Structural changes in the canine lung and pulmonary arteries after pneumonectomy

1982 ◽  
Vol 53 (4) ◽  
pp. 859-864 ◽  
Author(s):  
P. Davies ◽  
J. McBride ◽  
G. F. Murray ◽  
B. R. Wilcox ◽  
J. A. Shallal ◽  
...  
Keyword(s):  
Structural Changes ◽  
Pulmonary Arteries ◽  
Postoperative Recovery ◽  
Arterial System ◽  
Alveolar Volume ◽  
Prolonged Recovery ◽  
Mean Linear Intercept ◽  
Compensatory Enlargement ◽  
Medial Hypertrophy ◽  
The Right

The study set out to describe the structural changes in the remaining lung of beagle dogs after left-sided pneumonectomy, performed at 6–10 wk or 1 yr of age. After a 5-yr postoperative recovery, lung volume and weight had increased in the operated groups, though only the latter was significant in comparison with 5-yr-old controls. In both operated groups, total alveolar number in the right lung was normal. The total volume of alveolar ducts, mean linear intercept, and (in the young operated group) mean alveolar volume were increased, indicating a compensatory enlargement of distal air spaces. Lobar differences reinforced these conclusions. In the 1-yr operated group, medial hypertrophy was present in preacinar arteries, with a similar trend in intra-acinar arteries where peripheral extension of medial smooth muscle was also present. Despite the lack of structural change in their pulmonary arterial system, the young operated group had right ventricular hypertrophy. Previously reported evidence of alveolar proliferation shortly after pneumonectomy probably represents a speeding up of normal developmental patterns, but after prolonged recovery the final alveolar number is no greater than normal.

Primary repair of tetralogy of Fallot in infancy – the effect on growth of the pulmonary arteries and the risk for late reinterventions

2001 ◽  
Vol 11 (4) ◽  
pp. 391-398 ◽  
Author(s):  
Renate Kaulitz ◽  
Christian Jux ◽  
Harald Bertram ◽  
Thomas Paul ◽  
Gerhard Ziemer ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Tetralogy Of Fallot ◽  
Pulmonary Valve ◽  
Primary Repair ◽  
Pulmonary Arteries ◽  
Arterial System ◽  
Asymptomatic Patients ◽  
The Right ◽  
Normal Controls

We sought to analyse the long-term follow-up after primary repair of tetralogy of Fallot in infancy in the first year of life, paying particular attention to growth of the pulmonary arteries and the need for reintervention. We performed a combined retro- and prospective echocardiographic study, including measurements of the pulmonary valve and right and left pulmonary arteries, indexed to the square root of body surface area, in 62 patients prior to primary repair, 18 to 24 months after this event, and at the most recent follow-up, with a mean of 80.4 ± 24 months. Of these, 38 patients, with an age at operation of 5.0 ± 3.4 months, had presented preoperatively with hypoxic spells or increasing cyanosis. The remaining 24 patients had been asymptomatic, with adequate flow of blood to the lungs. Their age at elective operation was 7.4 ± 3.0 months. A transannular patch was needed in 37 patients (63%). There were 3 early postoperative deaths (4.8%).Cross-sectional echocardiography revealed a significantly smaller diameter for the pulmonary valve in patients who had been symptomatic preoperatively compared to the asymptomatic patients (1.09 versus 1.3 cm/BSA0.5; p = 0.019). The diameters of the right and left pulmonary arteries did not differ significantly between the groups. Examination of echocardiographic data obtained 18 to 24 months postoperatively in 43 patients revealed a significant increase in the diameter of the pulmonary arteries; 0.83 ± 0.17 cm/BSA0.5 versus 1.1 ± 0.26 cm/BSA0.5 for the diameter of the right pulmonary artery, 0.85 ± 0.2 cm/BSA0.5 versus 1.0 ± 0.25 cm/BSA0.5 for the left pulmonary artery. On comparison between individuals, 18.6% and 25.6% of the patients, respectively, did not show any change in the diameters of their right and left pulmonary arteries, whereas the increase in diameter reached or exceeded the measurements in normal controls in 55.8% and 46.5% of the patients, respectively. On recent follow-up, with a range from 56 to 147 months, no further increase in the indexed diameters of the pulmonaries could be documented in 21 of 33 patients. Of these, 9.1% and 18.2%, respectively, presented with small right and left pulmonary arteries compared with measurements obtained in normal controls. Moderate pulmonary incompetence was found on colour flow mapping in one-third. Of 56 longterm survivors, 8 (14%) had required reinterventions, which were surgical in 6 and achieved by transcatheter techniques in the other 2 patients. Thus, primary correction of tetralogy of Fallot in infancy, with restoration of normal pressures and flows, resulted in sustained increase in the diameters of the right and left pulmonary arteries. It allowed for early normal development of the proximal pulmonary arterial system in most patients regardless of their age and symptomatic status at operation. Patients with persistent subnormal diameter of the pulmonary arteries did not present with significantly elevated right ventricular pressure. Early one-stage repair of tetralogy of Fallot in infancy was associated with a low rate of reinterventions.

