Glucagon-like peptide-1 stimulates acute secretion of pro-atrial natriuretic peptide from the isolated, perfused pig lung exposed to warm ischemia
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Glucagon-like peptide-1 stimulates acute secretion of pro-atrial natriuretic peptide from the isolated, perfused pig lung exposed to warm ischemia. / Balk-Møller, Emilie; Hebsgaard, Mathilde M. B.; Lilleør, Nikolaj B.; Møller, Christian H.; Gøtze, Jens P.; Kissow, Hannelouise.
In: Frontiers in Transplantation, Vol. 1, 1082634, 2022.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Glucagon-like peptide-1 stimulates acute secretion of pro-atrial natriuretic peptide from the isolated, perfused pig lung exposed to warm ischemia
AU - Balk-Møller, Emilie
AU - Hebsgaard, Mathilde M. B.
AU - Lilleør, Nikolaj B.
AU - Møller, Christian H.
AU - Gøtze, Jens P.
AU - Kissow, Hannelouise
PY - 2022
Y1 - 2022
N2 - Glucagon-like peptide-1 (GLP-1) has proven to be protective in animal models of lung disease but the underlying mechanisms are unclear. Atrial natriuretic peptide (ANP) is mainly produced in the heart. As ANP possesses potent vaso- and bronchodilatory effects in pulmonary disease, we hypothesised that the protective functions of GLP-1 could involve potentiation of local ANP secretion from the lung. We examined whether the GLP-1 receptor agonist liraglutide was able to improve oxygenation in lungs exposed to 2 h of warm ischemia and if liraglutide stimulated ANP secretion from the lungs in the porcine ex vivo lung perfusion (EVLP) model. Pigs were given a bolus of 40 µg/kg liraglutide or saline 1 h prior to sacrifice. The lungs were then left in vivo for 2 h, removed en bloc and placed in the EVLP machinery. Lungs from the liraglutide treated group were further exposed to liraglutide in the perfusion buffer (1.125 mg). Main endpoints were oxygenation capacity, and plasma and perfusate concentrations of proANP and inflammatory markers. Lung oxygenation capacity, plasma concentrations of proANP or concentrations of inflammatory markers were not different between groups. ProANP secretion from the isolated perfused lungs were markedly higher in the liraglutide treated group (area under curve for the first 30 min in the liraglutide group: 635 ± 237 vs. 38 ± 38 pmol/L x min in the saline group) (p < 0.05). From these results, we concluded that liraglutide potentiated local ANP secretion from the lungs.
AB - Glucagon-like peptide-1 (GLP-1) has proven to be protective in animal models of lung disease but the underlying mechanisms are unclear. Atrial natriuretic peptide (ANP) is mainly produced in the heart. As ANP possesses potent vaso- and bronchodilatory effects in pulmonary disease, we hypothesised that the protective functions of GLP-1 could involve potentiation of local ANP secretion from the lung. We examined whether the GLP-1 receptor agonist liraglutide was able to improve oxygenation in lungs exposed to 2 h of warm ischemia and if liraglutide stimulated ANP secretion from the lungs in the porcine ex vivo lung perfusion (EVLP) model. Pigs were given a bolus of 40 µg/kg liraglutide or saline 1 h prior to sacrifice. The lungs were then left in vivo for 2 h, removed en bloc and placed in the EVLP machinery. Lungs from the liraglutide treated group were further exposed to liraglutide in the perfusion buffer (1.125 mg). Main endpoints were oxygenation capacity, and plasma and perfusate concentrations of proANP and inflammatory markers. Lung oxygenation capacity, plasma concentrations of proANP or concentrations of inflammatory markers were not different between groups. ProANP secretion from the isolated perfused lungs were markedly higher in the liraglutide treated group (area under curve for the first 30 min in the liraglutide group: 635 ± 237 vs. 38 ± 38 pmol/L x min in the saline group) (p < 0.05). From these results, we concluded that liraglutide potentiated local ANP secretion from the lungs.
U2 - 10.3389/frtra.2022.1082634
DO - 10.3389/frtra.2022.1082634
M3 - Journal article
VL - 1
JO - Frontiers in Transplantation
JF - Frontiers in Transplantation
SN - 2813-2440
M1 - 1082634
ER -
ID: 331489621