Localized multiple minute pulmonary embolism and breathing

1961 ◽  
Vol 16 (5) ◽  
pp. 842-846 ◽  
Author(s):  
Alan D. Horres ◽  
Theodore Bernthal
Keyword(s):  
Pulmonary Embolism ◽  
Glass Bead ◽  
Quantitative Relationship ◽  
Pure Oxygen ◽  
Lung Area ◽  
Pulmonary Embolization ◽  
Lung Lobes

During continuous spirometric recording of breathing, 75–μ glass bead emboli were delivered selectively to single lungs or lung lobes while the remaining lung areas were maintained functionally intact and free of emboli. Postmortem digestion of the lungs revealed the distribution of the emboli and demonstrated complete localization within single lungs or lobes in 12 of 16 experiments. In all instances the frequency of breathing increased and tidal air decreased in a pattern indistinguishable from that attending bilateral multiple minute pulmonary embolism. These effects were abolished by vagotomy but survived inhalation of pure oxygen. Comparison of the quantitative relationship between emboli dose and magnitude of response in localized with that in generalized pulmonary embolization suggests that, within limits, the intensity of the tachypnea is determined by the number of emboli injected regardless of the identity of the gross lung area in which they lodge or the degree of their concentration or dispersion within areas in which they lodge and seems not to favor associated hemodynamic factors as the agency initiating the reflex. Submitted on January 3, 1961

Mechanisms leading to lung edema in pulmonary embolization

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz
Keyword(s):  
Pulmonary Edema ◽  
Capillary Permeability ◽  
Lysergic Acid ◽  
Lung Edema ◽  
Pulmonary Infarction ◽  
Edema Formation ◽  
Lung Lobe ◽  
Pulmonary Embolization ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.

scholarly journals Pulmonary embolism after thrombolysis of hemodialysis grafts.

1997 ◽  
Vol 8 (9) ◽  
pp. 1458-1461
Author(s):  
H F Smits ◽  
P P Van Rijk ◽  
J W Van Isselt ◽  
W P Mali ◽  
H A Koomans ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Clinical Symptoms ◽  
Interventional Procedure ◽  
Pulmonary Perfusion ◽  
Perfusion Scintigraphy ◽  
Substantial Risk ◽  
Pulmonary Embolization ◽  
Hemodialysis Graft

The aim of this study was to determine the incidence of pulmonary embolization occurring after mechanical or pharmacomechanical percutaneous intravascular thrombolysis in 23 patients with occluded hemodialysis grafts. In all patients, pulmonary perfusion scintigraphy was performed before and immediately after thrombolysis. In eight (35%) of the patients, there was evidence of pulmonary embolism resulting from the interventional procedure; however, in only one was there clinical symptoms. It is concluded that there is substantial risk of pulmonary embolism in patients undergoing percutaneous intravascular thrombolysis for an occluded hemodialysis graft.

The Effect of Defibrinogenation on Pulmonary Embolism in Dogs

1976 ◽  
Vol 36 (01) ◽  
pp. 140-149 ◽  
Author(s):  
Alfred G. Meissner ◽  
Gerald O’Sullivan ◽  
Robert A. Macbeth
Keyword(s):  
Pulmonary Embolism ◽  
Mortality Rate ◽  
Superior Vena ◽  
Vena Cava ◽  
Treated Group ◽  
Canine Model ◽  
Control Group ◽  
Cent Mortality ◽  
Pulmonary Embolization

SummaryThe role of fibrinogen in the pathophysiology of pulmonary embolism is not clearly understood. A study was therefore performed in order to determine the effect of defibrinogenation on the sequelae of experimental pulmonary embolization in the canine model. Total defibrinogenation was achieved by treating 15 dogs with Defibrase over a period of three days, and these were studied and compared with 15 control animals. The embolus was produced by injection of a homologous clot into the superior vena cava. A 27 per cent mortality rate was observed after embolism in the control group, but there were no deaths in the Defibrase-treated animals. Hemodynamic and pulmonary gas exchange disturbances occuring in the control group were more severe than those in the treated group and were associated with marked fibrinogen consumption. It is suggested, therefore, that defibrinogenation reduces the mortality and severity of the pathophysiological changes associated with pulmonary embolization probably by inhibition of pulmonary intravascular coagulation and by changing the rheological properties of the blood.

