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Background & Aims: Paracentesis is commonly used to manage patient discomfort due to ascites. The relationship between ascites pressure, ascites volume, and patient discomfort has not been elucidated., Methods: We prospectively enrolled adult patients with non-malignant ascites undergoing outpatient therapeutic paracenteses from 2021 to 2024 at a tertiary care hospital. Patients completed a validated symptom questionnaire (ASI-7, maximum score 35) before, immediately after, and 1 week after paracentesis. An open-ended manometer was used to measure ascites pressure at the beginning and end of paracentesis. Mixed effect linear regression was performed to evaluate the relationships between patient characteristics, pressure, volume, and symptoms., Results: One hundred and fifty paracentesis procedures among 48 unique patients with an average Model for End Stage Liver Disease-Sodium 3.0 of 16.7 were included. An average of 6.5 L was drained, which reduced abdominal pressure from a mean of 13.7 to 6.0 cm H 2 O (10.1 to 4.4 mmHg, p < 0.001) and mean symptom score from 22.6 to 6.5 (p < 0.001). Regression models identified that symptoms and abdominal pressure linearly correlated above a pressure of 6 cm H 2 O or ASI-7 score of 16 (p < 0.01). Taller patients required about 670 ml additional drainage per inch above the cohort mean height (5'8″) to achieve the same symptom relief., Conclusions: Pressure measured at the bedside can be used to explore changes in abdominal pressure during paracentesis. Pressure, volume, and patient level factors such as height contribute to patient symptoms but cannot fully explain discomfort associated with ascites and relief after paracentesis., (© 2024 The Author(s). United European Gastroenterology Journal published by Wiley Periodicals LLC on behalf of United European Gastroenterology.)

Introduction: The left (LV) and right (RV) ventricles are linked biologically, hemodynamically, and mechanically, a phenomenon known as ventricular interdependence. While LV function has long been known to impact RV function, the reverse is increasingly being realized to have clinical importance. Investigating ventricular interdependence clinically is challenging given the invasive measurements required, including biventricular catheterization, and confounding factors such as comorbidities, volume status, and other aspects of subject variability. Methods: Computational modeling allows investigation of mechanical and hemodynamic interactions in the absence of these confounding factors. Here, we use a threesegment biventricular heart model and simple circulatory system to investigate ventricular interdependence under conditions of systolic and diastolic dysfunction of the LV and RV in the presence of compensatory volume loading. We use the end-diastolic pressure-volume relationship, end-systolic pressure-volume relationship, Frank Starling curves, and cardiac power output as metrics. Results: The results demonstrate that LV systolic and diastolic dysfunction lead to RV compensation as indicated by increases in RV power. Additionally, RV systolic and diastolic dysfunction lead to impaired LV filling, interpretable as LV stiffening especially with volume loading to maintain systemic pressure. Discussion: These results suggest that a subset of patients with intact LV systolic function and diagnosed to have impaired LV diastolic function, categorized as heart failure with preserved ejection fraction (HFpEF), may in fact have primary RV failure. Application of this computational approach to clinical data sets, especially for HFpEF, may lead to improved diagnosis and treatment strategies and consequently improved outcomes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Kim, Randall, Jezek, Beard and Chesler.)

Introduction: As liver disease progresses, scarring results in worsening hemodynamics ultimately culminating in portal hypertension. This process has classically been quantified through the portosystemic pressure gradient (PSG), which is clinically estimated by hepatic venous pressure gradient (HVPG); however, PSG alone does not predict a given patient's clinical trajectory regarding the Baveno stage of cirrhosis. We hypothesize that a patient's PSG sensitivity to venous remodeling could explain disparate disease trajectories., Methods: We created a computational model of the portal system in the context of worsening liver disease informed by physiologic measurements from the field of portal hypertension. We simulated progression of clinical complications, HVPG, and transjugular intrahepatic portosystemic shunt placement while only varying a patient's likelihood of portal venous remodeling., Results: Our results unify hemodynamics, venous remodeling, and the clinical progression of liver disease into a mathematically consistent model of portal hypertension. We find that by varying how sensitive patients are to create venous collaterals with rising PSG we can explain variation in patterns of decompensation for patients with liver disease. Specifically, we find that patients who have higher proportions of portosystemic shunting earlier in disease have an attenuated rise in HVPG, delayed onset of ascites, and less hemodynamic shifting after transjugular intrahepatic portosystemic shunt placement., Discussion: This article builds a computational model of portal hypertension which supports that patient-level differences in venous remodeling may explain disparate clinical trajectories of disease., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)

