In vivo application of the generalised radial-aorta and carotid-aorta pressure transfer function

Author(s):  
P. Segers ◽  
S. Carlier ◽  
G. Armstrong ◽  
P. Verdonck ◽  
J. Thomas
Keyword(s):  
EMBO Reports ◽  
2020 ◽  
Vol 21 (9) ◽  
Author(s):  
Vaisaly R Nath ◽  
Shirish Mishra ◽  
Bishal Basak ◽  
Deepti Trivedi ◽  
Padinjat Raghu

2012 ◽  
Vol 302 (7) ◽  
pp. H1492-H1509 ◽  
Author(s):  
Bryn A. Martin ◽  
Philippe Reymond ◽  
Jan Novy ◽  
Olivier Balédent ◽  
Nikolaos Stergiopulos

Coupling of the cardiovascular and cerebrospinal fluid (CSF) system is considered to be important to understand the pathophysiology of cerebrovascular and craniospinal disease and intrathecal drug delivery. A coupled cardiovascular and CSF system model was designed to examine the relation of spinal cord (SC) blood flow (SCBF) and CSF pulsations along the spinal subarachnoid space (SSS). A one-dimensional (1-D) cardiovascular tree model was constructed including a simplified SC arterial network. Connection between the cardiovascular and CSF system was accomplished by a transfer function based on in vivo measurements of CSF and cerebral blood flow. A 1-D tube model of the SSS was constructed based on in vivo measurements in the literature. Pressure and flow throughout the cardiovascular and CSF system were determined for different values of craniospinal compliance. SCBF results indicated that the cervical, thoracic, and lumbar SC each had a signature waveform shape. The cerebral blood flow to CSF transfer function reproduced an in vivo-like CSF flow waveform. The 1-D tube model of the SSS resulted in a distribution of CSF pressure and flow and a wave speed that were similar to those in vivo. The SCBF to CSF pulse delay was found to vary a great degree along the spine depending on craniospinal compliance and vascular anatomy. The properties and anatomy of the SC arterial network and SSS were found to have an important impact on pressure and flow and perivascular fluid movement to the SC. Overall, the coupled model provides predictions about the flow and pressure environment in the SC and SSS. More detailed measurements are needed to fully validate the model.


2010 ◽  
Vol 4 (2) ◽  
Author(s):  
Nick Chernyy ◽  
Bruce J. Gluckman

Feedback-control has been proved to be advantageous in various technical fields and is likely to increase the performance of electrical neural interface devices. The control algorithms in such a device will rely on metrics of neural activity, thereby necessitating their differentiation from artifacts caused by electrical stimulation. We demonstrate an efficient algorithm for determining the relationship between the electrical stimulus current waveform and the recorded artifact potential, or transfer function. This facilitates online stimulus artifact subtraction and concurrent neural recordings during electrical stimulation. Furthermore, we demonstrate significant changes in this transfer function, in vivo, that occur on time scales of hours and are indicative of changes in the electrical properties of neural tissue. Tracking these variations is paramount for the successful implementation of a feedback-enabled neural control system.


2020 ◽  
Author(s):  
Christopher Murphy Lewis ◽  
Jianguang Ni ◽  
Thomas Wunderle ◽  
Patrick Jendritza ◽  
Ilka Diester ◽  
...  

SummaryThe gamma rhythm has been implicated in neuronal communication, but causal evidence remains indirect. We measured spike output of local neuronal networks and emulated their synaptic input through optogenetics. Opsins provide currents through somato-dendritic membranes, similar to synapses, yet under experimental control with high temporal precision. We expressed Channelrhodopsin-2 in excitatory neurons of cat visual cortex and recorded neuronal responses to light with different temporal characteristics. Sine waves of different frequencies entrained neuronal responses with a reliability that peaked for input frequencies in the gamma band. Crucially, we also presented white-noise sequences, because their temporal unpredictability enables analysis of causality. Neuronal spike output was caused specifically by the input’s gamma component. This gamma-specific transfer function is likely an emergent property of in-vivo networks with feedback inhibition. The method described here could reveal the transfer function between the input to any one and the output of any other neuronal group.


