In Vitro Pressure Flow Relationship in Model of Significant Coronary Artery Stenosis

2004 ◽  
Author(s):  
Abhijit Sinha Roy ◽  
Lloyd H. Back ◽  
Ronald W. Millard ◽  
Saeb Khoury ◽  
Rupak K. Banerjee
Keyword(s):  
Coronary Artery ◽  
Pressure Drop ◽  
Power Law ◽  
Flow Rate ◽  
In Vitro Model ◽  
Maximum Pressure ◽  
Vitro Model ◽  
Maximum Pressure Drop

Simultaneous measurement of pressure and flow rate has been found to be helpful in evaluating the physiologic significance of obstructive coronary artery disease and in the diagnosis of microvascular disease. This experimental study seeks to find important pressure-flow relationship in an in-vitro model of significant coronary artery stenoses using a non-Newtonian liquid, similar to blood showing a shear thinning behavior, using significant stenotic in-vitro model (minimal area stenosis = 90%). The geometry for the stenotic model is based on data provided in an in vivo study by Wilson et al., (1988). For 90% area stenosis, the maximum recorded pressure drop for steady flow rate of 55, 79 and 89 are 14, ~24 and ~32 mmHg respectively. The maximum pressure drop at flow rate of 115 ml/min (the physiological limit) is 50.3 mmHg respectively. Using a power law curve fit, the maximum pressure drop (in mmHg) related with flow rate (in ml/min) provided a power law index of 1.72. Shorter distal length than required in the in-vitro model did not allow the recording of complete pressure recovery. This preliminary data provides reference values for further experimentation both in vitro with pulsatile flow as in physiological conditions, and in vivo.

Nitric oxide donors attenuate increase in pressure drop across membrane oxygenators

Perfusion ◽  
1999 ◽  
Vol 14 (5) ◽  
pp. 331-336 ◽  
Author(s):  
F De Somer ◽  
L Foubert ◽  
E Schacht ◽  
G Van Nooten
Keyword(s):  
Nitric Oxide ◽  
Pressure Drop ◽  
In Vitro Model ◽  
Membrane Oxygenator ◽  
In Vivo Models ◽  
Initial Resistance ◽  
Membrane Oxygenators ◽  
Vitro Model

We have evaluated the effect of nitric oxide (NO) on the pressure drop across a membrane oxygenator in one in vitro model and two in vivo models (using four dogs and five pigs). In all the experiments sodium nitroprusside (SNP) was used as a NO source, whereas gaseous NO was only used in the in vitro model. The drugs were given when the pressure drop or resistance across the device increased to at least twice the baseline values. In the in vitro model, both SNP and gaseous NO decreased the pressure drop to 75% of its peak value after 10 min and to 67% after 20 min. In the dog model, resistance decreased from 390 to 153 mmHg/l/min after 5 min and to 85 mmHg/l/min after 20 min for a baseline value of 75 mmHg/l/min. The initial resistance across the membrane oxygenator in the pig model increased from 6.6 ± 1.3 to 74 ± 38 mmHg/l/min. An infusion of 10 μg/kg/min SNP reduced the resistance to 16 ± 5 mmHg/l/min.

scholarly journals Generation of a Novel In Vitro Model to Study Endothelial Dysfunction from Atherothrombotic Specimens

2021 ◽  
Author(s):  
Susan Gallogly ◽  
Takeshi Fujisawa ◽  
John D. Hung ◽  
Mairi Brittan ◽  
Elizabeth M. Skinner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
In Vitro Model ◽  
Umbilical Vein ◽  
Coronary Syndrome ◽  
Coronary Endothelial Cells ◽  
Vitro Model ◽  
Umbilical Vein Endothelial Cells

Abstract Purpose Endothelial dysfunction is central to the pathogenesis of acute coronary syndrome. The study of diseased endothelium is very challenging due to inherent difficulties in isolating endothelial cells from the coronary vascular bed. We sought to isolate and characterise coronary endothelial cells from patients undergoing thrombectomy for myocardial infarction to develop a patient-specific in vitro model of endothelial dysfunction. Methods In a prospective cohort study, 49 patients underwent percutaneous coronary intervention with thrombus aspiration. Specimens were cultured, and coronary endothelial outgrowth (CEO) cells were isolated. CEO cells, endothelial cells isolated from peripheral blood, explanted coronary arteries, and umbilical veins were phenotyped and assessed functionally in vitro and in vivo. Results CEO cells were obtained from 27/37 (73%) atherothrombotic specimens and gave rise to cells with cobblestone morphology expressing CD146 (94 ± 6%), CD31 (87 ± 14%), and von Willebrand factor (100 ± 1%). Proliferation of CEO cells was impaired compared to both coronary artery and umbilical vein endothelial cells (population doubling time, 2.5 ± 1.0 versus 1.6 ± 0.3 and 1.2 ± 0.3 days, respectively). Cell migration was also reduced compared to umbilical vein endothelial cells (29 ± 20% versus 85±19%). Importantly, unlike control endothelial cells, dysfunctional CEO cells did not incorporate into new vessels or promote angiogenesis in vivo. Conclusions CEO cells can be reliably isolated and cultured from thrombectomy specimens in patients with acute coronary syndrome. Compared to controls, patient-derived coronary endothelial cells had impaired capacity to proliferate, migrate, and contribute to angiogenesis. CEO cells could be used to identify novel therapeutic targets to enhance endothelial function and prevent acute coronary syndromes.

