Inhaled nitric oxide attenuates reperfusion injury in non-heartbeating- donor lung transplantation

Emile A. Bacha, Hassan Sellak, Shinya Murakami, Guy Michel Mazmanian, Hélène Détruit, Vincent De Montpreville, Alain R. Chapelier, Jean Marie Libert, Philippe G. Dartevelle, Philippe Hervé

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Abstract

Background. Non-heartbeating-donor (NHBD) lung transplantation could help reduce the current organ shortage. Polymorphonuclear neutrophil (PMN) activation plays a pivotal role in ischemia-reperfusion injury (I-R), and can be inhibited by nitric oxide (NO). We hypothesized that inhaled NO might be beneficial in NHBD lung transplantation. Methods. The effect of inhaled NO on PMNs was studied by measuring in vivo PMN lung sequestration (myeloperoxidase activity) and adhesion of recipient circulating PMNs to cultured pulmonary artery endothelial cells (PAECs) in vitro. Pigs were randomly assigned to an NO or a control group (n=9 each). In the NO group, cadavers and recipients were ventilated with oxygen and 30 parts per million of NO. After 3 hr of postmortem in situ warm ischemia and 2 hr of cold ischemia, left allotransplantation was performed. The right pulmonary artery was ligated, and hemodynamic and gas exchange data were recorded hourly for 9 hr. Recipient PMN adherence to tumor necrosis factor-α- and calcium ionophore- stimulated PAECs was measured before and after reperfusion, and lung PMN sequestration was determined after death. Results. NO-treated animals exhibited lowered pulmonary vascular resistance (P<0.01), as well as improved oxygenation (P<0.01) and survival (P<0.05). Adhesion of PMNs to PAECs was inhibited in the NO group before (P<0.001) and after reperfusion (P<0.0001). Lung PMN sequestration was reduced by NO (P<0.05). Conclusions. Inhaled NO attenuates I-R injury after NHBD lung transplantation. This is likely due to the prevention of I-R-induced pulmonary vasoconstriction and to the direct effect on peripheral blood PMN adhesion to endothelium, which results in reduced sequestration and tissue injury.

Original languageEnglish (US)
Pages (from-to)1380-1386
Number of pages7
JournalTransplantation
Volume63
Issue number10
DOIs
StatePublished - May 27 1997

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Lung Transplantation
Reperfusion Injury
Nitric Oxide
Neutrophils
Pulmonary Artery
Lung
Endothelial Cells
Reperfusion
Cold Ischemia
Warm Ischemia
Neutrophil Activation
Calcium Ionophores
Wounds and Injuries
Vasoconstriction
Cadaver
Vascular Resistance
Peroxidase
Endothelium
Swine
Tumor Necrosis Factor-alpha

ASJC Scopus subject areas

  • Transplantation

Cite this

Bacha, E. A., Sellak, H., Murakami, S., Mazmanian, G. M., Détruit, H., De Montpreville, V., ... Hervé, P. (1997). Inhaled nitric oxide attenuates reperfusion injury in non-heartbeating- donor lung transplantation. Transplantation, 63(10), 1380-1386. https://doi.org/10.1097/00007890-199705270-00002

Inhaled nitric oxide attenuates reperfusion injury in non-heartbeating- donor lung transplantation. / Bacha, Emile A.; Sellak, Hassan; Murakami, Shinya; Mazmanian, Guy Michel; Détruit, Hélène; De Montpreville, Vincent; Chapelier, Alain R.; Libert, Jean Marie; Dartevelle, Philippe G.; Hervé, Philippe.

In: Transplantation, Vol. 63, No. 10, 27.05.1997, p. 1380-1386.

Research output: Contribution to journalArticle

Bacha, EA, Sellak, H, Murakami, S, Mazmanian, GM, Détruit, H, De Montpreville, V, Chapelier, AR, Libert, JM, Dartevelle, PG & Hervé, P 1997, 'Inhaled nitric oxide attenuates reperfusion injury in non-heartbeating- donor lung transplantation', Transplantation, vol. 63, no. 10, pp. 1380-1386. https://doi.org/10.1097/00007890-199705270-00002
Bacha EA, Sellak H, Murakami S, Mazmanian GM, Détruit H, De Montpreville V et al. Inhaled nitric oxide attenuates reperfusion injury in non-heartbeating- donor lung transplantation. Transplantation. 1997 May 27;63(10):1380-1386. https://doi.org/10.1097/00007890-199705270-00002
Bacha, Emile A. ; Sellak, Hassan ; Murakami, Shinya ; Mazmanian, Guy Michel ; Détruit, Hélène ; De Montpreville, Vincent ; Chapelier, Alain R. ; Libert, Jean Marie ; Dartevelle, Philippe G. ; Hervé, Philippe. / Inhaled nitric oxide attenuates reperfusion injury in non-heartbeating- donor lung transplantation. In: Transplantation. 1997 ; Vol. 63, No. 10. pp. 1380-1386.
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abstract = "Background. Non-heartbeating-donor (NHBD) lung transplantation could help reduce the current organ shortage. Polymorphonuclear neutrophil (PMN) activation plays a pivotal role in ischemia-reperfusion injury (I-R), and can be inhibited by nitric oxide (NO). We hypothesized that inhaled NO might be beneficial in NHBD lung transplantation. Methods. The effect of inhaled NO on PMNs was studied by measuring in vivo PMN lung sequestration (myeloperoxidase activity) and adhesion of recipient circulating PMNs to cultured pulmonary artery endothelial cells (PAECs) in vitro. Pigs were randomly assigned to an NO or a control group (n=9 each). In the NO group, cadavers and recipients were ventilated with oxygen and 30 parts per million of NO. After 3 hr of postmortem in situ warm ischemia and 2 hr of cold ischemia, left allotransplantation was performed. The right pulmonary artery was ligated, and hemodynamic and gas exchange data were recorded hourly for 9 hr. Recipient PMN adherence to tumor necrosis factor-α- and calcium ionophore- stimulated PAECs was measured before and after reperfusion, and lung PMN sequestration was determined after death. Results. NO-treated animals exhibited lowered pulmonary vascular resistance (P<0.01), as well as improved oxygenation (P<0.01) and survival (P<0.05). Adhesion of PMNs to PAECs was inhibited in the NO group before (P<0.001) and after reperfusion (P<0.0001). Lung PMN sequestration was reduced by NO (P<0.05). Conclusions. Inhaled NO attenuates I-R injury after NHBD lung transplantation. This is likely due to the prevention of I-R-induced pulmonary vasoconstriction and to the direct effect on peripheral blood PMN adhesion to endothelium, which results in reduced sequestration and tissue injury.",
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T1 - Inhaled nitric oxide attenuates reperfusion injury in non-heartbeating- donor lung transplantation

