Pharmacology of Streptokinase

Klöcking, H.-P.

doi:10.1007/978-3-642-66863-0_6

Cited by 6 publications

(1 citation statement)

References 54 publications

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“…The canine genome exhibits greater fibrinolytic system homology with the human genome as compared to other mammalian models of thrombotic disease [ 11 , 12 ]. Interestingly, Virchow’s original description of a canine model focused on the development of animal models of thrombosis that mimicked the human condition [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Close concordance between pulmonary angiography and pathology in a canine model with chronic pulmonary thromboembolism and pathological mechanisms after lung ischemia reperfusion injury

Deng

Zhai

et al. 2015

J Thromb Thrombolysis

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To investigate the pulmonary angiography and pathology in a canine model with chronic pulmonary thromboembolism (PTE). The cylindrical blood clots were selectively introduced into the left (n = 10) or right (n = 20) lower pulmonary arteries of dogs. Pulmonary arteriography (PA) was performed before or after embolization. The values after embolization and baseline of mean pulmonary arterial pressure, pulmonary vascular resistance, cardiac output had changed. After 1 or 2 weeks’ embolization, local PA demonstrated the abrupt cut-off perfusion defects or webs, bands, and abrupt vascular narrowing. 2 weeks after embolization, the pathology showed that the fibrin networks of the thrombi had multiple recanalization channels, and pulmonary artery had the concentric, lamellar (onion-like) intimal hyperplasia, multilayered, irregular arrangements of endothelial cells, and the infiltration of inflammatory cells. After embolectomy-mediated reperfusion, 2 weeks’ subgroup showed destroyed and incomplete alveolar structures, and a large number of exudative cells, primarily neutrophils, and exudate. There close concordance between pulmonary angiography and pathology in a canine model with chronic PTE. The LIRI mechanisms after embolectomy-mediated reperfusion involve the destroyed, incomplete alveolar structures, and infiltration of inflammatory cells, primarily neutrophils.

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Section: Introductionmentioning

confidence: 99%