Chronic pulmonary thromboembolism due to intracardiac and pulmonary hydatidosis

2020 ◽  
Vol 28 (9) ◽  
pp. 610-612
Author(s):  
Ameya Kaskar ◽  
Varun Shetty ◽  
Devi Shetty
Keyword(s):  
Hydatid Disease ◽  
Pulmonary Thromboembolism ◽  
Circulatory Arrest ◽  
Wedge Resection ◽  
Pulmonary Arteries ◽  
Lower Lobe ◽  
Postoperative Recovery ◽  
Rare Presentation ◽  
Pulmonary Hydatid Disease ◽  
The Right

Hydatid disease remains a problem in endemic areas. The combination of both intracardiac and pulmonary hydatid disease in association with chronic pulmonary thromboembolism is a rare presentation. We report a case of a 14-year-old girl with hydatid disease of the lungs, right ventricle, and pulmonary arteries, presenting as chronic pulmonary thromboembolism. She underwent surgery for wedge resection of the pulmonary hydatid in the right lower lobe, removal of the right ventricular hydatid (under cardiopulmonary bypass), and pulmonary endarterectomy (under total circulatory arrest). Her postoperative recovery was uneventful.

Pulmonary Arterial Changes in Feline Dirofilariasis

1993 ◽  
Vol 30 (1) ◽  
pp. 64-69 ◽  
Author(s):  
M. D. McCracken ◽  
S. Patton
Keyword(s):  
Pulmonary Arteries ◽  
Inflammatory Cells ◽  
Pulmonary Trunk ◽  
Ventricular Dilation ◽  
Pulmonary Arterial ◽  
Medial Hypertrophy ◽  
The Right ◽  
Partially Occluded ◽  
Passive Congestion ◽  
Right Ventricular Dilation

Eleven cats with spontaneous dirofilariasis were necropsied; ten were domestic shorthairs and one was a Persian. The cats ranged in age from 1 to 10 years, and 6/11 cats were male. One to three heartworms were present in the right ventricle and pulmonary arteries of each of the 11 cats. Patchy areas of rugose thickening of the intima of the pulmonary trunk and marked villous endarteritis of lobar and medium-sized pulmonary arteries were observed. Affected larger vessels were partially occluded by large villous intimal proliferations that were lined by hyperplastic endothelial cells supported by connective tissue stroma. Moderate to marked infiltration of eosinophils and mononuclear inflammatory cells was consistently observed in the intima of affected larger pulmonary arteries. Thrombosis of pulmonary arteries was seen in five cats. Medial hypertrophy, mild intimal proliferative changes, and focal infiltrations of leukocytes were seen in small pulmonary arteries. Lesions indicative of right-sided heart failure consisting of right ventricular dilation and chronic passive congestion of the liver were observed in four cats.

scholarly journals Anatomical correlation between left atrium pulmonary vein ablation targets of atrial fibrillation and adjacent bronchi and pulmonary arteries by MSCT

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yan-Jing Wang ◽  
Huan Sun ◽  
Xiao-Fei Fan ◽  
Meng-Chao Zhang ◽  
Ping Yang ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrium ◽  
Pulmonary Vein ◽  
Pulmonary Arteries ◽  
Contact Points ◽  
Pulmonary Vein Ablation ◽  
Adjacent Structures ◽  
Anatomical Correlation ◽  
The Right

Abstract Background The ablation targets of atrial fibrillation (AF) are adjacent to bronchi and pulmonary arteries (PAs). We used computed tomography (CT) to evaluate the anatomical correlation between left atrium (LA)-pulmonary vein (PV) and adjacent structures. Methods Data were collected from 126 consecutive patients using coronary artery CT angiography. The LA roof was divided into three layers and nine points. The minimal spatial distances from the nine points and four PV orifices to the adjacent bronchi and PAs were measured. The distances from the PV orifices to the nearest contact points of the PVs, bronchi, and PAs were measured. Results The anterior points of the LA roof were farther to the bronchi than the middle or posterior points. The distances from the nine points to the PAs were shorter than those to the bronchi (5.19 ± 3.33 mm vs 8.62 ± 3.07 mm; P < .001). The bilateral superior PV orifices, especially the right superior PV orifices were closer to the PAs than the inferior PV orifices (left superior PV: 7.59 ± 4.14 mm; right superior PV: 4.43 ± 2.51 mm; left inferior PV: 24.74 ± 5.26 mm; right inferior PV: 22.33 ± 4.75 mm) (P < .001). Conclusions The right superior PV orifices were closer to the bronchi and PAs than other PV orifices. The ablation at the mid-posterior LA roof had a higher possibility to damage bronchi. CT is a feasible method to assess the anatomical adjacency in vivo, which might provide guidance for AF ablation.