AU - Bacha, Emile A.

AU - Sellak, Hassan

AU - Murakami, Shinya

AU - Mazmanian, Guy Michel

AU - Détruit, Hélène

AU - De Montpreville, Vincent

AU - Chapelier, Alain R.

AU - Libert, Jean Marie

AU - Dartevelle, Philippe G.

AU - Hervé, Philippe

PY - 1997/5/27

Y1 - 1997/5/27

N2 - Background. Non-heartbeating-donor (NHBD) lung transplantation could help reduce the current organ shortage. Polymorphonuclear neutrophil (PMN) activation plays a pivotal role in ischemia-reperfusion injury (I-R), and can be inhibited by nitric oxide (NO). We hypothesized that inhaled NO might be beneficial in NHBD lung transplantation. Methods. The effect of inhaled NO on PMNs was studied by measuring in vivo PMN lung sequestration (myeloperoxidase activity) and adhesion of recipient circulating PMNs to cultured pulmonary artery endothelial cells (PAECs) in vitro. Pigs were randomly assigned to an NO or a control group (n=9 each). In the NO group, cadavers and recipients were ventilated with oxygen and 30 parts per million of NO. After 3 hr of postmortem in situ warm ischemia and 2 hr of cold ischemia, left allotransplantation was performed. The right pulmonary artery was ligated, and hemodynamic and gas exchange data were recorded hourly for 9 hr. Recipient PMN adherence to tumor necrosis factor-α- and calcium ionophore- stimulated PAECs was measured before and after reperfusion, and lung PMN sequestration was determined after death. Results. NO-treated animals exhibited lowered pulmonary vascular resistance (P<0.01), as well as improved oxygenation (P<0.01) and survival (P<0.05). Adhesion of PMNs to PAECs was inhibited in the NO group before (P<0.001) and after reperfusion (P<0.0001). Lung PMN sequestration was reduced by NO (P<0.05). Conclusions. Inhaled NO attenuates I-R injury after NHBD lung transplantation. This is likely due to the prevention of I-R-induced pulmonary vasoconstriction and to the direct effect on peripheral blood PMN adhesion to endothelium, which results in reduced sequestration and tissue injury.

AB - Background. Non-heartbeating-donor (NHBD) lung transplantation could help reduce the current organ shortage. Polymorphonuclear neutrophil (PMN) activation plays a pivotal role in ischemia-reperfusion injury (I-R), and can be inhibited by nitric oxide (NO). We hypothesized that inhaled NO might be beneficial in NHBD lung transplantation. Methods. The effect of inhaled NO on PMNs was studied by measuring in vivo PMN lung sequestration (myeloperoxidase activity) and adhesion of recipient circulating PMNs to cultured pulmonary artery endothelial cells (PAECs) in vitro. Pigs were randomly assigned to an NO or a control group (n=9 each). In the NO group, cadavers and recipients were ventilated with oxygen and 30 parts per million of NO. After 3 hr of postmortem in situ warm ischemia and 2 hr of cold ischemia, left allotransplantation was performed. The right pulmonary artery was ligated, and hemodynamic and gas exchange data were recorded hourly for 9 hr. Recipient PMN adherence to tumor necrosis factor-α- and calcium ionophore- stimulated PAECs was measured before and after reperfusion, and lung PMN sequestration was determined after death. Results. NO-treated animals exhibited lowered pulmonary vascular resistance (P<0.01), as well as improved oxygenation (P<0.01) and survival (P<0.05). Adhesion of PMNs to PAECs was inhibited in the NO group before (P<0.001) and after reperfusion (P<0.0001). Lung PMN sequestration was reduced by NO (P<0.05). Conclusions. Inhaled NO attenuates I-R injury after NHBD lung transplantation. This is likely due to the prevention of I-R-induced pulmonary vasoconstriction and to the direct effect on peripheral blood PMN adhesion to endothelium, which results in reduced sequestration and tissue injury.

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