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

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.

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz

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.


1963 ◽  
Vol 204 (4) ◽  
pp. 619-625 ◽  
Author(s):  
John W. Hyland ◽  
George T. Smith ◽  
Lockhart B. McGuire ◽  
Donald C. Harrison ◽  
Florence W. Haynes ◽  
...  

Pulmonary embolism was produced in 30 closed-chest 8-kg dogs with polystyrene spheres, glass beads, or blood clots of precise graded size. The sizes matched selectively the internal diameter of pulmonary arteries from lobar branches (5–6 mm) down to atrial arteries (0.17 mm). Emboli were injected into the right atrium until the pressure in the pulmonary artery rose 5–10 mm Hg. The number of emboli of a given size required to produce this incipient pulmonary hypertension was compared with the number of vessels of that same size as determined from the literature as well as by postmortem injection with Schlesinger mass. The number of emboli bore a constant relation to the number of vessels of that same size. With each size, the majority of vessels had to be occluded before pulmonary hypertension appeared. This was true even in the absence of anesthesia. The results support the thesis that mechanical blockade rather than vasoconstriction is the mechanism by which pulmonary hypertension is produced by emboli occluding pulmonary arterial (as opposed to arteriolar) vessels.


1964 ◽  
Vol 207 (3) ◽  
pp. 641-646 ◽  
Author(s):  
H. Weisberg ◽  
J. F. Lopez ◽  
M. H. Luria ◽  
L. N. Katz

Bilateral pulmonary edema was present in dogs autopsied 24 hr after pulmonary embolization. Mean pulmonary artery pressure remained elevated during this period. Most others, which survived up to the 3rd day and died spontaneously after embolization, showed edema at autopsy. Longer survivors showed no edema. Edema severity during the first 2 days was roughly related to the pressure rise during the 1st hr after embolization. Immediate significant pulmonary artery pressure rise, predominant in dogs succumbing by the 3rd day, was not as common in those surviving longer. Thus, survival time showed an inverse relationship to immediate pulmonary artery pressure elevation. In another 17 dogs followed as long as 10–23 months after embolization, 53% showed a significant rise in pressure at the end and some animals also had histologic pulmonary vascular changes. In some instances acute elevation of pulmonary artery pressure at embolization may anticipate chronic pulmonary arterial hypertension. The problem is the creation of embolism which elevates pulmonary arterial pressure without animals succumbing acutely to the associated pulmonary edema.


2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Hyun Ju Yoon ◽  
Kye Hun Kim ◽  
Myung Ho Jeong ◽  
Jeong Gwan Cho ◽  
Jong Chun Park

Abstract Background Primary thrombosis of the pulmonary vasculatures without extra-pulmonary sources of embolism are uncommon. Here, we report 2 cases of thrombosis of the stump of the remnant pulmonary vasculatures after lung resection complicated by embolic events with review of the literature. Case presentation A 75-year-old female was consulted to evaluate cardiac source of embolism for acute cerebral infarction. The patient underwent left upper lobectomy because of lung cancer 2 years ago. Cardiovascular imaging revealed about 1.6 cm × 1.4 cm sized thrombus within the remnant stump of the left superior pulmonary vein. The patient was treated by anticoagulation with warfarin, because the patients refused surgical removal of thrombus. A 57-year-old female who had a history of right pneumonectomy 10 years ago presented with dyspnea. Cardiovascular imaging revealed 1.7 × 1.5 cm sized thrombus in the right pulmonary artery stump and small pulmonary embolism in the left lower segmental pulmonary artery. The patient was treated by long-term anticoagulation with warfarin, and the thrombus and pulmonary embolism were resolved. Conclusion The present cases demonstrated that very late thrombosis of the remnant pulmonary vascular structures and subsequent fatal embolic complications can develope even several years later after lung resection. Therefore, the dead space of the remnant vascular structures should be minimized during lung resection surgery, and the developement of delayed thromboembolic complications associated with vascular stump thrombosis should be carefully monitored.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Julie Van Maercke ◽  
Anne-Sophie Van Rompuy ◽  
Willy Poppe ◽  
Tom Verbelen ◽  
Marion Delcroix ◽  
...  

