<i>In Vivo</i>
            and Post Mortem Dissolution Rates of Pulmonary Emboli and Venous Thrombi in the Dog

Moser, Kenneth Μ.; Guisan, Michel; Bartimmo, Ernest E.; Longo, Antonio; Harsanyi, Paul G.; Chiorazzi, Nicholas

doi:10.1161/01.cir.48.1.170

Cited by 75 publications

(45 citation statements)

References 15 publications

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“…Thus, 3 hours after acute pulmonary embolism in dogs, 14 only 30% of the initial injected thrombus volume remained inside the PA. Adding tranexamic acid 15 or plasminogen activator inhibitor-1 16 to delay thrombus resorption between injections failed to solve this problem.…”

Section: Discussionmentioning

confidence: 95%

Piglet Model of Chronic Pulmonary Hypertension

et al. 2013

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None of the animal models have been able to reproduce all aspects of CTEPH because of the rapid resolution of the thrombi in the pulmonary vasculature. The aim of this study was to develop an easily reproducible large-animal model of chronic pulmonary hypertension (PH) related to the development of a postobstructive and overflow vasculopathy. Chronic PH was induced in 5 piglets by ligation of the left pulmonary artery (PA) through a midline sternotomy followed by weekly transcatheter embolization of the right lower-lobe arteries. Sham-operated piglets (n = 5) served as controls. Hemodynamics, RV function, lung morphometry, and endothelin-1 (ET-1) pathway gene expression (ET-1 and its receptors ETA and ETB) were assessed after 5 weeks in the obstructed (left lung and right lower lobe) and unobstructed (right upper lobe) territories. All animals developed chronic PH within 5 weeks. Compared to controls, chronic-PH animals had higher mean PA pressure (28.5 ± 1.7 vs. 11.6 ± 1.8 mmHg, P = 0.0001) and total pulmonary resistance (784 ± 160 vs. 378 ± 51 dyn s −1 cm −5 , P = 0.05). Echocardiography showed RV enlargement, RV wall thickening (56 ± 5 vs. 30 ± 4 mm, P = 0.0003), decreased tricuspid annular plane systolic excursion (11.3 ± 0.9 vs. 14.4 ± 0.4 mm, P = 0.01), and paradoxical septal motion.In obstructed territories, morphometry demonstrated increases in the number of bronchial arteries per bronchus (8.7 ± 0.9 vs. 2 ± 0.17, P < 0.0001) and in distal PA media thickness (60% ± 2.8% vs. 29% ± 0.9%, P < 0.0001), consistent with postobstructive vasculopathy. Distal PA media thickness was increased in unobstructed territories (70% ± 2.4% vs. 29% ± 0.9%, P < 0.0001). ET-1 was overexpressed in unobstructed territories, compared to controls and obstructed territories. In conclusion, the large-animal model described here is reproducible and led to the development of PH in a relatively short time frame.

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Section: Discussionmentioning

confidence: 95%

Piglet Model of Chronic Pulmonary Hypertension

et al. 2013

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“…Since the 1990s, several attempts to develop animal models of CTEPH [48][49][50][51][52] failed because of clot lysis by the very efficient endogenous fibrinolytic system [53] and of the remarkable territories in a patient with chronic thromboembolic pulmonary hypertension. The obstructed territory is subjected to chronic ischaemia and the unobstructed territory to an increase in blood flow.…”

Section: Animal Model Replicating All Features Of Ctephmentioning

confidence: 99%

Chronic thromboembolic pulmonary hypertension: animal models

Mercier

Fadel

2013

Eur Respir J

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Chronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening disease due to pulmonary artery obstruction by persistent organised clots related to one or more episodes of acute pulmonary embolism. To date, the pathogenesis of CTEPH remains unexplained. Pulmonary endarterectomy removes obstruction from pulmonary vessels and can cure patients. However, some unreachable distal pulmonary obstruction and/or associated distal pulmonary vasculopathy could induce persistent pulmonary hypertension, the main postoperative complication.The pathophysiology of CTEPH is not fully understood and improving knowledge of this disease could improve our future surgical and medical management. Many attempts, conducted over several decades, have failed to reproduce this chronic disease in animals. However, several animal models have provided insights into the pathophysiology and pathogenesis of CTEPH. Here, we review all the animal models that have improved the comprehension of CTEPH and hold promise for further investigations. This short review analyses strengths and weaknesses of all animal models available to study the pathophysiology of CTEPH. , chronic thromboembolic pulmonary hypertension (CTEPH) is a type-4 subtype of pulmonary hypertension (PH), in which pulmonary endarterectomy (PEA) [2] is effective in preventing death by right ventricle (RV) failure. CTEPH is due to obstruction of pulmonary arteries by persistent organised clots formed during one or more episodes of acute pulmonary embolism. The reason for clot persistence is unknown and the pathogenesis of CTEPH remains unexplained. To date, the lack of risk factors predicting the evolution from acute pulmonary embolism to CTEPH does not allow the development of preventive care and/or screening programmes.The increase in pulmonary vascular resistance is believed to result from a combination of proximal pulmonary artery obstruction and distal pulmonary vasculopathy [3,4], which have to be quantified before PEA to estimate risks and predict surgical success. However, the mechanisms underlying lesion development in the obstructed and unobstructed peripheral vascular beds remain unknown. Hence, medical management of inoperable CTEPH or operable CTEPH with an important distal vasculopathy remains troublesome because of a lack of efficient therapy.To elucidate the pathophysiology of CTEPH, considerable effort has been expended in attempting to develop reliable animal models. Acute pulmonary embolism is easily produced in several animal species. In contrast, the induction of a disease replicating all the components of human CTEPH has proved challenging. These

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“…However, it has also been reported that heparin may relieve the bronchial spasm by preventing the release of vasoactive amines from platelets in the embolus (Thomas 1965). Studies in dogs by Moser et al (1973) indicated an enhancement of the embolic disintegration during heparin treatment by preventing accretion of fibrin-platelet layers on the surface of the embolus. Untreated patients demonstrated scintigraphic improvement less often and had more new perfusion defects than patients treated with anticoagulants (Secker-Walker et al 1970).…”

Section: Discussionmentioning

confidence: 99%

Screening and Treatment of Pulmonary Embolism After Total Hip Replacement

Fredin

1983

Acta Orthopaedica Scandinavica

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In Vivo and Post Mortem Dissolution Rates of Pulmonary Emboli and Venous Thrombi in the Dog

Cited by 75 publications

References 15 publications

Piglet Model of Chronic Pulmonary Hypertension

Piglet Model of Chronic Pulmonary Hypertension

Chronic thromboembolic pulmonary hypertension: animal models

Screening and Treatment of Pulmonary Embolism After Total Hip Replacement

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