scholarly journals Blood Clotting Decreases Pulmonary Circulation during the Coronavirus Disease

Mathematics ◽  
2021 ◽  
Vol 9 (19) ◽  
pp. 2401
Author(s):  
Anastasia Mozokhina ◽  
Anass Bouchnita ◽  
Vitaly Volpert
Keyword(s):  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Blood Clotting ◽  
Multiscale Model ◽  
Diagnostic Techniques ◽  
Blood Oxygenation ◽  
Suggested Approach ◽  
Vessel Network ◽  
Mortality Causes ◽  
Vessel Networks

Spontaneous blood clotting in pulmonary circulation caused by thrombo-inflammation is one of the main mortality causes during the COVID-19 disease. Blood clotting leads to reduced pulmonary circulation and blood oxygenation. Lung inflammation can be evaluated with noninvasive diagnostic techniques. However, the correlation of the severity of the inflammation with the pulmonary blood flow has not been established. To address this question, in this work, we develop a multiscale model taking into account the interaction of a local model of thrombus growth with 1D hemodynamics in a vessel network. Flux reduction depending on the level of lung obstruction is evaluated. In particular, the model obtains that an obstruction level of 5% leads to a 12% reduction of blood flux. The suggested approach can be used to investigate the interaction of blood clotting and flow not only in the pulmonary network but also in other complex vessel networks.

Influence of pulmonary blood flow on management and outcome

2011 ◽  
Keyword(s):  
Blood Flow ◽  
Heart Disease ◽  
Pulmonary Circulation ◽  
Early Life ◽  
Pulmonary Blood Flow ◽  
Venous Blood ◽  
Cyanotic Heart Disease ◽  
Capillary Membrane ◽  
Pulmonary Vascular Development ◽  
Alveolar Capillary

Introduction 50Pulmonary vascular development in early life 50Cyanotic heart disease and pulmonary blood flow 52Delivery of systemic venous blood to the alveolar capillary membrane to allow release of waste CO2 and uptake of O2 depends on the integrity of the pulmonary circulation. Too little blood flow to the lungs and the patient is hypoxic; too much and the lungs become oedematous....

scholarly journals Organ-wide 3D-imaging and topological analysis of the continuous microvascular network in a murine lymph node

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Inken D. Kelch ◽  
Gib Bogle ◽  
Gregory B. Sands ◽  
Anthony R. J. Phillips ◽  
Ian J. LeGrice ◽  
...  
Keyword(s):  
Lymph Node ◽  
Blood Vessel ◽  
Topological Analysis ◽  
Computational Techniques ◽  
Vascular Networks ◽  
High Endothelial Venules ◽  
Pixel Resolution ◽  
Vessel Network ◽  
Vessel Networks ◽  
Blood Vessel Network

Abstract Understanding of the microvasculature has previously been limited by the lack of methods capable of capturing and modelling complete vascular networks. We used novel imaging and computational techniques to establish the topology of the entire blood vessel network of a murine lymph node, combining 63706 confocal images at 2 μm pixel resolution to cover a volume of 3.88 mm3. Detailed measurements including the distribution of vessel diameters, branch counts and identification of voids were subsequently re-visualised in 3D revealing regional specialisation within the network. By focussing on critical immune microenvironments we quantified differences in their vascular topology. We further developed a morphology-based approach to identify High Endothelial Venules, key sites for lymphocyte extravasation. These data represent a comprehensive and continuous blood vessel network of an entire organ and provide benchmark measurements that will inform modelling of blood vessel networks as well as enable comparison of vascular topology in different organs.

scholarly journals INFLUENCE OF LIPOSUCTION OF LARGE VOLUME ON SYSTEMIC AND LUNG CIRCULATION, OXIGENATED LUNG FUNCTION

2015 ◽  
Vol 174 (6) ◽  
pp. 17-21
Author(s):  
I. P. Nikolaeva ◽  
A. S. Kapranova ◽  
V. B. Popova ◽  
A. N. Lodyagin ◽  
T. A. Frolova
Keyword(s):  
Lung Function ◽  
Large Volume ◽  
Pulmonary Circulation ◽  
Blood Oxygenation ◽  
Before And After

The authors measured the changes of hemodynamics in 72 patients. It was also estimated a blood oxygenation and volume of liquid sectors of the organism in different degree of obesity before and after liposuction of the large volume. It was shown, that this operation facilitated to an improvement of respiratory lung function due to changes of pulmonary circulation.

