scholarly journals STUDIES IN INFARCTION

1913 ◽  
Vol 18 (5) ◽  
pp. 507-511 ◽  
Author(s):  
Howard T. Karsner ◽  
Albert A. Ghoreyeb
Keyword(s):  
Pulmonary Artery ◽  
High Pressures ◽  
Bronchial Artery ◽  
Normal Lung ◽  
Bronchial Arteries ◽  
Pulmonary Vessels ◽  
Pulmonary Pressure ◽  
Two Systems ◽  
Bronchial System ◽  
Bronchial Vessels

From series 1 it is concluded that increases in pulmonary pressure improve the circulation in the embolic areas and that decreases in pulmonary pressure limit the circulation in the same areas. In this series the bronchial vessels showed no tendency to take up the circulation in the area of pulmonary embolism until the pulmonary pressure was as low as zero, and then only to a limited degree. It has been shown, however, that in the circulation of an entire lobe the fall to zero pressure in the pulmonary circuit is followed by almost complete taking over of the circulation by the bronchial arterial supply and the most reasonable explanation of why this does not occur when embolism is present in a smaller branch of the pulmonary is the inference that the physiological anastomosis between the two systems takes place in part before the pulmonary artery breaks up into branches small enough to be occluded by seeds of about three millimeters in diameter. From series 2 it is concluded that although increases in pressure in the bronchial arteries cause somewhat greater inflow of bronchial injection mass into the embolic area, extremely high pressures are not sufficient to provide for complete circulation in the same district. This fact would tend to support further the belief that the anastomosis between the two vascular systems occurs before the smaller divisions of the pulmonary artery are reached. From series 3 it is concluded that with a zero pressure in the pulmonary artery there is improved injection of the embolic area through the bronchial artery which is to be expected when it is remembered that zero pressure in the pulmonary artery favors a taking over of the circulation by the bronchial system. What pressure is found in the smaller pulmonary vessels is supplied by the bronchials. It has been shown that the anastomosis between the two systems probably occurs before the branches are reached which would provide lodgment for the turnip radish seeds. The pressure supplied by the bronchials would naturally be less beyond this point and hence the injection would be less complete in the embolic area than in the normal lung. This is shown to be the case by the results of the experiment. From series 4 it is concluded that the absence of pressure in the bronchial circulation favors a better injection of the embolic area through the pulmonary vessels, which is to be expected when it is recalled that not until zero pressure is reached in the bronchial circuit does the pulmonary artery supply the bronchial vessels with blood. Throughout the study it was found that whenever the two vascular systems were injected simultaneously the pleural vessels over the embolic area, as well as those over the normal lung, received their supply from the pulmonary vessels. When only one system was used for injection the pleural vessels over the embolic area showed about the same degree of injection as those of the embolic area itself.

scholarly journals A STUDY OF THE RELATION OF PULMONARY AND BRONCHIAL CIRCULATION

1913 ◽  
Vol 18 (5) ◽  
pp. 500-506 ◽  
Author(s):  
Albert A. Ghoreyeb ◽  
Howard T. Karsner
Keyword(s):  
Pulmonary Artery ◽  
Lung Tissue ◽  
Bronchial Artery ◽  
Venous Blood ◽  
Pulmonary Arteries ◽  
The Other ◽  
Main Trunk ◽  
Intimate Contact ◽  
Bronchial Arteries ◽  
Bronchial Circulation

