Single-Compartment Model

1991 ◽  
pp. 65-89 ◽  
Author(s):  
Thomas A. Depner
2013 ◽  
Vol 35 (3) ◽  
pp. 295-316 ◽  
Author(s):  
Febe Francis ◽  
Míriam R. García ◽  
Richard H. Middleton

1983 ◽  
Vol 212 (3) ◽  
pp. 585-598 ◽  
Author(s):  
J M Crawford ◽  
J J Blum

Hepatocytes were isolated from the livers of fed rats and incubated with a mixture of glucose (10 mM), ribose (1 mM), mannose (4 mM), glycerol (3 mM), acetate (1.25 mM), and ethanol (5 mM) with one substrate labelled with 14C in any given incubation. Incorporation of label into CO2, glucose, glycogen, lipid glycerol and fatty acids, acetate and C-1 of glucose was measured at 20 and 40 min after the start of the incubation. The data (about 48 measurements for each interval) were used in conjunction with a single-compartment model of the reactions of the gluconeogenic, glycolytic and pentose phosphate pathways and a simplified model of the relevant mitochondrial reactions. An improved method of computer analysis of the equations describing the flow of label through each carbon atom of each metabolite under steady-state conditions was used to compute values for the 34 independent flux parameters in this model. A good fit to the data was obtained, thereby permitting good estimates of most of the fluxes in the pathways under consideration. The data show that: net flux above the level of the triose phosphates is gluconeogenic; label in the hexose phosphates is fully equilibrated by the second 20 min interval; the triose phosphate isomerase step does not equilibrate label between the triose phosphates; substrate cycles are operating at the glucose-glucose 6-phosphate, fructose 6-phosphate-fructose 1,6-bisphosphate and phosphoenolpyruvate-pyruvate-oxaloacetate cycles; and, although net flux through the enzymes catalysing the non-oxidative steps of the pentose phosphate pathway is small, bidirectional fluxes are large.


1994 ◽  
Vol 77 (3) ◽  
pp. 1185-1197 ◽  
Author(s):  
S. Kano ◽  
C. J. Lanteri ◽  
A. W. Duncan ◽  
P. D. Sly

To investigate the influence of nonlinearities on estimates of respiratory mechanics, differing patterns of mechanical ventilation patterns were analyzed from 8 puppies and 14 children. Respiratory mechanics were calculated using multiple linear regression to fit a linear single-compartment model, a volume-dependent single-compartment model (VDSCM), and a flow-dependent single-compartment model. The ratio of the compliance of the last 20% of the dynamic volume-pressure (V-P) curve to the total compliance (C20/C) and the contribution of a volume-dependent elastance to total elastance [%E2 = E2 (VT)/[(E1 + E2)VT], where E1 + E2 is total elastance, E2 is the volume-dependent component, and VT is tidal volume] were used as the indexes of over-distension. By positioning the dynamic loops on the static V-P curves, ventilation patterns were classified as overdistended or nonoverdistended. In the overdistended group, the C20/C was significantly lower (0.71 +/- 0.10 vs. 0.92 +/- 0.16; P < 0.0001) and %E2 was significantly higher (43.4 +/- 15.0 vs. 0.51 +/- 18.02%, P < 0.0001) than in the nonoverdistended group. The mode of ventilation (pressure controlled vs. volume controlled) and the resistive pressures that resulted in widening of the dynamic V-P loop were found to alter C20/C but not %E2. When the respiratory system was overdistended, i.e., ventilated up to the flattened portion of the V-P curve, the VDSCM gave more accurate estimates of respiratory mechanisms. Furthermore, %E2 calculated from VDSCM is a useful parameter for estimating respiratory system overdistension that is not affected by resistive pressures.


2019 ◽  
Vol 127 (1) ◽  
pp. 58-70 ◽  
Author(s):  
Michelle M. Mellenthin ◽  
Siyeon A. Seong ◽  
Gregory S. Roy ◽  
Elizabeth Bartolák-Suki ◽  
Katharine L. Hamlington ◽  
...  

Identifying safe ventilation patterns for patients with acute respiratory distress syndrome remains challenging because of the delicate balance between gas exchange and selection of ventilator settings to prevent further ventilator-induced lung injury (VILI). Accordingly, this work seeks to link ventilator settings to graded levels of VILI to identify injury cost functions that predict injury by using a computational model to process pressures and flows measured at the airway opening. Pressure-volume loops were acquired over the course of ~2 h of mechanical ventilation in four different groups of BALB/c mice. A cohort of these animals were subjected to an injurious bronchoalveolar lavage before ventilation. The data were analyzed with a single-compartment model that predicts recruitment/derecruitment and tissue distension at each time step in measured pressure-volume loops. We compared several injury cost functions to markers of VILI-induced blood-gas barrier disruption. Of the cost functions considered, we conclude that mechanical power dissipation and strain heterogeneity are the best at distinguishing between graded levels of injury and are good candidates for forecasting the development of VILI. NEW & NOTEWORTHY This work uses a predictive single-compartment model and injury cost functions to assess graded levels of mechanical ventilator-induced lung injury. The most promising measures include strain heterogeneity and mechanical power dissipation.


1986 ◽  
Vol 251 (4) ◽  
pp. H800-H807 ◽  
Author(s):  
B. Rucinski ◽  
L. C. Knight ◽  
S. Niewiarowski

Human 125I-labeled platelet factor 4 (PF4) injected into rabbits showed a biphasic exponential pattern of disappearance from the circulation [half-life of the fast components was 0.75 min, that of the slow components was 20 min] that was not affected by a 1,000-fold excess of unlabeled PF4. Heparin resulted in a single-compartment disappearance of 125I-labeled PF4 (half-life = 25-40 min). Five minutes after injection of 125I-labeled PF4 greater than 40% radioactivity had accumulated in the liver and 4% in the kidney. At that time, accumulation of 125I-labeled beta-thromboglobulin (beta-TG) in the organs was low, approximately 4% in the kidneys and less than 3.0% in the liver. Nuclear imaging studies revealed rapid clearance of 131I-labeled PF4 from blood and its predominant accumulation in the liver. The half-lives of 131I-labeled PF4 radioactivity in liver and kidney were 96 and 252 min, fitting a single-compartment model. 131I-labeled beta-TG accumulated predominantly in the kidney. The half-lives of 131I-labeled beta-TG radioactivity in the kidney and in the liver were 84 and 414 min. Simultaneous or subsequent injection of heparin did not affect the distribution of 131I-labeled beta-TG but caused partial loss of 131I-labeled PF4 radioactivity from the liver and accelerated its appearance in the urinary bladder. Injection of heparin resulted in a 100-fold increase of excretion in the urine of 125I-labeled Pf4 precipitable by 10% trichloroacetic acid.(ABSTRACT TRUNCATED AT 250 WORDS)


Sign in / Sign up

Export Citation Format

Share Document