Intravenous Injection of Sonicated Blood Induces Pulmonary Microthromboembolism in Rabbits With Ligation of the Splenic Artery

Kisanuki, Atsushi; Kietthubthew, Suparp; Asada, Yujiro; Marutsuka, Kousuke; Funahara, Y; Sumiyoshi, Akinobu

doi:10.1016/s0049-3848(96)00226-5

Cited by 22 publications

(9 citation statements)

References 8 publications

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“…Levy and Simmons [27] observed a bronchoconstriction of 30-min duration after injection of 30 mL of fresh clots. Kisanuki A et al found that bronchoconstriction occurred up to 60 min after embolization, as suggested by the progressive increase in effective alveolar ventilation [28]. In our study we tried to establish a kind of process to induce PTE in rats by blood clot injection.…”

Section: Discussionmentioning

confidence: 83%

Hsp90 mediates the balance of nitric oxide and superoxide anion in the lungs of rats with acute pulmonary thromboembolism

Jin

Xia

Tao

et al. 2009

International Immunopharmacology

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Section: Discussionmentioning

confidence: 83%

Hsp90 mediates the balance of nitric oxide and superoxide anion in the lungs of rats with acute pulmonary thromboembolism

Jin

Xia

Tao

et al. 2009

International Immunopharmacology

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“…In addition, in a murine model of CTEPH, inhibition of angiogenesis was associated with delay in thrombus resolution[143,144]. In a rabbit model with splenic artery ligation, transfusion of sonicated blood resulted in platelet rich thrombi in pulmonary circulation; in contrast, transfusion of normal blood did not have any effect[145]. …”

Section: Hematological Disorders and Phmentioning

confidence: 99%

Hematological disorders and pulmonary hypertension

Mathew

Huang

et al. 2016

WJC

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Pulmonary hypertension (PH), a serious disorder with a high morbidity and mortality rate, is known to occur in a number of unrelated systemic diseases. Several hematological disorders such as sickle cell disease, thalassemia and myeloproliferative diseases develop PH which worsens the prognosis. Associated oxidant injury and vascular inflammation cause endothelial damage and dysfunction. Pulmonary vascular endothelial damage/dysfunction is an early event in PH resulting in the loss of vascular reactivity, activation of proliferative and antiapoptotic pathways leading to vascular remodeling, elevated pulmonary artery pressure, right ventricular hypertrophy and premature death. Hemolysis observed in hematological disorders leads to free hemoglobin which rapidly scavenges nitric oxide (NO), limiting its bioavailability, and leading to endothelial dysfunction. In addition, hemolysis releases arginase into the circulation which converts L-arginine to ornithine, thus bypassing NO production. Furthermore, treatments for hematological disorders such as immunosuppressive therapy, splenectomy, bone marrow transplantation, and radiation have been shown to contribute to the development of PH. Recent studies have shown deregulated iron homeostasis in patients with cardiopulmonary diseases including pulmonary arterial hypertension (PAH). Several studies have reported low iron levels in patients with idiopathic PAH, and iron deficiency is an important risk factor. This article reviews PH associated with hematological disorders and its mechanism; and iron homeostasis and its relevance to PH.

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“…The underlying pathogenic mechanism is unclear but function of spleen, abnormal erythrocytes may remain in circulation for longer period of time and may trigger platelet activation which could then be trapped in pulmonary vascular bed [8,9]. Such mechanism could be active in any patient who is splenectomised but would be aggravated in presence of hemolytic disorders [10][11][12].…”

Section: Discussionmentioning

confidence: 99%

Pulmonary hypertension in patients with hematological disorders following splenectomy

Meera¹,

Jijina²,

Ghosh³

2010

Indian J Hematol Blood Transfus

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Prevalence of pulmonary arterial hypertension (PAH) was studied by Echocardiography and Doppler in 43 splenectomised patients with various disorders 1-20 years after splenectomy. PAH was detected only in thalassemia major, intermedia, hereditary sphereocytosis and myelofibrosis groups comprising a total of 21 patients. Six patients out of 21 was found to have PAH with mean pulmonary arterial pressure of 46.28 ± 28.17 mmHg. Twenty one controls having similar duration and type of disease also were assessed for PAH in this case control study 3/21 had PAH in this control group. The difference in number of patients showing pulmonary hypertension between case and control was not statistically significant (chi-square test p = 0.29-though the difference in pulmonary arterial pressure between case and control were significantly different (t-test p<0.0029) with control group showing a mean pulmonary arterial pressure of 25 ± 19 mmHg.Platelet count in the splenectomised group was significantly higher (p = 0.0029) than the controls. Pulmonary thromboembolism was equally high in the PAH patients with and without splenectomy. Patients undergoing splenectomy due to trauma, immune thrombocytopenia, sideroblastic anemia, extra hepatic portal hypertension, autoimmune hemolytic anemia did not show PAH after splenectomy even years after the procedure PAH following splenectomy is common after certain disorders and control patients with these diseases have tendency to develop PAH even without splenectomy. Pulmonary thromboembolism may be an important pathophysiological mechanism leading to this condition. Patients having hemolytic anemia and myelofibrosis should have regular evaluation of pulmonary arterial pressure whether he/she has been splenectomised or not. This is particularly important as availability of phosphodiesterase inhibitors like sildenafil allows one to manage these cases.

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Intravenous Injection of Sonicated Blood Induces Pulmonary Microthromboembolism in Rabbits With Ligation of the Splenic Artery

Cited by 22 publications

References 8 publications

Hsp90 mediates the balance of nitric oxide and superoxide anion in the lungs of rats with acute pulmonary thromboembolism

Hsp90 mediates the balance of nitric oxide and superoxide anion in the lungs of rats with acute pulmonary thromboembolism

Hematological disorders and pulmonary hypertension

Pulmonary hypertension in patients with hematological disorders following splenectomy

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