Increasing oxygen tension dilates fetal pulmonary circulation via endothelium-derived relaxing factor

1993 ◽  
Vol 265 (1) ◽  
pp. H376-H380 ◽  
Author(s):  
M. H. Tiktinsky ◽  
F. C. Morin
Keyword(s):  
Blood Flow ◽  
Oxygen Tension ◽  
Hyperbaric Oxygen ◽  
Pulmonary Circulation ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Absolute Pressure ◽  
Relaxing Factor ◽  
Pulmonary Arterial ◽  
Endothelium Derived Relaxing Factor

We examined the role of endothelium-derived relaxing factor (EDRF) in the increase in pulmonary blood flow caused by increasing oxygen tension in the lungs of the fetus. Fetal lambs at 133 days of gestation were instrumented for intrauterine measurement of pulmonary arterial, left atrial, and amniotic fluid pressure and pulmonary blood flow. Three days later oxygen tension in the pulmonary arterial blood of the fetus was doubled by having the ewe breathe 100% oxygen at 3 atm absolute pressure. In the control fetuses (n = 5), hyperbaric oxygenation increased pulmonary blood flow eightfold. Blocking EDRF production by infusing 45 mg of NG-monomethyl-L-arginine into the superior vena cava of the fetus over 5 min starting 30 min after the beginning of hyperbaric oxygen reversed the increase in pulmonary blood flow (n = 5). Blocking EDRF production by infusing NG-nitro-L-arginine at 1 mg/min for 60 min starting 30 min before hyperbaric oxygen blunted the initial increase in pulmonary blood flow and eliminated it by the end of the experiment (n = 5). As hyperbaric oxygen did not significantly alter pulmonary arterial or left atrial pressure, changes in pulmonary vascular conductance paralleled those in pulmonary blood flow. We conclude that the majority of the vasodilation of the fetal pulmonary circulation caused by increasing oxygen tension is mediated by EDRF. We speculate that EDRF is involved in maintaining low vascular tone at the relatively high oxygen tension of the postnatal lung.

Leukotriene end organ antagonists increase pulmonary blood flow in fetal lambs

1985 ◽  
Vol 249 (3) ◽  
pp. H570-H576 ◽  
Author(s):  
S. J. Soifer ◽  
R. D. Loitz ◽  
C. Roman ◽  
M. A. Heymann
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Blood Gases ◽  
Physiological Control ◽  
Arterial Blood ◽  
High Pulmonary Vascular Resistance

The factors responsible for maintaining the normally low pulmonary blood flow and high pulmonary vascular resistance in the fetus are not well understood. Since leukotrienes are potent pulmonary vasoconstrictors in many adult animal species, we determined whether leukotrienes were perhaps involved in the control of the fetal pulmonary circulation by studying the effects of putative leukotriene end organ antagonists in two groups of fetal lambs. In six fetal lambs studied at 130-134 days gestation, FPL 55712 increased pulmonary blood flow by 61% (P less than 0.05) and reduced pulmonary vascular resistance by 45% (P less than 0.05). There was a small increase in heart rate but no changes in pulmonary and systemic arterial pressures and systemic arterial blood gases. In six other fetal lambs studied at 130-140 days gestation, FPL 57231 increased pulmonary blood flow by 580% (P less than 0.05) and decreased pulmonary vascular resistance by 87% (P less than 0.05). Pulmonary and systemic arterial pressures decreased (P less than 0.05), and heart rate increased (P less than 0.05). Leukotriene end organ antagonism significantly increases fetal pulmonary blood flow and decreases pulmonary vascular resistance. Leukotrienes may play a role in the physiological control of the fetal pulmonary circulation.

