scholarly journals Establishment and Evaluation of a Rat Model of Extracorporeal Membrane Oxygenation (ECMO) Thrombosis Using a 3D-printed Mock Oxygenator

Author(s):  
Nao Umei ◽  
Angela Lai ◽  
Jennifer Miller ◽  
Suji Shin ◽  
Kalliope Georgette Roberts ◽  
...  

Abstract Background: Extracorporeal membrane oxygenation (ECMO) research using large animals requires a significant amount of resources, slowing down the development of new means of ECMO anticoagulation. Therefore, this study developed and evaluated a new rat ECMO model using a 3D-printed mock oxygenator.Methods: The circuit consisted of tubing, a 3D-printed mock oxygenator, and a roller pump. The mock oxygenator was designed to simulate the geometry and blood flow patterns of the fiber bundle in full-scale oxygenators but with a low (2.5 mL) priming volume. Rats were placed on arteriovenous ECMO at a 1.9 mL/min flow rate at two different heparin doses (n = 3 each): low (15 IU/kg/h for eight hours) versus high (50 IU/kg/h for one hour followed by 25 IU/kg/h for seven hours). The experiment continued for eight hours or until the mock oxygenator failed. The mock oxygenator was considered to have failed when its blood flow resistance reached three times its baseline resistance.Results: During ECMO, rats maintained near-normal mean arterial pressure and arterial blood gases with minimal hemodilution. The mock oxygenator thrombus weight was significantly different (p < 0.05) between the low (0.02 ± 0.006 g) and high (0.003 ± 0.001 g) heparin delivery groups, and blood flow resistance was also larger in the low anticoagulation group.Conclusions: This model is a simple, inexpensive system for investigating new anticoagulation agents for ECMO and provides low and high levels of anticoagulation that can serve as control groups for future studies.

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Nao Umei ◽  
Angela Lai ◽  
Jennifer Miller ◽  
Suji Shin ◽  
Kalliope Roberts ◽  
...  

Abstract Background Extracorporeal membrane oxygenation (ECMO) research using large animals requires a significant amount of resources, slowing down the development of new means of ECMO anticoagulation. Therefore, this study developed and evaluated a new rat ECMO model using a 3D-printed mock-oxygenator. Methods The circuit consisted of tubing, a 3D-printed mock-oxygenator, and a roller pump. The mock-oxygenator was designed to simulate the geometry and blood flow patterns of the fiber bundle in full-scale oxygenators but with a low (2.5 mL) priming volume. Rats were placed on arteriovenous ECMO at a 1.9 mL/min flow rate at two different heparin doses (n = 3 each): low (15 IU/kg/h for eight hours) versus high (50 IU/kg/h for one hour followed by 25 IU/kg/h for seven hours). The experiment continued for eight hours or until the mock-oxygenator failed. The mock-oxygenator was considered to have failed when its blood flow resistance reached three times its baseline resistance. Results During ECMO, rats maintained near-normal mean arterial pressure and arterial blood gases with minimal hemodilution. The mock-oxygenator thrombus weight was significantly different (p < 0.05) between the low (0.02 ± 0.006 g) and high (0.003 ± 0.001 g) heparin delivery groups, and blood flow resistance was also larger in the low anticoagulation group. Conclusions This model is a simple, inexpensive system for investigating new anticoagulation agents for ECMO and provides low and high levels of anticoagulation that can serve as control groups for future studies.


PEDIATRICS ◽  
1996 ◽  
Vol 97 (3) ◽  
pp. 295-300
Author(s):  
G. Ganesh Konduri ◽  
Daisy C. Garcia ◽  
Nadya J. Kazzi ◽  
Seetha Shankaran

