Simple computer model for the nonlinear beam-beam interaction in isabelle

Complexation of Iron with the Orally Active Decorporation Drug L1 (3-Hydroxy-1,2-Dimethyl-4-Pyridinone)

Clinical Chemistry ◽

10.1093/clinchem/38.4.562 ◽

1992 ◽

Vol 38 (4) ◽

pp. 562-565 ◽

Cited By ~ 17

Author(s):

M A Kline ◽

C Orvig

Keyword(s):

Blood Plasma ◽

Potentiometric Titration ◽

Stability Constants ◽

Computer Model ◽

Chelating Agent ◽

Glass Electrode ◽

Simple Computer ◽

Active Iron ◽

The Stability ◽

Orally Active

Abstract The stability constants for the Fe(III) complexes of the orally active iron decorporation drug L1 (3-hydroxy-1,2-dimethyl-4-pyridinone) have been determined by potentiometric titration [glass electrode, 25.0 degrees C, mu = 0.15 mol/L (isotonic) NaCl]. A simple computer model of blood plasma (citrate 100 mumol/L, transferrin 37 mumol/L) has been used to compare the Fe(III) binding efficacies in blood of L1 and the clinically used intravenously administered chelating agent deferoxamine.

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A simple computer model for albumin and water distribution and flux in man

International Journal of Bio-Medical Computing ◽

10.1016/0020-7101(85)90061-3 ◽

1985 ◽

Vol 16 (3-4) ◽

pp. 277-291 ◽

Cited By ~ 3

Author(s):

D. Mangnall ◽

P.J. Moore ◽

R.G. Clark

Keyword(s):

Computer Model ◽

Water Distribution ◽

Simple Computer

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Simple computer model of an IR-photoconductor

10.1117/12.517325 ◽

2003 ◽

Author(s):

L. I. Diakonov ◽

E. V. Susov ◽

Galina V. Chekanova

Keyword(s):

Computer Model ◽

Simple Computer

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Low-frequency oscillations in arterial pressure and heart rate: a simple computer model

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.256.6.h1573 ◽

1989 ◽

Vol 256 (6) ◽

pp. H1573-H1579 ◽

Cited By ~ 27

Author(s):

J. B. Madwed ◽

P. Albrecht ◽

R. G. Mark ◽

R. J. Cohen

Keyword(s):

Heart Rate ◽

Nervous System ◽

Computer Model ◽

Low Frequency ◽

Beta Adrenergic ◽

Simple Computer ◽

Effector Mechanism ◽

Arterial Blood ◽

Low Frequency Oscillations ◽

Effector Mechanisms

We have previously reported that low-frequency oscillations in arterial blood pressure (ABP) and heart rate (HR) occur when conscious dogs experience severe blood loss. These low-frequency oscillations are generated by enhancement of the sympathetic nervous system and inhibition of the parasympathetic nervous system. We have developed a simple computer model to elucidate those properties critical to the generation of these oscillations. Our model incorporates several important features: 1) arterial baroreceptor feedback loops, which relate ABP to targeted HR and total peripheral resistance (TPR) values; 2) two effector outputs, HR and TPR, which are controlled by the outputs of vagal, beta-adrenergic, and alpha-adrenergic effector mechanisms; 3) a fixed beat-to-beat stroke volume; and 4) a wind-kessel model, which represents the peripheral circulation. Each effector mechanism is modeled as a low-pass filter in series with a delay. The vagal effector mechanism slows the HR after a 100-ms delay and reaches maximal HR at that time. The beta-adrenergic effector mechanism speeds HR after a 2.5-s delay and then increases to maximal HR 7.5 s later. The alpha-adrenergic effector mechanism begins vasoconstriction after a 5-s delay and then reaches maximal contraction 15 s later. Computer simulations of inhibition of the vagal effector mechanism and activation of the adrenergic effector mechanisms elicit low-frequency oscillations in ABP and HR. These oscillations are similar to those observed experimentally in the dog during hemorrhage. We conclude that the slow temporal response of the alpha-adrenergic effector mechanism controlling TPR is the critical element in predicting the observed low-frequency oscillations in ABP and HR.

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