Intravascular leiomyomatosis (IVL) is a very rare condition. It is characterized by the proliferation of benign smooth muscle cells within vascular structures without invasion of these tissues. Symptoms depend on the site of origin and the extent of invasion. Rarely, this neoplasm is located in the inferior vena cava or in the pulmonary vasculature potentially causing symptoms of dyspnea, chest pain, or syncope. We report the case of a 53-year-old woman who was referred to our hospital with extensive pulmonary embolism comprising of a subtotal occlusion of the right pulmonary artery with extension into the left pulmonary artery. Due to persistent dyspnea (New York Heart Association class II) despite anticoagulation, after a six-week period, imaging was repeated and showed stable findings. As she was not responding to adequate anticoagulant therapy, intima sarcoma of the pulmonary artery was suspected, and a pulmonary endarterectomy (PEA) was performed. A smooth, white, intravascular mass was easily and completely removed. Analysis demonstrated a lesion consisting of cells without atypia, showing expression of alpha-smooth muscle actin (alpha SMA) and desmin with partial expression of estrogen receptor (ER) and progesterone receptor (PR), leading to the diagnosis of intravascular leiomyomatosis. The patient fully recovered. Complete surgical removal of the intravascular tumor is recommended to relieve symptoms and prevent possible complications. Clinicians have to be aware that in unresolved pulmonary embolism, nonthrombotic and rare causes, like an intima sarcoma or intravascular leiomyomatosis, should be considered.


2016 ◽  
Vol 19 (10) ◽  
pp. 1007-1012 ◽  
Author(s):  
Tekla M Lee-Fowler ◽  
Robert C Cole ◽  
A Ray Dillon ◽  
D Michael Tillson ◽  
Rachel Garbarino ◽  
...  

Objectives Bronchial lumen to pulmonary artery diameter (BA) ratio has been utilized to investigate pulmonary pathology on high-resolution CT images. Diseases affecting both the bronchi and pulmonary arteries render the BA ratio less useful. The purpose of the study was to establish bronchial lumen diameter to vertebral body diameter (BV) and pulmonary artery diameter to vertebral body diameter (AV) ratios in normal cats. Methods Using high-resolution CT images, 16 sets of measurements (sixth thoracic vertebral body [mid-body], each lobar bronchi and companion pulmonary artery diameter) were acquired from young adult female cats and 41 sets from pubertal female cats. Results Young adult and pubertal cat BV ratios were not statistically different from each other in any lung lobe. Significant differences between individual lung lobe BV ratios were noted on combined age group analysis. Caudal lung lobe AV ratios were significantly different between young adult and pubertal cats. All other lung lobe AV ratios were not significantly different. Caudal lung lobe AV ratios were significantly different from all other lung lobes but not from each other in both the young adult and pubertal cats. Conclusions and relevance BV ratio reference intervals determined for individual lung lobes could be applied to both young adult and pubertal cats. Separate AV ratios for individual lung lobes would be required for young adult and pubertal cats. These ratios should allow more accurate evaluation of cats with concurrent bronchial and pulmonary arterial disease.


