Chapter V: Volume of Contrast Liquid Necessary in Angiography of the Pulmonary Vessels Distally of an Occluded Pulmonary Artery

1954 ◽  
Vol 41 (sup108) ◽  
pp. 41-46
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vessels

Pulmonary Embolization in the Dog: Its Effects on Blood Coagulation and on Pulmonary Artery Pressures

1961 ◽  
Vol 06 (01) ◽  
pp. 025-036 ◽  
Author(s):  
James W. Hampton ◽  
William E. Jaques ◽  
Robert M. Bird ◽  
David M. Selby
Keyword(s):  
Pulmonary Hypertension ◽  
Particulate Matter ◽  
Pulmonary Artery ◽  
Amniotic Fluid ◽  
Blood Coagulation ◽  
Glass Beads ◽  
Pulmonary Vessels ◽  
Pulmonary Embolization ◽  
Biological Nature

Summary1. Infusions containing particulate matter, viz. whole amniotic fluid, amniotic fluid sediment, and glass beads, produce in dogs changes in both early and late phases of the clotting reaction. These changes are associated with the development of pulmonary hypertension.2. When dogs were given an active fibrinolysin followed by an infusion of whole amniotic fluid, the alterations in the clotting mechanism were either delayed or did not appear. No pulmonary hypertension developed in these animals.3. We infer that infusions containing particulate matter will produce in dogs both pulmonary hypertension and changes in the clotting mechanism. Although these are independent changes, both are as closely related to the damage to the pulmonary vessels as they are to the biological nature of the infusions.

Role of the pericytes of intra-acinar pulmonary artery in the structural remodeling of pulmonary vessels

1995 ◽  
Vol 15 (1) ◽  
pp. 16-18 ◽  
Author(s):  
Wu Yong-ping ◽  
Che Dong-yuan ◽  
Zhang Wan-rong ◽  
Li Wen-ying
Keyword(s):  
Pulmonary Artery ◽  
Structural Remodeling ◽  
Pulmonary Vessels

Effect of small doses of 5-hydroxytryptamine (serotonin) on pulmonary circulation in the closed-chest dog

1959 ◽  
Vol 197 (5) ◽  
pp. 963-967 ◽  
Author(s):  
John T. Shepherd ◽  
David E. Donald ◽  
Erland Linder ◽  
H. J. C. Swan
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Veins ◽  
Pulmonary Vessels ◽  
Isolated Perfused Lung ◽  
Small Doses ◽  
Perfused Lung ◽  
Anesthetized Dogs ◽  
Flow Through ◽  
The Difference

5-Hydroxytryptamine (serotonin) was infused into anesthetized dogs at a rate of 20 µg/kg/min. In nine sets of observations on three dogs the increase in the difference of pressure between the pulmonary artery and the left atrium, which averaged 55%, consistently exceeded the increase in pulmonary blood flow, which averaged 16%. 5-HT therefore is a potent constrictor of pulmonary vessels, even in small concentrations. No changes in the pulmonary-artery wedge and pulmonary-vein pressures were detected during the infusions of 5-HT, nor was there any change in the volume of blood between the pulmonary artery and the root of the aorta. With this dose of 5-HT the principal site of the increased resistance to flow through the lungs appeared to be in the precapillary vessels. In the isolated perfused lung, moderate constriction of pulmonary veins also was produced by large doses of 5-HT.

scholarly journals Pulmonary Hemodynamics and Ventilation in Patients With COVID-19-related Respiratory Failure and ARDS

2020 ◽  
Author(s):  
André Becker ◽  
Frederik Seiler ◽  
Ralf M. Muellenbach ◽  
Guy Danziger ◽  
Sebastian Mang ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Respiratory Failure ◽  
Pulmonary Artery ◽  
Distress Syndrome ◽  
Respiratory Infections ◽  
Severe Respiratory Failure ◽  
Shunt Fraction ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vessels ◽  
Microcirculatory Dysfunction