scholarly journals 3D Environment Is Required In Vitro to Demonstrate Altered Bone Metabolism Characteristic for Type 2 Diabetics

2021 ◽  
Vol 22 (6) ◽  
pp. 2925
Author(s):  
Victor Häussling ◽  
Romina H Aspera-Werz ◽  
Helen Rinderknecht ◽  
Fabian Springer ◽  
Christian Arnscheidt ◽  
...  
Keyword(s):  
Bone Metabolism ◽  
In Vitro Model ◽  
Bone Diseases ◽  
3D Environment ◽  
Type 2 Diabetics ◽  
Mineralized Matrix ◽  
Vitro Model

A large British study, with almost 3000 patients, identified diabetes as main risk factor for delayed and nonunion fracture healing, the treatment of which causes large costs for the health system. In the past years, much progress has been made to treat common complications in diabetics. However, there is still a lack of advanced strategies to treat diabetic bone diseases. To develop such therapeutic strategies, mechanisms leading to massive bone alterations in diabetics have to be well understood. We herein describe an in vitro model displaying bone metabolism frequently observed in diabetics. The model is based on osteoblastic SaOS-2 cells, which in direct coculture, stimulate THP-1 cells to form osteoclasts. While in conventional 2D cocultures formation of mineralized matrix is decreased under pre-/diabetic conditions, formation of mineralized matrix is increased in 3D cocultures. Furthermore, we demonstrate a matrix stability of the 3D carrier that is decreased under pre-/diabetic conditions, resembling the in vivo situation in type 2 diabetics. In summary, our results show that a 3D environment is required in this in vitro model to mimic alterations in bone metabolism characteristic for pre-/diabetes. The ability to measure both osteoblast and osteoclast function, and their effect on mineralization and stability of the 3D carrier offers the possibility to use this model also for other purposes, e.g., drug screenings.

scholarly journals Exposure of ichnovirus particles to digitonin leads to enhanced infectivity and induces fusion from without in an in vitro model system

2007 ◽  
Vol 88 (11) ◽  
pp. 2977-2984 ◽  
Author(s):  
Don Stoltz ◽  
Renée Lapointe ◽  
Andrea Makkay ◽  
Michel Cusson
Keyword(s):  
Outer Membrane ◽  
In Vitro Model ◽  
Model System ◽  
Host Cells ◽  
Fusion Event ◽  
Susceptible Host ◽  
In Vitro Model System ◽  
Vitro Model

Unlike most viruses, the mature ichnovirus particle possesses two unit membrane envelopes. Following loss of the outer membrane in vivo, nucleocapsids are believed to gain entry into the cytosol via a membrane fusion event involving the inner membrane and the plasma membrane of susceptible host cells; accordingly, experimentally induced damage to the outer membrane might be expected to increase infectivity. Here, in an attempt to develop an in vitro model system for studying ichnovirus infection, we show that digitonin-induced disruption of the virion outer membrane not only increases infectivity, but also uncovers an activity not previously associated with any polydnavirus: fusion from without.

Uptake and Retention of Hematoporphyrin Derivative in an in Vivo/in Vitro Model of Cerebral Glioma

Neurosurgery ◽  
1985 ◽  
Vol 17 (6) ◽  
pp. 883-890 ◽  
Author(s):  
Andrew H. Kaye ◽  
George Morstyn ◽  
Robert G. Ashcroft
Keyword(s):  
In Vitro Model ◽  
Hematoporphyrin Derivative ◽  
Cerebral Glioma ◽  
Vitro Model

scholarly journals Adrenomedullin expression in a rat model of acute lung injury induced by hypoxia and LPS

2005 ◽  
Vol 288 (3) ◽  
pp. L536-L545 ◽  
Author(s):  
Jackeline Agorreta ◽  
Javier J. Zulueta ◽  
Luis M. Montuenga ◽  
Mercedes Garayoa
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Lines ◽  
Rat Model ◽  
In Vitro Model ◽  
Rat Lung ◽  
Vitro Model

Adrenomedullin (ADM) is upregulated independently by hypoxia and LPS, two key factors in the pathogenesis of acute lung injury (ALI). This study evaluates the expression of ADM in ALI using experimental models combining both stimuli: an in vivo model of rats treated with LPS and acute normobaric hypoxia (9% O2) and an in vitro model of rat lung cell lines cultured with LPS and exposed to hypoxia (1% O2). ADM expression was analyzed by in situ hybridization, Northern blot, Western blot, and RIA analyses. In the rat lung, combination of hypoxia and LPS treatments overcomes ADM induction occurring after each treatment alone. With in situ techniques, the synergistic effect of both stimuli mainly correlates with ADM expression in inflammatory cells within blood vessels and, to a lesser extent, to cells in the lung parenchyma and bronchiolar epithelial cells. In the in vitro model, hypoxia and hypoxia + LPS treatments caused a similar strong induction of ADM expression and secretion in epithelial and endothelial cell lines. In alveolar macrophages, however, LPS-induced ADM expression and secretion were further increased by the concomitant exposure to hypoxia, thus paralleling the in vivo response. In conclusion, ADM expression is highly induced in a variety of key lung cell types in this rat model of ALI by combination of hypoxia and LPS, suggesting an essential role for this mediator in this syndrome.

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