Systemic blood flow to the lung after bronchial artery occlusion in anesthetized sheep

1992 ◽  
Vol 72 (5) ◽  
pp. 1701-1707 ◽  
Author(s):  
E. M. Baile ◽  
D. Minshall ◽  
P. B. Harrison ◽  
P. M. Dodek ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Bronchial Artery ◽  
Experimental Studies ◽  
Middle Lobe ◽  
Arterial Blood Flow ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Complete Obstruction ◽  
Caudal Lobe ◽  
Arterial Blood

To compare the effectiveness of different embolizing agents in reducing or redistributing bronchial arterial blood flow, we measured systemic blood flow to the right lung and trachea in anesthetized sheep by use of the radioactive microsphere method before and 1 h after occlusion of the bronchoesophageal artery (BEA) as follows: injection of 4 ml ethanol (ETOH) into BEA (group 1, n = 5), injection of approximately 0.5 g polyvinyl alcohol particles (PVA) into BEA (group 2, n = 5), or ligation of BEA (group 3, n = 5). After occlusion, angiography showed complete obstruction of the bronchial vessels. There were no changes in tracheal blood flow in any of the groups. Injection of ETOH produced a 75 +/- 14% (SD) reduction in flow to the middle lobe (P less than 0.02) and a 75 +/- 13% reduction to the caudal lobe (P less than 0.01), whereas injection of PVA produced a smaller reduction in flow to these two lobes (41 +/- 66 and 51 +/- 54%, respectively). After BEA ligation there was a 52 +/- 29% reduction in flow to the middle lobe and a 53 +/- 38% reduction to the caudal lobe (P less than 0.05). This study has significant implications both clinically and experimentally; it illustrates the importance of airway collateral circulation, in that apparently complete radiological obstruction of the BEA does not necessarily mean complete obstruction of systemic blood flow. We also conclude that, in experimental studies in which the role of the bronchial circulation in airway pathophysiology is examined, ETOH is the agent of choice.

Forward blood flow provoked by changing intravascular pressure using an extracorporeal circulation during cardiopulmonary resuscitation

2020 ◽  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Resuscitation ◽  
Chest Compression ◽  
Intrathoracic Pressure ◽  
Arterial Blood Flow ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Closed Chest ◽  
Arterial Blood ◽  
Intravascular Pressure

Since both “cardiac pump” and “thoracic pump” theories have been proved during cardiopulmonary resuscitation (CPR), the mechanism of forward blood flow during closed chest compression still remains open to question. The cardiac pump seems to work by the direct compression of the cardiac ventricles between the sternum and vertebral column. A pressure gradient created between the ventricle and aorta generates systemic blood flow. However, the thoracic pump mechanism presumes chest compression causes a rise in intrathoracic pressure which generates a blood flow from the thoracic cavity to the systemic circulation. Retrograde blood flow from the right heart into the systemic veins is prevented by a concomitant collapse of veins at the thoracic inlet. We hypothesize that the intrinsic decrease of vascular resistance from the aorta to peripheral arteries and the existence of competent venous valves enable blood to flow unidirectionally by the fluctuation of intravascular pressures during closed chest compression. The purpose of this study is to prove an antegrade arterial blood flow without cardiac compression and intrathoracic pressure changes in an animal cardiac arrest model. We demonstrate that arterial pulses can be developed by using an extracorporeal circuit, resulting in forward blood flow from the aorta through the systemic vasculature. It can be suggested that changes in intravascular pressure provoked by either cardiac or thoracic pump generate systemic blood flow during closed chest compression, while systemic vascular patency and valve function may be required for successful CPR.

Abstract 183: Differences in Genetic Regulation of Carotid Stenosis and Thickening in Mice

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Janice Gerloff ◽  
Katrien Genyn ◽  
Aldons J Lusis ◽  
Vyacheslav A Korshunov
Keyword(s):  
Blood Flow ◽  
Carotid Stenosis ◽  
Inbred Mice ◽  
Experimental Studies ◽  
Arterial Stenosis ◽  
Arterial Blood Flow ◽  
Mouse Strains ◽  
Occipital Artery ◽  
Carotid Imt ◽  
Arterial Blood