Role of ATP-sensitive potassium channels in ovine fetal pulmonary vascular tone

1992 ◽  
Vol 263 (5) ◽  
pp. H1363-H1368 ◽  
Author(s):  
D. N. Cornfield ◽  
J. A. McQueston ◽  
I. F. McMurtry ◽  
D. M. Rodman ◽  
S. H. Abman
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Vascular Tone ◽  
Left Pulmonary Artery ◽  
Late Gestation ◽  
Flow Transducer ◽  
Pulmonary Vasodilation ◽  
Relaxing Factor

To study the potential role of ATP-sensitive K+ (K+ATP) channels in fetal pulmonary vasoregulation, we studied the effect of a K+ATP channel agonist, lemakalim, and antagonist, glibenclamide, on the fetal pulmonary circulation in nine chronically instrumented late-gestation fetal lambs. Left pulmonary artery (LPA) blood flow was measured with an electromagnetic flow transducer. Brief (10 min) infusions of lemakalim at 3, 10, and 30 micrograms/min into the LPA produced dose-dependent increases in flow from 68 +/- 7 to 96 +/- 11, 160 +/- 15, and 204 +/- 34 ml/min, respectively. The duration of pulmonary vasodilation after the 10-min infusions of lemakalim at 3, 10, and 30 micrograms/min was 20 +/- 3, 47 +/- 10, and 55 +/- 15 min, respectively. Pulmonary blood pressure and flow did not change with intrapulmonary infusion of glibenclamide (10 mg), a K+ATP channel antagonist. Lemakalim-induced pulmonary vasodilation was not affected by nitro-L-arginine (10 mg), a competitive inhibitor of endothelium-dependent relaxing factor, but was blocked by glibenclamide. Prolonged (2 h) intrapulmonary infusions of lemakalim (2-6 micrograms/min) increased pulmonary blood flow by 137%. The increase in pulmonary blood flow was sustained throughout the infusion. Systemic and pulmonary arterial pressures decreased during prolonged infusion. We conclude that K+ATP channels are present in the fetal pulmonary circulation, but do not participate in the regulation of basal pulmonary vascular tone. K+ATP channel activation produces sustained vasodilation that is not mediated by endothelium-derived relaxing factor. We speculate that birth-related stimuli activate K+ATP channels to enhance the pulmonary vasodilation that occurs at birth.

Acute effects of partial compression of ductus arteriosus on fetal pulmonary circulation

1989 ◽  
Vol 257 (2) ◽  
pp. H626-H634 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Base Line ◽  
Acute Effects ◽  
Artery Pressure

To determine the acute effects of increased pulmonary artery pressure and flow on the fetal pulmonary circulation, we studied the response of pulmonary blood flow and vascular reactivity to partial compression of the ductus arteriosus in 22 chronically prepared late-gestation fetal lambs. An inflatable occluder was placed loosely around the ductus arteriosus for compression. Partial compression of the ductus rapidly increased mean pulmonary artery pressure from 45 +/- 1 to 60 +/- 1 mmHg (mean +/- SE) and left pulmonary artery blood flow from 65 +/- 6 to 151 +/- 11 ml/min at 30 min (P less than 0.001; 12 animals). Despite keeping pulmonary artery pressure constant, pulmonary blood flow steadily declined and by 2 h was not different from base-line values. Pulmonary vascular resistance initially fell during the first 30 min of partial compression but then steadily increased and remained elevated above base-line values for at least 30 min after the release of the occluder (P less than 0.001). The decline of pulmonary vascular resistance during the first 30 min of compression was blunted after treatment with the cyclooxygenase inhibitor, meclofenamate (P less than 0.001; 6 animals). Rapid incremental ductus compressions demonstrated a decrease in the slope of the pressure-flow relationship from 3.30 +/- 0.27 (control) to 1.59 +/- 0.21 ml.min-1.mmHg-1 during the postcompression period (P less than 0.001; 12 animals). The vasodilation response to small increases of fetal PO2 was markedly blunted during the postcompression period (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Role of endothelium-derived relaxing factor during transition of pulmonary circulation at birth