2021 ◽  
Vol 93 (4) ◽  
pp. 363-368
Author(s):  
Evgeniy S. Mazur ◽  
Vera V. Mazur ◽  
Robert M. Rabinovich ◽  
Mariya A. Bachurina

Aim. To detect the effect of the feature of the pulmonary vascular obstruction on the clinical manifestations of pulmonary embolism (PE). Materials and methods. The 127 patients with PE were included in this study. PE verified with multidetector computed tomography with pulmonary angiography. Among them were 57 patients with high-risk PE, and 39 patients with intermediate-risk PE and 31 patients with low-risk PE. The pulmonary artery obstruction index and the obstruction level were determined. Results. The mean values of the pulmonary artery obstruction index in high and intermediate risk patients were 42.5%, and in low risk patients 12.5% (p0.001). The trunk or main branches obstruction was in 80.7% of high-risk PE patients, the main or lobar branches obstruction in 92.3% of intermediate-risk patients and lobar or segmental branches obstruction in 93.5% of low-risk patients. Pulmonary infarction was detected in 89.2% of patients with the segmental branches obstruction and with another level of obstruction in 28.0% of patients only (p0.001). Conclusion. The hemodynamic disorder in pulmonary embolism associate with the pulmonary artery obstruction index of more than 30%. The development of obstructive shock is associated with the pulmonary artery trunk obstruction, and the development of pulmonary infarction associated with the segmental branches obstruction.


2021 ◽  
Vol 99 (1) ◽  
pp. 6-14
Author(s):  
Y. V. Ovchinnikov ◽  
M. V. Zelenov ◽  
V. S. Polovinka ◽  
E. V. Kryukov

The concept of high-risk pulmonary artery embolism determines that verification of the occlusion of the pulmonary arterial bed requires urgent restoration of pulmonary blood flow in such patients. Thrombolytic therapy is currently recognized as the main treatment for pulmonary artery thromboembolism. It can save patients’ lives, prevent the development of chronic post embolic pulmonary hypertension and thromboembolism recurrence. The literature review presents thrombolytic medications used in the treatment of pulmonary thromboembolism, describes indications for thrombolytic therapy, comparative efficiency and safety of various thrombolytics. The main complications of thrombolytic therapy are described and the issues of increasing its safety are raised. Criteria for the success of thrombolysis are early diagnosis, accurate risk stratification, and adequate use of reperfusion agents in patients with high-risk or transitionally high-risk of pulmonary embolism.


2019 ◽  
Vol 39 (4) ◽  
pp. 704-718 ◽  
Author(s):  
Yuan Huang ◽  
Yi-Wei Liu ◽  
Hai-Zhou Pan ◽  
Xiao-Ling Zhang ◽  
Jun Li ◽  
...  

Objective— Pulmonary arterial hypertension is characterized by progressive pulmonary vascular remodeling and persistently elevated mean pulmonary artery pressures and pulmonary vascular resistance. We aimed to investigate whether transthoracic pulmonary artery denervation (TPADN) attenuated pulmonary artery (PA) remodeling, improved right ventricular (RV) function, and affected underlying mechanisms. We also explored the distributions of sympathetic nerves (SNs) around human PAs for clinical translation. Approach and Results— We identified numerous SNs in adipose and connective tissues around the main PA trunks and bifurcations in male Sprague Dawley rats, which were verified in samples from human heart transplant patients. Pulmonary arterial hypertensive rats were randomized into TPADN and sham groups. In the TPADN group, SNs around the PA trunk and bifurcation were completely and accurately removed under direct visualization. The sham group underwent thoracotomy. Hemodynamics, RV function, and pathological changes in PA and RV tissues were measured via right heart catheterization, cardiac magnetic resonance imaging, and pathological staining, respectively. Compared with the sham group, the TPADN group had lower mean pulmonary arterial pressures, less PA and RV remodeling, and improved RV function. Furthermore, TPADN inhibited neurohormonal overactivation of the sympathetic nervous system and renin-angiotensin-aldosterone system and regulated abnormal expressions and signaling of neurohormone receptors in local tissues. Conclusions— There are numerous SNs around the rat and human main PA trunks and bifurcations. TPADN completely and accurately removed the main SNs around PAs and attenuated pulmonary arterial hypertensive progression by inhibiting excessive activation of the sympathetic nervous system and renin-angiotensin-aldosterone system neurohormone-receptor axes.


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