2006 ◽  
Vol 290 (4) ◽  
pp. R982-R991 ◽  
Author(s):  
Ying Shi ◽  
Xuemei Wang ◽  
Ki H. Chon ◽  
William A. Cupples

Nonselective inhibition of nitric oxide (NO) synthase (NOS) augments myogenic autoregulation, an action that implies enhancement of pressure-induced constriction and dilatation. This pattern is not explained solely by interaction with a vasoconstrictor pathway. To test involvement of the Rho-Rho kinase pathway in modulation of autoregulation by NO, the selective Rho kinase inhibitor Y-27632 and/or the NOS inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) were infused into the left renal artery of anesthetized rats. Y-27632 and l-NAME were also infused into isolated, perfused hydronephrotic kidneys to assess myogenic autoregulation over a wide range of perfusion pressure. In vivo, l-NAME reduced renal vascular conductance and augmented myogenic autoregulation, as shown by increased slope of gain reduction and associated phase peak in the pressure-flow transfer function. Y-27632 (10 μmol/l) strongly dilated the renal vasculature and profoundly inhibited autoregulation in the absence or presence of l-NAME in vivo and in vitro. Afferent arteriolar constriction induced by 30 mmol/l KCl was reversed (−92 ± 3%) by Y-27632. Phenylephrine caused strong renal vasoconstriction but did not affect autoregulation. Inhibition of neuronal NOS by N5-(1-imino-3-butenyl)-l-ornithine (l-VNIO) did not cause significant vasoconstriction but did augment myogenic autoregulation. Thus vasoconstriction is neither necessary (l-VNIO) nor sufficient (phenylephrine) to explain the augmented myogenic autoregulation induced by l-NAME. The effect of l-VNIO implicates tubuloglomerular feedback (TGF) and neuronal NOS at the macula densa in regulation of the myogenic mechanism. This conclusion was confirmed by the demonstration that systemic furosemide removed the TGF signature from the pressure-flow transfer function and significantly inhibited myogenic autoregulation. In the presence of furosemide, augmentation of myogenic autoregulation by l-NAME was significantly reduced. These results provide a potential mechanism to explain interaction between myogenic and TGF-mediated autoregulation.


1994 ◽  
Vol 77 (4) ◽  
pp. 1784-1789 ◽  
Author(s):  
T. Binzoni ◽  
P. Cerretelli

A mathematical model analogous to Chance's “transfer function” was derived on the basis of the energy consumption principle, which is suitable to describe the energetics of human skeletal muscle during aerobic activity. The implications and the characteristics of this model are that 1) the half time of phosphocreatine (PCr) hydrolysis at the onset of a mechanical constant-load exercise is independent of the imposed charge, 2) the changes of O2 consumption in the muscle at steady state when changing workload are linearly related to PCr concentration, 3) the kinetics of the intracellular oxygen consumption during a rest-to-work transient are influenced by anaerobic glycolysis, 4) it may explain the PCr-time relationship of different muscles types (e.g., skeletal, heart, trained vs. untrained), 5) it allows one to interpret correctly the significance of the oxygen consumption kinetics in the rest-to-work transient at the lung level, and 6) it is conceived for in vivo applications.


Author(s):  
S. Phyllis Steamer ◽  
Rosemarie L. Devine

The importance of radiation damage to the skin and its vasculature was recognized by the early radiologists. In more recent studies, vascular effects were shown to involve the endothelium as well as the surrounding connective tissue. Microvascular changes in the mouse pinna were studied in vivo and recorded photographically over a period of 12-18 months. Radiation treatment at 110 days of age was total body exposure to either 240 rad fission neutrons or 855 rad 60Co gamma rays. After in vivo observations in control and irradiated mice, animals were sacrificed for examination of changes in vascular fine structure. Vessels were selected from regions of specific interest that had been identified on photomicrographs. Prominent ultrastructural changes can be attributed to aging as well as to radiation treatment. Of principal concern were determinations of ultrastructural changes associated with venous dilatations, segmental arterial stenosis and tortuosities of both veins and arteries, effects that had been identified on the basis of light microscopic observations. Tortuosities and irregularly dilated vein segments were related to both aging and radiation changes but arterial stenosis was observed only in irradiated animals.


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