Aminoguanidine produces beneficial haemodynamic effects in a canine model of acute pulmonary thromboembolism

Dias‐Junior, Carlos A.; Sertório, Jonas T.; Tanus‐Santos, Jose E.

doi:10.1111/j.1748-1716.2007.01746.x

Cited by 7 publications

(4 citation statements)

References 42 publications

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“…Endogenous NO biosynthesis has been reported to play a protective role in haemodynamic homeostasis during APT . The activation of the NO‐cGMP pathway attenuates the haemodynamic derangement in APT .…”

Section: Discussionmentioning

confidence: 99%

“…33,34 Endogenous NO biosynthesis has been reported to play a protective role in haemodynamic homeostasis during APT. 35 The activation of the NO-cGMP pathway attenuates the haemodynamic derangement in APT. 6,36 Recent studies have shown that haemolysis and the release of arginase I caused by experimental pulmonary embolism contribute to subsequent depletion of L-arginine which is the substrate for NO synthesis.…”

Section: One Of the Main Mechanisms Of Pulmonary Hypertension Inmentioning

confidence: 99%

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N‐Acetylcysteine potentiates the haemodynamic‐improving effect of sildenafil in a rabbit model of acute pulmonary thromboembolism via the p38 MAPK pathway

Zhang

Wang

Pan

et al. 2018

Clin Exp Pharma Physio

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Summary The current study aimed to investigate the effects of sildenafil and N‐acetylcysteine (NAC) on the haemodynamics in a rabbit model of acute pulmonary thromboembolism (APT). We developed an APT model using healthy male China big‐ear rabbits (2.7 ± 0.4 kg). The rabbits were divided into five groups subjected to various interventions. We recorded the haemodynamic parameters and assessed the oxidative stress and lipid peroxidation response in the groups. Additionally, we detected apoptosis‐associated molecules, FoxO1, Bad and Bcl‐2, in the lung tissue. Gelatine zymography was used to detect matrix metalloproteinase (MMP) activity in bronchoalveolar lavage (BLA). Pulmonary artery endothelial cells were isolated, and their apoptosis rates and MMP activity were assayed. N‐acetylcysteine potentiated the haemodynamic‐improving effect of sildenafil and significantly inhibited the oxidative stress response. N‐acetylcysteine combined with sildenafil decreased MMP‐2 and MMP‐9 activity and NO consumption and inhibited apoptosis of pulmonary arterial endothelial cells. Moreover, NAC combined with sildenafil inhibited the expression of MCP‐1 and p‐p38 MAPK. Thus, NAC potentiates the haemodynamic‐improving effect of sildenafil in a rabbit model of acute pulmonary thromboembolism via the MCP‐1 and p38 MAPK signalling pathway. This study may provide a promising treatment method for APT.

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Section: Discussionmentioning

confidence: 99%

Section: One Of the Main Mechanisms Of Pulmonary Hypertension Inmentioning

confidence: 99%

N‐Acetylcysteine potentiates the haemodynamic‐improving effect of sildenafil in a rabbit model of acute pulmonary thromboembolism via the p38 MAPK pathway

Zhang

Wang

Pan

et al. 2018

Clin Exp Pharma Physio

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“…Kline et al 31 reported that the NOI combined with oxygen alleviated right ventricular dysfunction in patients with pulmonary thromboembolism and decreased the level of high-sensitivity troponin, which is not consistent with the results of the present study. Diasjunior et al 32 also demonstrated that intravenous administration of NO was not able to reduce pulmonary hypertension caused by AMPE. The use of high dose intravenous NO does not exhibit a selective effect on the pulmonary circulation, which can lead to severe systemic hypotension.…”

Section: ■ Discussionmentioning

confidence: 99%

The effects of inhaled NO on plasma vasoactive factor and CTnI level in rabbits with acute massive pulmonary embolism

Zhang

Chen

et al. 2018

Acta Cir. Bras.

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“…59 NO protects (partly) from PE-induced changes in hemodynamics and both expression of endothelial NO synthase mRNA and the fraction of expiratory NO increases in PE. [60][61][62] NO consumption increases in both animals and humans with PE, 63 and the endogenous NO production seems lifesaving in PE as antagonism of NO synthase causes death in PE-animals. 62,64 Accordingly, iNO has a potential therapeutic role in PE.…”

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

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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Aminoguanidine produces beneficial haemodynamic effects in a canine model of acute pulmonary thromboembolism

Abstract: These results indicate that endogenous NO protects against APT-induced cardiovascular responses. Moreover, iNOS-derived NO possibly produces unfavourable effects, which are counteracted by aminoguanidine. However, non-NO-related mechanisms may also be involved.

Cited by 7 publications

References 42 publications

N‐Acetylcysteine potentiates the haemodynamic‐improving effect of sildenafil in a rabbit model of acute pulmonary thromboembolism via the p38 MAPK pathway

N‐Acetylcysteine potentiates the haemodynamic‐improving effect of sildenafil in a rabbit model of acute pulmonary thromboembolism via the p38 MAPK pathway

The effects of inhaled NO on plasma vasoactive factor and CTnI level in rabbits with acute massive pulmonary embolism

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

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