Starling resistor vs. distensible vessel models for embolic pulmonary hypertension

1995 ◽  
Vol 268 (2) ◽  
pp. H817-H827 ◽  
Author(s):  
C. Melot ◽  
M. Delcroix ◽  
J. Closset ◽  
P. Vanderhoeft ◽  
P. Lejeune ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Left Atrial ◽  
Glass Bead ◽  
Inflection Point ◽  
Pulmonary Arterial Pressure ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Closing Pressure

We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065–1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15–26, 1991) best describes pulmonary vascular pressure-flow (Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (Ppa)-Q plots at constant left atrial pressure (Pla) and Ppa-Pla plots at constant Q were investigated in seven dogs before and after 500-micron glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P(i)) of Ppa-Q plots and increased the inflection point of Ppa-Pla plots, above which an increase in Pla is transmitted to Ppa in a ratio of approximately 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the Ppa-Q and Ppa-Pla coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of Ppa-Pla plots and P(i). We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.

scholarly journals Pulmonary embolism: Successful treatment of floating thrombus in SFJ after vena cava filter insertion and surgical thrombectomy

2020 ◽  
Vol 9 ◽  
pp. 204800402097625
Author(s):  
Andrea Ascoli Marchetti ◽  
Bernardo Orellana Davila ◽  
Fabio Massimo Oddi ◽  
Arnaldo Ippoliti
Keyword(s):  
Pulmonary Embolism ◽  
Femoral Vein ◽  
Vena Cava ◽  
Common Femoral Vein ◽  
Floating Thrombus ◽  
Surgical Thrombectomy ◽  
Filter Insertion ◽  
Pulmonary Embolization ◽  
The Common ◽  
Endovascular Devices

The floating venous thrombus in the common femoral vein has a high potential risk for pulmonary embolization. Clinical treatments, using anticoagulants or fibrinolytic, open thrombectomies, or thrombectomies by endovascular devices have all been used. Our case describe an obese patient affected by floating thrombus coming from GSV and diving in common femoral vein successful treated by combined both temporary vena cava insertion and open surgical thrombectomy.

Modulation and roles of the endothelins in the pathophysiology of pulmonary embolism

2003 ◽  
Vol 81 (6) ◽  
pp. 555-569 ◽  
Author(s):  
Bruno Battistini
Keyword(s):  
Pulmonary Embolism ◽  
Cell Biology ◽  
Inflammatory Cells ◽  
Coagulation Cascade ◽  
Pulmonary Endothelial Cells ◽  
Chest X Ray ◽  
Pulmonary Embolization ◽  
Primary Injury

Recent research on the endothelins (ETs) and their pathways in acute pulmonary embolism (APE) has led to significant advances in the understanding of this disease. ETs are potent vasoconstrictors and bronchoconstrictors found abundantly in the lung and can be released by stimuli such as endothelial injury, hypoxia, or thrombin, a key product in the coagulation cascade. Many studies using different approaches and methods of inducing pulmonary embolization, both in vitro and in vivo in various species, have mostly shown that ETs play an important role in the pathophysiology of APE. These results were obtained by comparing the hemodynamic data in the presence or absence of various ETs inhibitors, but also by assessing the modulation of the ET-related elements of this system by molecular, cell biology, and pharmacological methods. Based on the current understanding, a mechanism involving the ET pathway in the pathophysiology of APE is proposed for the reader's considerations. We postulate that ETs are primary mediators in APE based on the following: (i) their source from pulmonary endothelial cells where the primary injury takes place; (ii) their direct vasconstrictive, bronchoconstrictive, and promitogenic effects via distinct ET receptors; and (iii) their indirect effects associated with the secondary release of thromboxane and other mediators, which are released from inflammatory cells and platelets, which together can potentiate the overall hemodynamic response, most specifically the pulmonary vascular bed. Such combined effects of ETs on bronchomotor and vasomotor tone in the lung can adversely affect ventilation perfusion matching and lead to severe hypoxemia without causing significant changes in the chest X-ray of these patients. Thus, we may consider ET inhibitors as future current therapeutic agents in patients with PE.Key words: pulmonary embolism, thrombus, air, pulmonary hypertension, blood gas, hypoxia, endothelin, endothelin receptor, antagonists.

scholarly journals Acute Pulmonary Embolism Decreases Adenosine Plasma Levels in Anesthetized Pigs

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
François Kerbaul ◽  
Youlet By ◽  
Vlad Gariboldi ◽  
Choukri Mekkaoui ◽  
Pierre Fesler ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Plasma Levels ◽  
Coupling Efficiency ◽  
Systolic Pressure ◽  
Vascular Impedance ◽  
Pulmonary Vasoconstriction ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
Pulmonary Embolization ◽  
Pulmonary Arterial

