In vitro evaluation of blood flow through autoperfusion balloon catheters

1993 ◽  
Vol 30 (1) ◽  
pp. 58-62 ◽  
Author(s):  
Ebo D. de Muinck ◽  
Paolo Angelini ◽  
Kathy Dougherty ◽  
Bart J. Verkerke ◽  
Gerhard Rakhorst ◽  
...  
1994 ◽  
Vol 17 (2) ◽  
pp. 83-87 ◽  
Author(s):  
E.D. De Muinck ◽  
B.J. Verkerke ◽  
G. Rakhorst ◽  
K.I. Lie

During coronary angioplasty, perfusion distal to the inflated angioplasty balloon can be maintained with autoperfusion balloon catheters and coronary perfusion pumps. The blood flow rates through the autoperfusion balloon catheters and the flow rates achieved with a perfusion pump were compared in vitro with fresh human blood at 37° C. In a specially designed system, blood flow rates through Stack™ autoperfusion balloon catheters were measured at 40, 60 and 80 mmHg continuous pressure. In another system, driving pressures were measured during perfusion with the pump, through a specially designed forced perfusion catheter at 20, 40 and 60 ml/min flow. The pressure applied in the autoperfusion experiments was converted into atmospheres (atm) to facilitate comparison with the driving pressures measured during pumping (1 mmHg = 1.316 × 10−3 atm). Mean flow rates through the autoperfusion balloon catheters were: 46 ml/min at 0.05 atm, 66 ml/min at 0.09 atm and 75 ml/min at 0.1 atm. Mean pressures during pumping were: 1.8 atm at 20 ml/min, 3.5 atm at 40 ml/min, 5 atm at 60 ml/min. Due to the phasic nature of coronary blood flow, the flow through autoperfusion balloons is generally lower than the minimum required for adequate myocardial protection (= 60 ml/min). Thus, autoperfusion balloon catheters are simpler and cheaper devices than perfusion pumps, but generally they are not able to provide adequate myocardial protection.


Author(s):  
Maartje C. F. Geven ◽  
Arjen Van Der Horst ◽  
Marcel C. M. Rutten ◽  
Wilbert Aarnoudse ◽  
Nico H. J. Pijls ◽  
...  

During coronary catheterization, the epicardial coronary arteries are visually assessed for stenoses on the coronary angiogram. However, the functional significance of disease in the coronary arterial tree, the increased resistance to blood flow, may easily be over- or underestimated by using a 2D projection.


1993 ◽  
Vol 73 (4) ◽  
pp. 855-868 ◽  
Author(s):  
J. M. Kelly ◽  
B. G. Southorn ◽  
C. E. Kelly ◽  
L. P. Milligan ◽  
B. W. McBride

The effect of level of nutrition on in vitro and in vivo O2 consumption by the gastrointestinal tract in four nonlactating, nonpregnant ewes catheterized in the anterior mesenteric vein, hepatic portal vein and mesenteric artery with duodenal cannulae was investigated. Animals were fed a pelleted ration at maintenance (M) or twice maintenance (2M) or fasted (F) subsequent to the M measurement. Duodenal in vitro O2, ouabain-sensitive O2 (OSO2) and cycloheximide-sensitive O2 (CSO2) consumption was determined polarographically using a YSI O2 monitor; whole-gut O2 consumption was determined as (arterio-venous difference of O2 concentration) × (blood flow through the PV). Whole-body O2 consumption was determined using indirect calorimetry. Ewes fed 2M exhibited higher (P < 0.10) whole-body O2 consumption than either M or F ewes. Ewes fed M and 2M had higher (P < 0.10) duodenal in vitro O2 and ouabain-insensitive O2 (OIO2) consumption than F ewes. Hepatic portal blood flow was directly proportional to level of intake (P < 0.10): it was lowest for F ewes (81.0 L h−1), intermediate for M ewes (97.7 L h−1) and highest for 2M ewes (122.5 L h−1). Ouabain inhibition of O2 consumption by portal-drained viscera (PDV) was highest in M ewes and lowest in 2M ewes (P < 0.10). CSO2 consumption by the entire PDV was not affected by level of intake, corresponding to no change in OIO2 consumption by the PDV. As a proportion of whole-body O2 consumption, total O2, OSO2 and cycloheximide-insensitive O2 consumption by the PDV was higher in F ewes than in 2M ewes (P < 0.10). Fasted ewes expended a greater proportion of whole-body O2 consumption on gastrointestinal energetics than did 2M ewes. Key words: Sheep, gastrointestinal oxygen consumption, sodium–potassium ATPase, protein synthesis


2008 ◽  
Vol 130 (1) ◽  
pp. 2-8 ◽  
Author(s):  
Anne Neubert ◽  
Katrin Sternberg ◽  
Stefan Nagel ◽  
Claus Harder ◽  
Klaus-Peter Schmitz ◽  
...  