Objective. Adenosine infusion causes selective pulmonary vasodilation in fetal and neonatal lambs with pulmonary hypertension. We investigated the effects of a continuous infusion of adenosine on oxygenation in term infants with persistent pulmonary hypertension of newborn (PPHN). Design. A randomized, placebo-controlled, masked trial comparing the efficacy of intravenous infusion of adenosine to normal saline infusion over a 24-hour period. Setting. Inborn and outborn level III neonatal intensive care units at a university medical center. Participants. Eighteen term infants with PPHN and arterial postductal Po2 of 60 to 100 Torr on inspired O2 concentration of 100% and optimal hyperventilation (PaCo2 &lt;30 Torr) were enrolled into the study. Study infants were randomly assigned to receive a placebo infusion of normal saline, or adenosine infusion in doses of 25 to 50 µg/kg/min over a 24-hour period. Results. Nine infants each received adenosine or placebo. The two groups did not differ in birth weight, gestational age, or blood gases and ventilator requirements at the time of entry into the study. Four of nine infants in the adenosine group and none of the placebo group had a significant improvement in oxygenation, defined as an increase in postductal PaO2 of ≥20 Torr from preinfusion baseline. The mean PaO2 in the adenosine group increased from 69 ± 19 at baseline to 94 ± 15 during 50 µg/kg/min infusion rate of adenosine and did not change significantly in the placebo group. Arterial blood pressure and heart rate did not change during the study in either group. The need for extracorporeal membrane oxygenation, incidence of bronchopulmonary dysplasia, and mortality were not different in the two groups. Conclusion. Data from this pilot study indicate that adenosine infusion at a dose of 50 µg/kg/min improves PaO2 in infants with PPHN without causing hypotension or tachycardia. Larger trials are needed to determine its effects on mortality and/or need for extracorporeal membrane oxygenation in infants with PPHN.


2019 ◽  
Vol 13 ◽  
pp. 175346661988813 ◽  
Author(s):  
Soo Jin Na ◽  
Hee Jung Choi ◽  
Chi Ryang Chung ◽  
Yang Hyun Cho ◽  
Kiick Sung ◽  
...  

Background: No data are available on the duration of time needed to assess the adequacy of lung function after stopping sweep gas for weaning of venovenous extracorporeal membrane oxygenation (ECMO). The objective of this study was to investigate changes in arterial blood gases (ABGs) during sweep gas off trials in patients receiving venovenous ECMO. Methods: Data on patients receiving venovenous ECMO, with a weaning trial at least once, were collected prospectively from January 2012 through December 2017. Serial changes in ABGs during sweep gas off trial and clinical outcomes after weaning from venovenous ECMO were evaluated. Results: Over the study period, 192 sweep gas off trials occurred in 93 patients: 115 (60%) failed and 77 (40%) were successful. During the trial, significant changes in blood gases were observed within 1 h in all patients. When serial ABGs were compared according to trial off results, there were no significant differences in the pH, PaCO2, and HCO3− trends across time points between successful and failed trials. However, PaO2 (70.6 versus 93.4 mmHg), SaO2 (91.9 versus 95.2%), and PaO2/FiO2 ratio (164.0 versus 233.4) were significantly lower in failed trials than successful trials within 1 h after stopping sweep gas. After 2 h of trial off, no significant change in blood gases was observed until the end of the trial. Conclusions: No change in blood gases was observed 2 h after stopping sweep gas in patients receiving venovenous ECMO. Based on our institutional experience, however, we suggest monitoring for 2 h or more after stopping sweep gas flow to assess if patients are ready for decannulation. The reviews of this paper are available via the supplemental material section.


Perfusion ◽  
2021 ◽  
pp. 026765912110559
Author(s):  
Hoong Lim

Extracorporeal membrane oxygenation (ECMO) can be delivered in veno-arterial (VA) and veno-venous (VV) configurations based on the cannulation strategy. VA and VV ECMO are delivered primarily for haemodynamic and respiratory support in patients with severe heart and lung failure, respectively. The Fick principle describes the relationship between blood flow and oxygen consumption – key parameters in the physiological management of extracorporeal support. This review will discuss the application of the Fick principle in: (i) recirculation in VV ECMO; (ii) the quantification of oxygen delivery (DO2) in VV ECMO and (iii) the quantification of transpulmonary blood flow and systemic arterial oxygen saturation in VA ECMO.


1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.


1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.


The authors studied the state of blood flow in the system of arterial vessels of the head and neck in 30 patients with hypertensive disease (HD) stage I, arterial hypertension (AH), 1st degree – in 26 (86,7 %) and 2nd degree – in 4 (13,3 %) people, with comorbid migraine (M) – in 14 (46,7 %) people and tension-type headache (TTH) – in 16 (53,3 %) people, triplex scanning of extra- and intracranial vessels was performed and measurement of arterial blood pressure was conducted. In patients with AH and comorbid M or TTH, decrease in the velocity and volume parameters of blood flow in the arteries at the extracranial and intracranial level, as well as increase in the indexes of blood flow resistance in comparison with the control, were revealed. In patients with AH and TTH, blood flow in the left vertebral artery and right posterior cerebral artery was lower than in patients with AH and M.


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