The most striking point brought out in this study is that as long as a definite pressure is maintained in either the pulmonary or bronchial circulations, the admixture of bloods is extremely limited. It is easily conceivable that more mixture occurs normally than under the conditions of the experiment, but there is no reason for considering this to be a large difference. If, however, in either system the pressure sinks to zero the possibility of supply by the other system becomes evident. It takes much longer for the mass injected through the bronchial arteries to penetrate to all parts of the lung than when the mass is injected through the pulmonary artery; but when accomplished, the injection reaches to all capillaries including those of the pleura, the only vessels remaining uninjected being the larger trunks of the pulmonary artery. On the other hand, the injection of the bronchial vessels by way of the pulmonary arteries is not complete with normal pressure, but occurs rapidly when a high pulmonary pressure is employed. It is therefore probable that either circulation can suffice for the simple nutritive demands of the lung if the other system is interfered with. It has been shown that embolism of the pulmonary artery, without other circulatory disturbance, does not lead to necrosis of the affected area of the lung, but it is probable that the preservation of circulation is not due to collateral bronchial circulation so much as to the free anastomosis and early division into capillaries of the pulmonary artery. In support of this statement is the fact that the appearance is not altered when the bronchials are ligated at their origin. The same ligation shows no subsequent interference with the nutrition of the bronchi up to a period of five weeks, demonstrating that the pulmonary circulation is sufficient to provide for the nutrition of the bronchi. If, however, as Virchow has shown, the pulmonary artery supplying an entire lobe be occluded, the bronchial circulation can and does suffice for the nutrition of the lobe. In the case of the occlusion of a branch of the pulmonary artery the pressure in the area interfered with does not sink to zero because of the collateral circulation in this area; whereas, if the main trunk is occluded no collateral supply is available, the pressure sinks to zero, and the bronchial artery becomes available as a source of blood supply. It must be remembered that the lung tissue, as a whole, has ready access to oxygen and this gas is the nutritive element acquired by the blood in the lungs. From these studies it would appear that the part of the lung tissue not in intimate contact with oxygen in the air is supplied by oxygenated blood of the bronchial arteries, and that the tissues through which the pulmonary blood circulates take up whatever organized nutriment they need from the pulmonary blood and possibly provide for their oxygen and carbon dioxide interchange (which must be very slight) either directly with the alveolar air, or by finding sufficient oxygen in the venous blood of the pulmonary artery. The studies of the injected specimens confirm Küttner's findings of a very rapid breaking up of the pulmonary artery into capillaries. In all the specimens studied it was found that although the pleural vessels can be injected by way of the bronchial arteries when there is zero pressure in the pulmonary arteries, yet when the two sets of vessels are injected simultaneously in the dog, the pleural vessels invariably derive their supply of injection mass from the pulmonary artery.

scholarly journals A Rare Cause of Hemoptysis in Children; Bronchial Artery to Pulmonary Artery Fistula in Healthy Child

2021 ◽  
pp. 1-4
Author(s):  
Nader Francis ◽  
◽  
Ahmad Al Kamali ◽  
Sinan Yavuz ◽  
◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Healthy Child ◽  
Bronchial Artery ◽  
Artery Aneurysm ◽  
Normal Lung ◽  
Massive Hemoptysis ◽  
Pediatric Age Group ◽  
Risk Of Rupture ◽  
Life Threatening ◽  
Pulmonary Artery Fistula

Hemoptysis is a rare, life-threatening condition in childhood defined as bleeding into the lungs due to underlying disorders or respiratory tract abnormalities. The bleeding from an arterial malformation to normal lung segments without underlying cardiovascular or pulmonary disorders is widely reported in adults but extremely rare in the pediatric age group. Bronchial artery aneurysm (BAA) is a rare vascular malformation complicated with a bronchial artery to pulmonary artery (BA PA) fistula. BAAs are life-threatening conditions because of the substantial risk of rupture that can cause massive hemoptysis. In such a case, BAA embolization (BAAE) has become essential management. We report here previously healthy child presented with massive hemoptysis due to systemic-pulmonary fistula, which was bleeding controlled by BAAE

Ligation of the bronchial artery in sheep attenuates early pulmonary changes following exposure to smoke

2000 ◽  
Vol 88 (3) ◽  
pp. 888-893 ◽  
Author(s):  
Olga Efimova ◽  
A. B. Volokhov ◽  
Sakineh Iliaifar ◽  
C. A. Hales
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Bronchial Artery ◽  
Lymph Flow ◽  
Smoke Inhalation ◽  
Acute Pulmonary Edema ◽  
Artery Ligation ◽  
Bronchial Arteries ◽  
Right Pulmonary Artery ◽  
The Right

