PubMed Health⌕ Search

PubMed · 8572426

Nonlinear closed-loop control system for intracranial pressure regulation.

Abstract

A nonlinear closed-loop control system with flat pressure-versus-flow characteristics that is aimed at regulating intracranial pressure (ICP) by adjusting the volume of cerebral spinal fluid (CSF) was designed, built, and tested. The control system design allows both the pressure setpoint and hysteresis to be adjusted to overcome the difficulties inherent in differential pressure-activated, fixed resistance, open-loop shunts. A dynamic six-compartment bench-top fluid system, which mimics the cerebral spinal fluid system, was designed, built, and tested. A computer simulation was developed which included the nonlinear on-off controller with hysteresis and a sixth-order, linear, multicompartmental model of the CSF system. The computer model and in vitro system results showed the ability of the system to track and compensate for pressure variations above and below normal as well as for spurious outputs that mimic such in vivo problems as blood pressure changes, sneezing, or coughing. There was one discrepancy between the simulated and in vitro results. The in vitro system had a higher rate of increase in pressure due to the more rigid compliance of the materials used, whereas the computer model compliance, based on the basal in vivo compliance of the CSF system, was less rigid. Based on these findings, the controller was modified to account for short-duration, extremely elevated pressures.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G L Coté, R Durai, B Zoghi. Nonlinear closed-loop control system for intracranial pressure regulation.. https://doi.org/10.1007/bf02584475

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Bradykinin shifts endothelial fluid passage from para- to transcellular routes.

The signalling peptide bradykinin (BK) is implicated in inflammation and angiogenesis. It promotes fluid transport from blood vessels to interstitial space, and thus facilitates oedema formation. To clarify whether paracellular or transcellular pathways mediate this effect, we investigated the BK-stimulated fluid transport across endothelial monolayers in vitro by comparison of electrical and fluorescence methods. Electrical cell impedance sensing monitored a biphasic response of cell layers to BK with high time resolution: a short decrease (18%, 1 min) was followed by a more sustained increase in paracellular resistance (30%, 10 min). The two phases can be assigned to second messengers of the BK-signalling pathway: Ca(2+) for the decrease and cyclic adenosine monophosphate for the rise of resistance, respectively. Despite tightening of the intercellular clefts, BK increased the fluid permeability by 39%, indicating transcellular fluid transport. Additionally, BK stimulated both in- and outwardly directed membrane trafficking as assessed by vesicular fluid uptake (by 49%) and secretion of von Willebrandt factor (by 85%). In conclusion, the combination of electrical and fluorescence data suggests that BK induces a shift from para- to transcellular fluid transport across endothelium.

Body Fluid Compartments↗

Beta2-microglobulin, a uremic toxin with a double meaning.

beta(2)M is a strong and independent indicator of hemodialysis patient outcomes and an excellent surrogate for middle molecules, and deserves to be routinely monitored and incorporated into dialysis adequacy targets. beta(2)M has a double meaning, reflecting both dialysis efficacy in terms of solute mass transfer and patient bioactivity. The work of Ward et al. in this issue warrants a study to test the hypothesis that long daily hemodiafiltration treatment would be the optimal renal replacement modality to improve dialysis patient outcomes.

Body Fluid Compartments↗