Perspectives on endothelial-to-mesenchymal transition: potential contribution to vascular remodeling in chronic pulmonary hypertension

2007 ◽  
Vol 293 (1) ◽  
pp. L1-L8 ◽  
Author(s):  
Enrique Arciniegas ◽  
Maria G. Frid ◽  
Ivor S. Douglas ◽  
Kurt R. Stenmark
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Vascular Remodeling ◽  
Serine Proteases ◽  
Structural Changes ◽  
Transforming Growth Factor ◽  
Pulmonary Arteries ◽  
Potential Contribution ◽  
Mesenchymal Transition ◽  
Endothelial Mesenchymal Transition

All forms of pulmonary hypertension are characterized by structural changes in pulmonary arteries. Increased numbers of cells expressing α-smooth muscle (α-SM) actin is a nearly universal finding in the remodeled artery. Traditionally, it was assumed that resident smooth muscle cells were the exclusive source of these newly appearing α-SM actin-expressing cells. However, rapidly emerging experimental evidence suggests other, alternative cellular sources of these cells. One possibility is that endothelial cells can transition into mesenchymal cells expressing α-SM actin and that this process contributes to the accumulation of SM-like cells in vascular pathologies. We review the evidence that endothelial-mesenchymal transition is an important contributor to cardiac and vascular development as well as to pathophysiological vascular remodeling. Recent work has provided evidence for the role of transforming growth factor-β, Wnt, and Notch signaling in this process. The potential roles of matrix metalloproteinases and serine proteases are also discussed. Importantly, endothelial-mesenchymal transition may be reversible. Thus insights into the mechanisms controlling endothelial-mesenchymal transition are relevant to vascular remodeling and are important as we consider new therapies aimed at reversing pulmonary vascular remodeling.

scholarly journals Postnatal alveolar development of the rabbit

2002 ◽  
Vol 93 (2) ◽  
pp. 629-635 ◽  
Author(s):  
Jana Kovar ◽  
Peter D. Sly ◽  
Karen E. Willet
Keyword(s):  
Wall Thickness ◽  
Alveolar Wall ◽  
Alveolar Volume ◽  
Surface Fraction ◽  
Alveolar Development ◽  
The Right ◽  
Timing Of Onset ◽  
Alveolar Formation ◽  
Tissue Fraction

Previous studies of alveolarization have used rats or lambs; however, neither closely reflects human alveolar development. We characterized alveolar development in rabbits ( n = 3–7 /group) at 28 days gestation (dg) to 9 mo to determine whether they followed the human pattern more closely. The right lung was made up of 30% alveolar and 50% duct space at 28 dg to 3 days and of 50 and 30%, respectively, at 14 days to 9 mo. Tissue fraction and alveolar wall thickness decreased by 40% 28 dg to birth. At birth, ∼4.5% of the number of alveoli seen at 9 mo were present, with alveolar number increasing progressively well into adulthood. The rate of alveolar formation was high around birth, decreasing progressively with age. Alveolar volume increased more than twofold (28 dg to birth) and continued to increase postnatally to 16 wk. Surface fraction decreased by 17% (28 dg to 3 days), after which it remained uniform. Our findings suggest that the timing of onset of alveolarization in humans and rabbits is similar and that rabbits may be used to model postnatal influences on alveolar development.

scholarly journals Ventilation/perfusion mismatch during lung aeration at birth

2014 ◽  
Vol 117 (5) ◽  
pp. 535-543 ◽  
Author(s):  
Justin A. R. Lang ◽  
James T. Pearson ◽  
Arjan B. te Pas ◽  
Megan J. Wallace ◽  
Melissa L. Siew ◽  
...  
Keyword(s):  
Pulmonary Arteries ◽  
Left Lung ◽  
X Ray ◽  
Lung Aeration ◽  
X Ray Imaging ◽  
Iodine Level ◽  
Pulmonary Shunting ◽  
Left And Right ◽  
Near Term ◽  
The Right

At birth, the transition to newborn life is triggered by lung aeration, which stimulates a large increase in pulmonary blood flow (PBF). Current theories predict that the increase in PBF is spatially related to ventilated lung regions as they aerate after birth. Using simultaneous phase-contrast X-ray imaging and angiography we investigated the spatial relationships between lung aeration and the increase in PBF after birth. Six near-term (30-day gestation) rabbits were delivered by caesarean section, intubated and an intravenous catheter inserted, before they were positioned for X-ray imaging. During imaging, iodine was injected before ventilation onset, after ventilation of the right lung only, and after ventilation of both lungs. Unilateral ventilation increased iodine levels entering both left and right pulmonary arteries (PAs) and significantly increased heart rate, iodine ejection per beat, diameters of both left and right PAs, and number of visible vessels in both lungs. Within the 6th intercostal space, the mean gray level (relative measure of iodine level) increased from 68.3 ± 11.6 and 70.3 ± 7.5%·s to 136.3 ± 22.6 and 136.3 ± 23.7%·s in the left and right PAs, respectively. No differences were observed between vessels in the left and right lungs, despite the left lung not initially being ventilated. The increase in PBF at birth is not spatially related to lung aeration allowing a large ventilation/perfusion mismatch, or pulmonary shunting, to occur in the partially aerated lung at birth.

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