Blood flows and pressures throughout the human cardiovascular system are regulated in response to various dynamic perturbations, such as changes to peripheral demands in exercise, rapid changes in posture, or loss of blood from hemorrhage, via the coordinated action of the heart, the vasculature, and autonomic reflexes. To assess how the systemic and pulmonary arterial and venous circulation, the heart, and the baroreflex work together to effect the whole-body responses to these perturbations, we integrated an anatomically-based large-vessel arterial tree model with the TriSeg heart model, models capturing nonlinear characteristics of the large and small veins, and baroreflex-mediated regulation of vascular tone and cardiac chronotropy and inotropy. The model was identified by matching data from the Valsalva maneuver (VM), exercise, and head-up tilt (HUT). Thirty-one parameters were optimized using a custom parameter-fitting tool chain, resulting in an unique, high-fidelity whole-body human cardiovascular systems model. Because the model captures the effects of exercise and posture changes, it can be used to simulate numerous clinical assessments, such as HUT, the VM, and cardiopulmonary exercise stress testing. The model can also be applied as a framework for representing and simulating individual patients and pathologies. Moreover, it can serve as a framework for integrating multi-scale organ-level models, such as for the heart or the kidneys, into a whole-body model. Here, the model is used to analyze the relative importance of chronotropic, inotropic, and peripheral vascular contributions to the whole-body cardiovascular response to exercise. It is predicted that in normal physiological conditions chronotropy and inotropy make roughly equal contributions to increasing cardiac output and cardiac power output during exercise. Under upright exercise conditions, the nonlinear pressure-volume relationship of the large veins and sympathetic-mediated venous vasoconstriction are both required to maintain preload to achieve physiological exercise levels. The developed modeling framework is built using the open Modelica modeling language and is freely distributed., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

The relationship between regional variabilities in airflow (ventilation) and blood flow (perfusion) is a critical determinant of gas exchange efficiency in the lungs. Hypoxic pulmonary vasoconstriction is understood to be the primary active regulator of ventilation-perfusion matching, where upstream arterioles constrict to direct blood flow away from areas that have low oxygen supply. However, it is not understood how the integrated action of hypoxic pulmonary vasoconstriction affects oxygen transport at the system level. In this study we develop, and make functional predictions with a multi-scale multi-physics model of ventilation-perfusion matching governed by the mechanism of hypoxic pulmonary vasoconstriction. Our model consists of (a) morphometrically realistic 2D pulmonary vascular networks to the level of large arterioles and venules; (b) a tileable lumped-parameter model of vascular fluid and wall mechanics that accounts for the influence of alveolar pressure; (c) oxygen transport accounting for oxygen bound to hemoglobin and dissolved in plasma; and (d) a novel empirical model of hypoxic pulmonary vasoconstriction. Our model simulations predict that under the artificial test condition of a uniform ventilation distribution (1) hypoxic pulmonary vasoconstriction matches perfusion to ventilation; (2) hypoxic pulmonary vasoconstriction homogenizes regional alveolar-capillary oxygen flux; and (3) hypoxic pulmonary vasoconstriction increases whole-lobe oxygen uptake by improving ventilation-perfusion matching., Competing Interests: The authors have declared that no competing interests exist.

The effect of two types of modified atmosphere (MA1: 69% N2, 25% CO2, 5% O2, 1% CO; MA2: 70% N2, 30% CO2) on changes in physical and chemical parameters (pH, a(w)--water activity, TVBN - total volatile basic nitrogen, TMA - trimethylamine, FFA - free fatty acids, PV - peroxide value, TBA--thiobarbituric acid) in muscle tissues of the silver carp was monitored in the study. The samples were stored at temperatures +2 +/- 2 degrees C for 18 days. Changes in gas volumes (CO2 and O2) in MAs were also monitored. CO2 levels increased in MA1 but decreased in MA2. At the end of 18 days of storage, a significantly (P < 0.01) lower water activity (a(w)) levels were found in samples packaged under MA1, in contrast to samples packaged under MA2 where water activity values showed considerable fluctuation. Variations in pH values in the two types of MA showed similar trends. Sample pH gradually decreased until day 9 of storage. On day 11, muscle tissue pH increased markedly and then began to decrease again. The overall decrease in pH values was more profound in samples packaged under MA1. TVBN and TMA levels in samples packaged under the two types of MAs remained almost identical until day 9 of the experiment. Later, however, significantly (P < 0.01) higher levels of both parameters were found in muscle tissues packaged under MA1. FFA concentrations in silver carp samples in MA1 were significantly lower (P < 0.01) throughout the experiment. The PV increased significantly in both muscle samples tested. Greater fluctuations in this parameter's values throughout the experiment were observed in samples packaged under MA2. Faster rates of oxidation (P < 0.01) were found in samples packaged under MA1 starting on day 9. Maximum TBA values in MA1 and MA2 were observed on days 14 and 18 of the experiment, respectively. From the course of proteolytic and oxidative changes point of view, the more appropriate combination of gases for silver carp storage seems to be the mixture of 70% N2 and 30% CO2 (MA2), which allows for muscle storage of up to 9 days. We recommend TVBN as a suitable indicator of freshness, and TBA assay as a suitable indicator of the extent of oxidative processes.