Smoke inhalation can produce acute pulmonary edema. Previous studies have shown that the bronchial arteries are important in acute pulmonary edema occurring after inhalation of a synthetic smoke containing acrolein, a common smoke toxin. We hypothesized that inhalation of smoke from burning cotton, known to contain acrolein, would produce in sheep acute pulmonary edema that was mediated by the bronchial circulation. We reasoned that occluding the bronchial arteries would eliminate smoke-induced pulmonary edema, whereas occlusion of the pulmonary artery would not. Smoke inhalation increased lung lymph flow from baseline from 2.4 ± 0.7 to 5.6 ± 1.2 ml/0.5 h at 30 min ( P < 0.05) to 9.1 ± 1 ml/0.5 h at 4 h ( P < 0.05). Bronchial artery ligation diminished and delayed the rise in lymph flow with baseline at 2.8 ± 0.7 ml/0.5 h rising to 3.1 ± 0.8 ml/0.5 h at 30 min to 6.5 ± 1.5 ml/0.5 h at 240 min ( P < 0.05). Wet-to-dry ratio was 4.1 ± 0.2 in control, 5.1 ± 0.3 in smoke inhalation ( P< 0.05), and 4.4 ± 0.4 in bronchial artery ligation plus smoke-inhalation group. Smoke inhalation after occlusion of the right pulmonary artery resulted in a wet-to-dry ratio after 4 h in the right lung of 5.5 ± 0.8 ( P < 0.05 vs. control) and in the left nonoccluded lung of 5.01 ± 0.7 ( P < 0.05). Thus the bronchial arteries may be major contributors to acute pulmonary and airway edema following smoke inhalation because the edema occurs in the lung with the pulmonary artery occluded but not in the lungs with bronchial arteries ligated.

Bronchial artery ligation modifies pulmonary edema after exposure to smoke with acrolein

1989 ◽  
Vol 67 (3) ◽  
pp. 1001-1006 ◽  
Author(s):  
C. A. Hales ◽  
P. Barkin ◽  
W. Jung ◽  
D. Quinn ◽  
D. Lamborghini ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Bronchial Artery ◽  
Smoke Exposure ◽  
Smoke Inhalation ◽  
Lung Water ◽  
Artery Ligation ◽  
Bronchial Arteries ◽  
Common Component ◽  
Multiple Chemical ◽  
Bronchial Vessels

Pulmonary edema can follow smoke inhalation and is believed to be due to the multiple chemical toxins in smoke, not the heat. We have developed a synthetic smoke composed of aerosolized charcoal particles to which one toxin at a time can be added to determine whether it produces pulmonary edema. Acrolein, a common component of smoke, when added to the synthetic smoke, produced a delayed-onset pulmonary edema in dogs in which the extravascular lung water (EVLW) as detected by a double-indicator technique began to rise after 42 +/- 2 (SE) min from 148 +/- 16 to 376 +/- 60 ml at 165 min after smoke exposure. The resulting pulmonary edema was widespread macroscopically but appeared focal microscopically with fibrin deposits in alveoli adjacent to small bronchi and bronchioles. Bronchial vessels were markedly dilated and congested. Monastral blue B when injected intravenously leaked into the walls of the bronchial vessels down to the region of the small bronchioles (less than or equal to 0.5 mm ID) of acrolein-smoke-exposed dogs but not into the pulmonary vessels. Furthermore, ligation of the bronchial arteries delayed the onset of pulmonary edema (87 +/- 3 min, P less than 0.05) and lessened the magnitude (232 +/- 30 ml, P less than 0.05) at 166 +/- 3 min after acrolein-smoke exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Control of Tubercular Haemoptysis by Bronchial Artery Embolization

1997 ◽  
Vol 27 (3) ◽  
pp. 149-150 ◽  
Author(s):  
Sanjeev Mani ◽  
Rajesh Mayekar ◽  
Ravi Rananavare ◽  
Deepti Maniar ◽  
J Mathews Joseph ◽  
...  
Keyword(s):  
Bronchial Artery ◽  
Bronchial Artery Embolization ◽  
Artery Embolization ◽  
Selective Embolization ◽  
Bronchial Arteries ◽  
Bleeding Vessel ◽  
Life Threatening ◽  
Abnormal Bleeding ◽  
Recurrent Haemoptysis

Thirty-seven patients presenting with massive or recurrent haemoptysis secondary to tuberculous aetiology were subjected to bronchial artery angiography. Of these, failure to catheterize the bleeding vessel occurred in two patients while embolization was withheld in two patients due to the presence of anterior spinal artery arising from a common intercosto-bronchial trunk. Immediate arrest of bleeding was performed in the remaining 33 patients by selective embolization of the abnormal bronchial arteries with a resorbable material (Gelfoam). Regular follow up for a duration of 6 months after the procedure revealed relapse of haemoptysis in four patients; three were treated by re-embolization of the abnormal bleeding vessels while one patient died due to aspiration immediately on admission. No recurrence of bleeding was seen in the remaining 29 patients. It is concluded that bronchial artery embolization is an effective treatment for immediate control of life-threatening haemoptysis.

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.

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