Introduction Most clinical and experimental studies are focused on the artery wall using a carotid intima-media thickening (IMT) phenotype. In physiological remodeling increases in IMT are coupled with increased arterial dimensions that preserve arterial blood flow. In contrast, pathological remodeling results in arterial stenosis. The goal of this study was to investigate genetic mechanisms of the carotid stenosis in inbred mice. Methods and Results We ligated external and internal branches of the left carotid artery, leaving the occipital artery patent to induce carotid IMT in mice. We evaluated flow-induced carotid remodeling in 9-12 week old males of 30 inbred mouse strains (n=270). Relative reductions in the left carotid blood flow were very similar among the mouse strains (Mean+SD= -86+7%) after two weeks after ligation. All animals were perfusion fixed with formalin and carotid arteries were stained with hematoxylin and eosin. There was less than 2-fold variation in carotid traits in controls. However, ligation resulted in a greater variation of carotid IMT (~6-fold) compared to carotid stenosis (~3-fold). The highest carotid IMT values were in SEA/GnJ, while the lowest IMT was in C3H/HeJ mice. Carotid stenosis was >60% in SEA/GnJ and SJL/J strains. There was significant correlation (R 2 =0.40) between carotid stenosis and IMT across 30 strains. We performed genome-wide association by using Efficient Mixed Model Association method for carotid traits in 30 inbred mice. Comparable numbers of genetic loci were associated with carotid IMT and stenosis after ligation. However, none of these loci overlap between the carotid stenosis and carotid IMT. Conclusions We found that major genetic modifiers for carotid stenosis are different from those that control carotid IMT. Our data also suggest that identification of mechanisms that determine carotid stenosis is difficult through studies on the carotid IMT.

Systemic blood flow to sheep lung: comparison of flow probes and microspheres

1992 ◽  
Vol 73 (5) ◽  
pp. 1996-2003 ◽  
Author(s):  
K. D. Ashley ◽  
D. N. Herndon ◽  
L. D. Traber ◽  
D. L. Traber ◽  
K. Deubel-Ashley ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Bronchial Artery ◽  
Left Lung ◽  
Vena Cava ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Flow Probe ◽  
Time Flow ◽  
Conscious Sheep

Discrepancies exist between experimental measurements of the systemic blood flow to sheep lung by use of microsphere techniques and flow probes on the bronchial artery. In these studies, we simultaneously measured the blood flow through the bronchial artery, using a transit time flow probe, and the systemic blood flow to left lung, using radioactive microspheres. All measurements were made on conscious sheep previously prepared with chronic catheterizations of the left atrium, aorta, and vena cava and a flow probe around the bronchial artery. Inflatable occluder cuffs were placed around the pulmonary and bronchoesophageal arteries. Bronchial artery blood flow in six sheep was 25.3 +/- 5.2 ml/min or 0.4% of the cardiac output. Systemic blood flow to left lung, measured with microspheres, was 54.1 +/- 14.2 ml/min. Calculated systemic blood flow to that portion of sheep lung perfused by the bronchial artery was 127.6 +/- 35.3 ml/min or 1.9% of cardiac output. Occlusion of the bronchoesophageal artery reduced bronchial artery flow to near zero, whereas total systemic blood to the lung was reduced by only 55%. Blood flow to the intraparenchymal cartilaginous airways was reduced 60–90% after occlusion of the bronchoesophageal artery. Sheep, like most mammals, have multiple and complex systemic arterial inputs to the lungs. We conclude that multiple branches of the bronchoesophageal artery provide most but not all of the systemic blood flow to the intraparenchymal cartilaginous airways but that over one-half of the total systemic blood flow to sheep lung comes from sources other than the common bronchial artery.

Measurement of bronchial arterial blood flow and bronchovascular resistance in sheep

1985 ◽  
Vol 59 (2) ◽  
pp. 305-308 ◽  
Author(s):  
N. B. Charan ◽  
G. M. Turk ◽  
R. Ripley
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Bronchial Artery ◽  
Arterial Blood Flow ◽  
Reservoir Volume ◽  
Mean Pulmonary Arterial Pressure ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Artery Flow

We studied the bronchial arterial blood flow (Qbr) and bronchial vascular resistance (BVR) in sheep prepared with carotid-bronchial artery shunt. Nine adult sheep were anesthetized, and through a left thoracotomy a heparinized Teflon-tipped Silastic catheter was introduced into the bronchial artery. The other end of the catheter was brought out through the chest wall and through a neck incision was introduced into the carotid artery. A reservoir filled with warm heparinized blood was connected to this shunt. The height of blood column in the reservoir was kept constant at 150 cm by adding more blood. Qbr was measured, after interrupting the carotid-bronchial artery flow, by the changes in the reservoir volume. The bronchial arterial back pressure (Pbr) was measured through the shunt when both carotid-bronchial artery and reservoir Qbr had been temporarily interrupted. The mean Qbr was 34.1 +/- 2.9 (SE) ml/min, Pbr = 17.5 +/- 3.3 cmH2O, BVR = 3.9 +/- 0.5 cmH2O X ml-1 X min, mean pulmonary arterial pressure = 21.5 +/- 3.6 cmH2O, and pulmonary capillary wedge pressure (Ppcw) = 14.3 +/- 3.7 cmH2O. We further studied the effect of increased left atrial pressure on these parameters by inflating a balloon in the left atrium. The left atrial balloon inflation increased Ppcw to 25.3 +/- 3.1 cmH2O, Qbr decreased to 21.8 +/- 2.4 ml/min (P less than 0.05), and BVR increased to 5.5 +/- 1.0 cmH2O.ml-1.min (P less than 0.05).