Abstract Background: It has been suggested that COVID-19-associated severe respiratory failure (CARDS) might differ from usual acute respiratory distress syndrome (ARDS) due to failing auto-regulation of pulmonary vessels and higher shunt. We sought to investigate pulmonary hemodynamics and ventilation properties in patients with CARDS compared to patients with ARDS of pulmonary origin. Methods: Retrospective analysis of prospectively collected data of consecutive adults with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 patients treated on our ICU in 04/2020 and comparison of the data to matched controls with ARDS due to respiratory infections treated on our ICU from 01/2014 to 08/2019 and for whom pulmonary artery catheter data were available. Results: CARDS patients (n = 10) had similar ventilation characteristics as compared to ARDS (n = 10) patients. Still, mechanical power applied by ventilation was significantly higher in CARDS patients (23.4 ± 8.9 J/min) than in ARDS (15.9 ± 4.3 J/min; p<0.05). COVID-19 patients had similar pulmonary artery pressure but significantly lower pulmonary vascular resistance, as cardiac output was higher in CARDS vs. ARDS patients (p<0.05). Shunt fraction and dead space were similar in CARDS compared to ARDS (p>0.05) and was in both groups correlated with hypoxemia. The arterio-venous pCO2 difference (DpCO2) was elevated (CARDS 5.5±2.8 mmHg vs. ARDS 4.7±1.1 mmHg; p>0.05) as was P(v-a)CO2/C(a-v)O2 ratio (CARDS mean 2.2±1.5 vs. ARDS 1.7±0.8; p>0.05). Conclusions: Respiratory failure in COVID-19 patients seems to differ only slightly from ARDS regarding ventilation characteristics and pulmonary hemodynamics. Differences are mainly due to increased CO2 production in CARDS patients. Our data indicate microcirculatory dysfunction. More data needs to be collected to assure these findings and gain more pathophysiological insights in COVID-19 and respiratory failure.

What leads to different mediators of alkalosis-induced vasodilation in isolated and in situ pulmonary vessels?

2003 ◽  
Vol 284 (5) ◽  
pp. L799-L807 ◽  
Author(s):  
John B. Gordon ◽  
Michele A. VanderHeyden ◽  
Ted R. Halla ◽  
Edmundo P. Cortez ◽  
Guillermo Hernandez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pulmonary Artery ◽  
Signaling Pathways ◽  
Salt Solution ◽  
Physiological Salt Solution ◽  
Pulmonary Vessels ◽  
Pulmonary Vasodilation ◽  
Oxide Synthase

We previously found that nitric oxide synthase (NOS) inhibition fully blocked alkalosis-induced relaxation of piglet pulmonary artery and vein rings. In contrast, NOS inhibition alone had no effect on alkalosis-induced pulmonary vasodilation in isolated piglet lungs. This study sought to identify factors contributing to the discordance between isolated and in situ pulmonary vessels. The roles of pressor stimulus (hypoxia vs. the thromboxane mimetic U-46619), perfusate composition (blood vs. physiological salt solution), and flow were assessed. Effects of NOS inhibition on alkalosis-induced dilation were also directly compared in 150–350-μm-diameter cannulated arteries and 150–900-μm-diameter, angiographically visualized, in situ arteries. Finally, effects of NOS inhibition on alkalosis-induced vasodilation were measured in intact piglets. NOS inhibition with N ω-nitro-l-arginine fully abolished alkalosis-induced vasodilation in all cannulated arteries but failed to alter alkalosis-induced vasodilation in intact lungs. The results indicate that investigation of other factors, such as perivascular tissue (e.g., adventitia and parenchyma) and remote signaling pathways, will need to be carried out to reconcile this discordance between isolated and in situ arteries.

Carbon dioxide--a major determinant of collateral ventilation

1978 ◽  
Vol 45 (1) ◽  
pp. 69-74 ◽  
Author(s):  
R. J. Traystman ◽  
P. B. Terry ◽  
H. A. Menkes
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Left Atrial ◽  
Co2 Concentration ◽  
Left Atrial Pressure ◽  
Pulmonary Vessels ◽  
Primary Determinant ◽  
Stop Flow ◽  
Collateral Ventilation

The effects of local or systemic CO2 and changes in pulmonary vascular pressure and flow on the mechanics of collateral ventilation were studied in anesthetized, paralyzed dogs. The resistance to collateral ventilation (Rcoll) decreased by 36.1% when the air being infused into the obstructed segment was replaced with 10% CO2 while the animal was ventilated with air. When the air used to ventilate the animals was replaced with 10% CO2 while air was infused into the segment, Rcoll decreased by 38.6%. When blood flow into the pulmonary artery was stopped (stop flow), pulmonary artery and left atrial pressure decreased. Rcoll increased following stop flow to 125% of control; however, the fall in pulmonary vascular pressures preceded the change in Rcoll. The increase in Rcoll with stop flow was markedly reduced when 10% CO2 was infused into the segment. We conclude that collateral channels respond both to the local infusion of CO2 and to the CO2 concentration in the surrounding lung and/or blood, and that the state of distention of pulmonary vessels surrounding collateral ventilatory channels is not a primary determinant of Rcoll. In addition we conclude that bronchiolar channels rather than interalveolar pores are the pathways for collateral ventilation.

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