2000 ◽  
Vol 83 (03) ◽  
pp. 469-474 ◽  
Author(s):  
Dingeman Rijken ◽  
Dmitry Sakharov

SummaryFibrinolysis initially generates channels in an occluding thombus which results in blood flow through the thrombus. Since the impact of flow along the surface of a thrombus on thrombolysis has not been investigated in detail, we studied in vitro how such a flow affects lysis. Compacted and noncompacted plasma clots were used as model thrombi. With compacted clots, fibrin-specific lysis induced by alteplase in the outer plasma was accelerated about 2-fold by strong flow (arterial shear rate). Non-fibrin-specific lysis induced either by a high concentration of alteplase or by streptokinase was slow, was accompanied by rapid depletion of plasminogen in the outer plasma, and was only slightly accelerated by flow. With noncompacted clots, similar acceleration factors were documented, when mild flow (venous shear rate) was applied. Strong flow further accelerated fibrin-specific lysis, up to 10-fold as compared to lysis without flow, but paradoxically retarded non-fibrin-specific lysis. The data suggest that flow accelerates lysis by enhancing transport of plasminogen from the outer plasma to the surface of the clot. Both opposite effects of the strong flow were mediated by forceful intrusion of the outer plasma into the noncompacted clot due to flow irregularities. In the case of non-fibrin-specific lysis this resulted in the replacement of the plasminogen-containing milieu by plasminogen-depleted outer plasma in certain areas of the clot turning them into virtually unlysable fragments. This flow-enforced “plasminogen steal” may contribute to the relatively high percentage of incomplete thrombolysis (TIMI-2 grade flow) documented in a number of trials for non-fibrin-specific thrombolytic agents. In the case of fibrin-specific lysis, the effect of flow on the speed of fibrinolysis is always beneficial.


2005 ◽  
Vol 2004.17 (0) ◽  
pp. 209-210
Author(s):  
Shinichi IIDA ◽  
Kenkichi OHBA ◽  
Tsutomu TAJIKAWA ◽  
Masataka YOSHIDA ◽  
Fuyo TSUKIYAMA

2021 ◽  
Author(s):  
Gaia Franzetti ◽  
Mirko Bonfanti ◽  
Cyrus Tanade ◽  
Chung Sim Lim ◽  
Janice Tsui ◽  
...  

Purpose: Peripheral arteriovenous malformations (pAVMs) are congenital lesions characterised by abnormal high-flow, low-resistance vascular connections - constituting the so-called nidus - between arteries and veins. The mainstay treatment typically involves the embolisation of the nidus with embolic and sclerosant agents, however the complexity of AVMs often leads to uncertain outcomes. This study aims at developing a simple, yet effective computational framework to aid the clinical decision making around the treatment of pAVMs. Methods: A computational model was developed to simulate the pre-, intra-, and post-intervention haemodynamics of an AVM. A porous medium of varying permeability was used to simulate the effect that the sclerosant has on the blood flow through the nidus. The computational model was informed by computed tomography (CT) scans and digital subtraction angiography (DSA) images, and the results were compared against clinical data and experimental results. Results: The computational model was able to simulate the blood flow through the AVM throughout the intervention and predict (direct and indirect) haemodynamic changes due to the embolisation. The simulated transport of the dye in the AVM was compared against DSA time-series obtained at different intervention stages, providing confidence in the results. Moreover, experimental data obtained via a mock circulatory system involving a patient specific 3D printed phantom of the same AVM provided further validation of the simulation results. Conclusion: We developed a simple computational framework to simulate AVM haemodynamics and predict the effects of the embolisation procedure. The developed model lays the foundation of a new, computationally driven treatment planning tool for AVM embolisation procedures.


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