1990 ◽  
Vol 259 (6) ◽  
pp. H1921-H1927 ◽  
Author(s):  
S. H. Abman ◽  
B. A. Chatfield ◽  
S. L. Hall ◽  
I. F. McMurtry
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Circulation ◽  
Atrial Natriuretic Factor ◽  
Pulmonary Blood Flow ◽  
Relaxing Factor ◽  
Natriuretic Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Atrial Natriuretic

To examine the potential role of endothelium-derived relaxing factor (EDRF) in regulation of the perinatal pulmonary circulation, we studied the hemodynamic effects of a selective inhibitor of EDRF production, nitro-L-arginine (L-NA), on pulmonary vascular tone and dilator reactivity in the late-gestation ovine fetus and on the pulmonary vasodilation that normally occurs at birth. L-NA infusion decreased pulmonary blood flow from 78 +/- 8 to 65 +/- 6 ml/min (P less than 0.01) and increased pulmonary artery pressure from 48 +/- 2 to 54 +/- 3 mmHg (P less than 0.002, n = 8 animals). To study the selectivity of L-NA on vasodilator responses to endothelium-dependent (acetylcholine) and -independent (atrial natriuretic factor) stimuli, we measured responses to brief infusions of each dilator before and after L-NA treatment. Acetylcholine increased pulmonary blood flow during the control period but not after L-NA treatment. In contrast, L-NA had little effect on the vasodilator response to atrial natriuretic factor. To study the role of EDRF in the transition of the pulmonary circulation from fetal to neonatal conditions, we infused L-NA into the left pulmonary artery immediately before cesarean-section delivery. In comparison with control animals, the rise in pulmonary blood flow at 1 h after delivery was reduced in the L-NA-treated animals (331 +/- 28 in control vs. 185 +/- 16 ml/min in treated, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Development of pulmonary vascular response to oxygen

1988 ◽  
Vol 254 (3) ◽  
pp. H542-H546 ◽  
Author(s):  
F. C. Morin ◽  
E. A. Egan ◽  
W. Ferguson ◽  
C. E. Lundgren
Keyword(s):  
Blood Flow ◽  
Right Ventricular ◽  
Oxygen Tension ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Absolute Pressure ◽  
Fetal Lamb ◽  
Near Term

The ability of the pulmonary circulation of the fetal lamb to respond to a rise in oxygen tension was studied from 94 to 146 days of gestation. The unanesthetized ewe breathed room air at normal atmospheric pressure, followed by 100% oxygen at three atmospheres absolute pressure in a hyperbaric chamber. In eleven near-term lambs (132 to 146 days of gestation), fetal arterial oxygen tension (PaO2) increased from 25 +/- 1 to 55 +/- 6 Torr (mean +/- SE), which increased the proportion of right ventricular output distributed to the fetal lungs from 8 +/- 1 to 59 +/- 5%. In five very immature lambs (94 to 101 days of gestation), fetal PaO2 increased from 27 +/- 1 to 174 +/- 70 Torr, but the proportion of right ventricular output distributed to the lung did not change, 8 +/- 1 to 9 +/- 1%. In five of the near-term lambs, pulmonary blood flow was measured. It increased from 34 +/- 3 to 298 +/- 35 ml.kg fetal wt-1.min-1, an 8.8-fold increase. We conclude that the pulmonary circulation of the fetal lamb does not respond to an increase in oxygen tension before 101 days of gestation; however, near term an increase in oxygen tension alone can induce the entire increase in pulmonary blood flow that normally occurs after the onset of breathing at birth.

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