Inhaled Nitric Oxide as an Adjunct to Suction Thrombectomy for Pulmonary Embolism

Faintuch, Salomão; Lang, Elvira V.; Cohen, Robert; Pinto, Duane S.

doi:10.1097/01.rvi.0000137979.63175.b6

Cited by 8 publications

(7 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the NO inhalation group, the PaO 2 /FiO 2 significantly decreased 2 and 4 h after reperfusion. However, due to the improvement in ratio of ventilation and blood flow (V/Q matching) [ 3 , 37 , 38 ], the PaO 2 /FiO 2 increased gradually to the baseline 6 h after reperfusion. Compared with the reperfusion group, the PaO 2 /FiO 2 increased significantly after inhalation of 20 ppm NO for 4 or 6 h, related to elevated inducible nitric oxide synthase (iNOS) expression and its activity [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory response and pneumocyte apoptosis during lung ischemia–reperfusion injury in an experimental pulmonary thromboembolism model

Deng

Zhai

et al. 2015

J Thromb Thrombolysis

View full text Add to dashboard Cite

Lung ischemia–reperfusion injury (LIRI) may occur in the region of the affected lung after reperfusion therapy. The inflammatory response mechanisms related to LIRI in pulmonary thromboembolism (PTE), especially in chronic PTE, need to be studied further. In a PTE model, inflammatory response and apoptosis may occur during LIRI and nitric oxide (NO) inhalation may alleviate the inflammatory response and apoptosis of pneumocytes during LIRI. A PTE canine model was established through blood clot embolism to the right lower lobar pulmonary artery. Two weeks later, we performed embolectomy with reperfusion to examine the LIRI changes among different groups. In particular, the ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2), serum concentrations of tumor necrosis factor-α (TNF-α), myeloperoxidase concentrations in lung homogenates, alveolar polymorphonuclear neutrophils (PMNs), lobar lung wet to dry ratio (W/D ratio), apoptotic pneumocytes, and lung sample ultrastructure were assessed. The PaO2/FiO2 in the NO inhalation group increased significantly when compared with the reperfusion group 4 and 6 h after reperfusion (368.83 ± 55.29 vs. 287.90 ± 54.84 mmHg, P < 0.05 and 380.63 ± 56.83 vs. 292.83 ± 6 0.34 mmHg, P < 0.05, respectively). In the NO inhalation group, TNF-α concentrations and alveolar PMN infiltration were significantly decreased as compared with those of the reperfusion group, 6 h after reperfusion (7.28 ± 1.49 vs. 8.90 ± 1.43 pg/mL, P < 0.05 and [(19 ± 6)/10 high power field (HPF) vs. (31 ± 11)/10 HPF, P < 0.05, respectively]. The amount of apoptotic pneumocytes in the lower lobar lung was negatively correlated with the arterial blood PaO2/FiO2, presented a positive correlation trend with the W/D ratio of the lower lobar lung, and a positive correlation with alveolar PMN in the reperfusion group and NO inhalation group. NO provided at 20 ppm for 6 h significantly alleviated LIRI in the PTE model. Our data indicate that, during LIRI, an obvious inflammatory response and apoptosis occur in our PTE model and NO inhalation may be useful in treating LIRI by alleviating the inflammatory response and pneumocyte apoptosis. This potential application warrants further investigation.

show abstract

Section: Discussionmentioning

confidence: 99%

Inflammatory response and pneumocyte apoptosis during lung ischemia–reperfusion injury in an experimental pulmonary thromboembolism model

Deng

Zhai

et al. 2015

J Thromb Thrombolysis

View full text Add to dashboard Cite

show abstract

“…In our experimental model, when inhaled NO at 20 ppm was administered, the PaO2/FiO2 decreased significantly at the time points of 2, 4 hours after reperfusion by embolectomy and, at the time point of 6 hours after reperfusion, increased gradually to the baseline mainly due to the improvement in V/Q matching [3,14,15]. When compared with the Reperfusion group, the PaO2/FiO2 increased significantly after inhaling 20 ppm NO for 4 or 6 hours, one of the mechanisms relating to elevating inducible nitric oxide synthase (iNOS) expression, and NOS activity in the lungs [41].…”

Section: Discussionmentioning

confidence: 99%

“…When compared with the Reperfusion group, the PaO2/FiO2 increased significantly after inhaling 20 ppm NO for 4 or 6 hours, one of the mechanisms relating to elevating inducible nitric oxide synthase (iNOS) expression, and NOS activity in the lungs [41]. After inhaling NO for 6 hours, the mPAP decreased to the level much lower than that of the 4 hours and the PVR decreased significantly possibly due to the regional vasodilatation effect of inhaled NO [3,14,15] when compared with that in the Reperfusion group , which are in accordance with the clinical investigations of RPE after pulmonary suction thrombectomy and pulmonary thromboendarterectomy for chronic PTE.…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of inhaled NO on apoptotic pneumocytes in pulmonary thromboembolism model

Deng

Yang

Lin

et al. 2014

Theor Biol Med Model

View full text Add to dashboard Cite

BackgroundLung ischemia–reperfusion injury (LIRI) may occur in the region of the affected lung after reperfusion therapy. Inhaled NO may be useful in treating acute and chronic pulmonary thromboembolism (PTE) due to the biological effect property of NO.MethodsA PTE canine model was established through selectively embolizing blood clots to an intended right lower lobar pulmonary artery. PaO2/FiO2, the mPAP and PVR were investigated at the time points of 2, 4, 6 hours after inhaled NO. Masson’s trichrome stain, apoptotic pneumocytes and lung sample ultrastructure were also investigated among different groups.ResultsThe PaO2/FiO2 in the Inhaled NO group increased significantly when compared with the Reperfusion group at time points of 4 and 6 hours after reperfusion, mPAP decreased significantly at point of 2 hours and the PVR decreased significantly at point of 6 hours after reperfusion. The amounts of apoptotic type II pneumocytes in the lower lobar lung have negative correlation trend with the arterial blood PaO2/FiO2 in Reperfusion group and Inhaled NO group. Inhaled nitric oxide given at 20 ppm for 6 hours can significantly alleviate the LIRI in the model.ConclusionsDramatic physiological improvements are seen during the therapeutic use of inhaled NO in pulmonary thromboembolism canine model. Inhaled NO may be useful in treating LIRI in acute or chronic PTE by alleviating apoptotic type II pneumocytes. This potential application warrants further investigation.

show abstract

“…A large variety of case reports have been published on the use of iNO, ranging from iNO administered to patients with RV failure (including PE-induced) as primary indication; as bridge to embolectomy or thrombolysis; with acute-on-chronic PE; during PE-induced cardiac arrest; on extra-corporal membrane oxygenation (ECMO) support or in case of contraindication to thrombolysis. 92–98 Some cases describe the use of iNO to treat increased PAP after embolectomy of acute PE 99–101 though not all with impressive hemodynamic responses. 102 iNO has been used in children and even infants with PE without success.…”

Section: Resultsmentioning

confidence: 99%

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

et al. 2020

View full text Add to dashboard Cite

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.

show abstract

Inhaled Nitric Oxide as an Adjunct to Suction Thrombectomy for Pulmonary Embolism

Cited by 8 publications

References 19 publications

Inflammatory response and pneumocyte apoptosis during lung ischemia–reperfusion injury in an experimental pulmonary thromboembolism model

Inflammatory response and pneumocyte apoptosis during lung ischemia–reperfusion injury in an experimental pulmonary thromboembolism model

Beneficial effects of inhaled NO on apoptotic pneumocytes in pulmonary thromboembolism model

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

Contact Info

Product

Resources

About