Adenosine plays a role in pulmonary arterial (PA) resistance due to its vasodilator properties. However, the behavior of adenosine plasma levels (APLs) during pulmonary embolism remains unknown. We investigated the effects of gradual pulmonary embolism on right ventricular (RV) contractility and PA coupling and on APLs in an piglet experimental model of RV failure. PA distal resistance by pressure-flow relationships and pulmonary vascular impedance were measured. RV contractility was determined by the end-systolic pressure-volume relationship (Ees), PA effective elastance by the end-diastolic to end-systolic relationship (Ea), and RV-PA coupling efficiency by the Ees/Ea ratio. APLs were measured before and during gradual pulmonary embolization. PA embolism increased PA resistance and elastance, increased Ea from to  mmHg/mL, decreased Ees from to  mmHg/mL, and decreased Ees/Ea from to . APLs decreased from to  μM in the systemic bed and from to  μM in the pulmonary bed during embolism procedure. Pulmonary embolism worsens PA hemodynamics and RV-PA coupling. APLs were reduced, both in the systemic and in the pulmonary bed, leading then to pulmonary vasoconstriction.

Effect of sympathectomy on pulmonary embolism-induced lung edema

1962 ◽  
Vol 202 (4) ◽  
pp. 687-689 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
M. Kandelman ◽  
H. Weisberg
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Artery ◽  
Lung Edema ◽  
Surgical Removal ◽  
Pulmonary Infarction ◽  
Lung Lobe ◽  
Contralateral Lung ◽  
Pulmonary Arterial ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of bilateral surgical removal of the sympathetic chain was determined. Edema is significantly inhibited in ipsilateral and contralateral lung lobes of sympathectomized dogs. It is concluded that the sympathetic nervous system plays a major role as an efferent path in reflex production of pulmonary edema by starch emboli in the dog. There is, incidentally, evidence that sympathectomy lowers the pressure gradient between the pulmonary artery and pulmonary arterial wedge position in the dog.

Pulmonary hemodynamics and arterial oxygen saturation in pulmonary embolism

1965 ◽  
Vol 20 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Paolo Caldini
Keyword(s):  
Pulmonary Embolism ◽  
Oxygen Saturation ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Repeated Injection ◽  
Venous Admixture ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Embolization ◽  
Mechanical Pump ◽  
The Right

Thoracotomized dogs with a reservoir and mechanical pump substitution of the right heart were subjected to pulmonary embolization by repeated injection of glass microspheres (80-120 뀅) or autologous clots (2-3 mm). Airway pressure was controlled by means of a Starling resistor connected to the expiratory line of the respirator. Following embolization with microspheres, the initial abrupt rise in pulmonary arterial pressure was followed by a more gradual increase, interpreted as due to delayed constriction of pulmonary vascular bed. Following emboli injection, systemic arterial oxygen saturation decreased to 82%, venous admixture rose to 30%. When the end-expiratory pressure was increased from 5 to 20 cm of water, the arterial oxygen saturation rose and venous admixture decreased to values not significantly different from pre-embolic levels. These findings suggest that pulmonary hypertension in pulmonary embolism is due not only to a mechanical obstruction of pulmonary vessels, but that some degree of pulmonary vasoconstriction also occurs when small-sized emboli are used. Arterial hypoxemia associated with pulmonary embolism appears to be due to perfusion of non- or poorly ventilated areas of the lung and not to significant blood flow through arteriovenous anastomoses. blood tensions; pulmonary edema; pulmonary venoarterial shunts Submitted on May 4, 1964

A High Voltage Electron Microscopy Study of Sub-Oxide Formation in Vanadium

1971 ◽  
Vol 29 ◽  
pp. 212-213
Author(s):  
R. H. Geiss ◽  
R. L. Ladd ◽  
K. R. Lawless
Keyword(s):  
High Vacuum ◽  
Microscopy Study ◽  
Electron Microscopy Study ◽  
Ultra High Vacuum ◽  
Pure Oxygen ◽  
Pressure Oxidation ◽  
High Voltage Electron Microscopy ◽  
Oxidation Study ◽  
Voltage Electron ◽  
Good Agreement

Detailed electron microscope and diffraction studies of the sub-oxides of vanadium have been reported by Cambini and co-workers, and an oxidation study, possibly complicated by carbon and/or nitrogen, has been published by Edington and Smallman. The results reported by these different authors are not in good agreement. For this study, high purity polycrystalline vanadium samples were electrochemically thinned in a dual jet polisher using a solution of 20% H2SO4, 80% CH3OH, and then oxidized in an ion-pumped ultra-high vacuum reactor system using spectroscopically pure oxygen. Samples were oxidized at 350°C and 100μ oxygen pressure for periods of 30,60,90 and 160 minutes. Since our primary interest is in the mechanism of the low pressure oxidation process, the oxidized samples were cooled rapidly and not homogenized. The specimens were then examined in the HVEM at voltages up to 500 kV, the higher voltages being necessary to examine thick sections for which the oxidation behavior was more characteristic of the bulk.

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