Correlations of inhaled NO with the cTnI levels and the plasma clotting factor in rabbits with acute massive pulmonary embolism

Zhang, Zeming; Meng, Zhaoqing; Wang, Yancun

doi:10.1590/s0102-865020180080000002

Cited by 4 publications

(8 citation statements)

References 26 publications

(27 reference statements)

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“…73 The reduced RV afterload might explain less myocardial damage evident by lowered cardiac troponins. 65,76,77 One study using fat-emboli in a canine model did, however, not detect any effects on pulmonary or cardiac function. 78 Due to the rationale of inhaled administration, only one study noticed effect on the systemic vasculature with decreased mean arterial pressure (MAP).…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

“…76 NO affects apoptotic pneumocytes, 74 and both endogenous and exogenous NO inhibits platelet aggregation in animals and humans 67,[89][90][91] which might be relevant in PE. 66,[68][69][70][71]73,80,[84][85][86] No effect on mPAP but increase in CO. 87 Lowers PVR, mPAP, increases CO. 51,65,67,72,[74][75][76]79,[81][82][83] Lowers cardiac damage. 65,76,77 No hemodynamic effects.…”

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

“…In general, iNO lowered PAP and PVR in animal models [65][66][67][68][69][70][71][72][73][74][75][76] and increased cardiac output (CO) in some studies. 70,72 The effect is possibly caused by reduced pulmonary vascular tone in the periphery of the pulmonary artery tree, especially regions with distally localized emboli.…”

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

“…iNO lowers von Willebrand factor and glycoprotein IIb/IIIa as central parts in endothelial function and thrombosis. 76 NO affects apoptotic pneumocytes, 74 and both endogenous and exogenous NO inhibits platelet aggregation in animals and humans 67,[89][90][91] which might be relevant in PE. NO has been used clinically in acute PE inspired by the experimental results and by the experience from using NO as a pulmonary vasodilator in acute respiratory distress syndrome and pulmonary hypertension.…”

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

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Pulmonary vasodilation in acute pulmonary embolism – a systematic review

et al. 2020

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Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricular afterload, which causes right ventricular failure, circulatory collapse and death. Most treatments focus on removal of the mechanical obstruction caused by the embolism, but pulmonary vasoconstriction is a significant contributor to the increased right ventricular afterload and is often left untreated. Pulmonary thromboembolism causes mechanical obstruction of the pulmonary vasculature coupled with a complex interaction between humoral factors from the activated platelets, endothelial effects, reflexes and hypoxia to cause pulmonary vasoconstriction that worsens right ventricular afterload. Vasoconstrictors include serotonin, thromboxane, prostaglandins and endothelins, counterbalanced by vasodilators such as nitric oxide and prostacyclins. Exogenous administration of pulmonary vasodilators in acute pulmonary embolism seems attractive but all come with a risk of systemic vasodilation or worsening of pulmonary ventilation-perfusion mismatch. In animal models of acute pulmonary embolism, modulators of the nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway, endothelin pathway and prostaglandin pathway have been investigated. But only a small number of clinical case reports and prospective clinical trials exist. The aim of this review is to give an overview of the causes of pulmonary embolism-induced pulmonary vasoconstriction and of experimental and human investigations of pulmonary vasodilation in acute pulmonary embolism.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

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Pulmonary vasodilation in acute pulmonary embolism – a systematic review

et al. 2020

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Rodent models of pulmonary embolism and chronic thromboembolic pulmonary hypertension

Карпов

Vaulina

Smirnov

et al. 2022

Heliyon

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Approaches to modeling pulmonary embolism and chronic thromboembolic pulmonary hypertension in rodents and medium-sized laboratory animals

Карпов

Smirnov

Shilenko

et al. 2021

Transl. med. (Print)

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Pulmonary embolism (PE) is the third most common cardiovascular disease. It is still associated with high hospital mortality, as well as with the development of acute and chronic complications. Treatment and prevention of PE and its complications requires high-tech approaches aimed at improving the prognosis of patients. In this regard, experimental studies aimed at studying the pathogenesis, improving diagnostic methods and searching for new pharmacological substances for the prevention and treatment of PE are in demand from the point of view of clinical practice. Considering the current trends in preclinical research, experimental work on rodents — mice, rats, hamsters, as well as on medium-sized laboratory animals (rabbits) is becoming more and more common. The use of these animal species is ethically acceptable and economically viable. The choice of a specific type of animal and a method for modeling PE is primarily determined by the objectives of the study. This article provides an overview of the main approaches to modeling PE, as well as discusses the advantages and disadvantages of each method. Special attention is paid to the modeling of chronic thromboembolic pulmonary hypertension (CTEPH) as one of the most dangerous complications of PE. The work analyzed publications from 1978 to 2020, in which PE was simulated in rodents and medium laboratory animals.

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Correlations of inhaled NO with the cTnI levels and the plasma clotting factor in rabbits with acute massive pulmonary embolism

Abstract: Inhaled nitric oxide can lead to a decrease in levels of cardiac troponin I, von Willebrand factor, glycoprotein, and granule membrane protein 140, after an established myocardial damage, provoked by acute massive pulmonary embolism.

Cited by 4 publications

References 26 publications

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

Rodent models of pulmonary embolism and chronic thromboembolic pulmonary hypertension

Approaches to modeling pulmonary embolism and chronic thromboembolic pulmonary hypertension in rodents and medium-sized laboratory animals

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