions and adding ethylene glycol tetraacetic acid (EGTA).34 Essentially, stretching vascular smooth muscles activates stretch-sensitive ion channels, which, in turn, depolarizes the membrane through nonselective cation channels, resulting in the entry of calcium through voltage-gated calcium channels, and, consequently, smooth muscle contraction.35,36 Some investigators believe that the myogenic mechanism limits autoregulation, whereas the metabolic mediators are responsible for cerebral autoregulation itself.
Mechanistic links between systemic hypertension and open angle glaucoma
Published in Clinical and Experimental Optometry, 2022
Ying-kun Cui, Li Pan, Tim Lam, Chun-yi Wen, Chi-wai Do
However, under physiological conditions, there is a lack of a linear relationship between ocular perfusion pressure and ocular blood flow.43 This is attributed to the ability of maintaining a relatively constant ocular blood flow despite fluctuating ocular perfusion pressure, which is known as autoregulation.42 Autoregulation is a complicated process and refers to the intrinsic property of organs to maintain a constant blood flow in response to changes in perfusion pressure. It is controlled by both myogenic and metabolic mechanisms. Since the retina has no autonomic innervation, the blood supply to the inner retina is regulated by local vascular mechanisms. In the myogenic mechanism, the smooth muscle cells in the blood vessels contract when being stretched. This process is possibly mediated by activating voltage-gated Ca2+ channels, resulting in an increased vascular resistance due to vasoconstriction.44
The emerging significance of circadian rhythmicity in microvascular resistance
Published in Chronobiology International, 2022
Jeffrey T. Kroetsch, Darcy Lidington, Steffen-Sebastian Bolz
It must be noted that the myogenic mechanism is not the sole determinant of microvascular resistance and capillary perfusion: when an increase in perfusion is necessary, metabolic, hormonal and neuronal mechanisms engage and superimpose on myogenic mechanisms, to either locally or broadly change perfusion. As examples, carbon dioxide tension, adenosine (a metabolic product), nitric oxide and sympathetic activity all locally influence microvascular tone and hence, regional perfusion within an organ (Lecrux and Hamel 2011; Phillips et al. 2016). Aerobic exercise and the fight-or-flight reaction are prime examples of a more broad modulation of microvascular tone, where the pronounced accumulation of metabolites or adrenaline acting on beta 2 adrenergic receptors acutely and transiently lowers skeletal muscle resistance artery tone to broadly increase skeletal muscle perfusion (Rowell 1974). Oscillations in cerebral blood flow during human sleep provide an illustration of a rhythm that is non-vascular in origin (Fultz et al. 2019): during sleep, low-frequency oscillations in neuronal activity (0.2–4.0 Hz) modulate vascular resistance via neurovascular coupling (Phillips et al. 2016) and consequently, induce oscillations in cerebral blood flow (Fultz et al. 2019). It is important to recognize, therefore, that vascular resistance in vivo is governed by the summation of multiple influences from a variety of cells, including non-vascular types. Because of these multiple influences, (i) intrinsic rhythms identified ex vivo may be nullified in the in vivo setting and (ii) the presence of a vascular rhythm in vivo may not emanate from the vascular molecular clock and may actually be independent of the molecular clock altogether. Consequently, it will be imperative to clearly connect myogenic rhythms ex vivo to hemodynamic parameters in vivo.
CBF regulation in hypertension and Alzheimer’s disease
Published in Clinical and Experimental Hypertension, 2020
Noushin Yazdani, Mark S. Kindy, Saeid Taheri
Chronic high MAP increases the transmural pressure, but the shear stress may remain unaffected. This happens because the shear pressure is only related to flow velocity. In the case of a chronic high MAP, the myogenic mechanism constricts the vessel which results in an increased vessel resistance that keeps the flow velocity low. This new condition pushes CBF myogenic autoregulation to switch to a higher acceptable vascular hydrostatic pressure.