IN SITU AND PILOT ORGAN PERFUSION TECHNIQUES FOR THE STUDY OF METABOLIC DYNAMICS

1972 ◽  
Vol 68 (2_Supplb) ◽  
pp. S9-S25 ◽  
Author(s):  
John Urquhart ◽  
Nancy Keller
Keyword(s):  
Cardiac Output ◽  
Large Fraction ◽  
Experimental Studies ◽  
Test Substance ◽  
Organ Perfusion ◽  
Systemic Blood ◽  
Experimental Control ◽  
Arterial Blood ◽  
Vascular Connections

ABSTRACT Two techniques for organ perfusion with blood are described which provide a basis for exploring metabolic or endocrine dynamics. The technique of in situ perfusion with autogenous arterial blood is suitable for glands or small organs which receive a small fraction of the animal's cardiac output; thus, test stimulatory or inhibitory substances can be added to the perfusing blood and undergo sufficient dilution in systemic blood after passage through the perfused organ so that recirculation does not compromise experimental control over test substance concentration in the perfusate. Experimental studies with the in situ perfused adrenal are described. The second technique, termed the pilot organ method, is suitable for organs which receive a large fraction of the cardiac output, such as the liver. Vascular connections are made between the circulation of an intact, anaesthetized large (> 30 kg) dog and the liver of a small (< 3 kg) dog. The small dog's liver (pilot liver) is excised and floated in a bath of canine ascites, and its venous effluent is continuously returned to the large dog. Test substances are infused into either the hepatic artery or portal vein of the pilot liver, but the small size of the pilot liver and its blood flow in relation to the large dog minimize recirculation effects. A number of functional parameters of the pilot liver are described.

Modeling Elastic Walls in Lattice Boltzmann Simulations of Arterial Blood Flow

2013 ◽  
Vol 23 (2) ◽  
Author(s):  
Xenia Descovich ◽  
Giuseppe Pontrelli ◽  
Sauro Succi ◽  
Simone Melchionna ◽  
Manfred Bammer
Keyword(s):  
Blood Flow ◽  
Lattice Boltzmann ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Lattice Boltzmann Simulations ◽  
Elastic Walls

scholarly journals Sustained Inflation Reduces Pulmonary Blood Flow during Resuscitation with an Intact Cord

Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 353
Author(s):  
Jayasree Nair ◽  
Lauren Davidson ◽  
Sylvia Gugino ◽  
Carmon Koenigsknecht ◽  
Justin Helman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Perinatal Asphyxia ◽  
Arterial Blood Flow ◽  
Positive Pressure ◽  
Optimal Timing ◽  
Delayed Cord Clamping ◽  
Arterial Blood ◽  
Cord Clamping ◽  
Sustained Inflation ◽  
Near Term

The optimal timing of cord clamping in asphyxia is not known. Our aims were to determine the effect of ventilation (sustained inflation–SI vs. positive pressure ventilation–V) with early (ECC) or delayed cord clamping (DCC) in asphyxiated near-term lambs. We hypothesized that SI with DCC improves gas exchange and hemodynamics in near-term lambs with asphyxial bradycardia. A total of 28 lambs were asphyxiated to a mean blood pressure of 22 mmHg. Lambs were randomized based on the timing of cord clamping (ECC—immediate, DCC—60 s) and mode of initial ventilation into five groups: ECC + V, ECC + SI, DCC, DCC + V and DCC + SI. The magnitude of placental transfusion was assessed using biotinylated RBC. Though an asphyxial bradycardia model, 2–3 lambs in each group were arrested. There was no difference in primary outcomes, the time to reach baseline carotid blood flow (CBF), HR ≥ 100 bpm or MBP ≥ 40 mmHg. SI reduced pulmonary (PBF) and umbilical venous (UV) blood flow without affecting CBF or umbilical arterial blood flow. A significant reduction in PBF with SI persisted for a few minutes after birth. In our model of perinatal asphyxia, an initial SI breath increased airway pressure, and reduced PBF and UV return with an intact cord. Further clinical studies evaluating the timing of cord clamping and ventilation strategy in asphyxiated infants are warranted.

Incidence and risk factors of early arterial blood flow stasis during first radioembolization of primary and secondary liver malignancy using resin microspheres: an initial single-center analysis

2015 ◽  
Vol 26 (8) ◽  
pp. 2779-2789 ◽  
Author(s):  
Claus Christian Pieper ◽  
Winfried A. Willinek ◽  
Daniel Thomas ◽  
Hojjat Ahmadzadehfar ◽  
Markus Essler ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Flow ◽  
Arterial Blood Flow ◽  
Single Center ◽  
Liver Malignancy ◽  
Arterial Blood ◽  
Resin Microspheres ◽  
Flow Stasis
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