Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock
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Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock. / Kronas, Nils; Peters, Birte; Richter, Hans Peter; Goetz, Alwin Eduard; Kubitz, Jens Christian.
in: EXP THER MED, Jahrgang 13, Nr. 4, 04.2017, S. 1369-1375.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock
AU - Kronas, Nils
AU - Peters, Birte
AU - Richter, Hans Peter
AU - Goetz, Alwin Eduard
AU - Kubitz, Jens Christian
PY - 2017/4
Y1 - 2017/4
N2 - The effects of inhaled and intravenous application of a guanylate cyclase stimulator (BAY 41-8543) on pulmonary vascular resistance (PVR) and cardiac output (CO) were investigated in an experimental model of septic shock. Following induction of septic shock, anaesthetized pigs (n=31) were randomly place into two groups receiving different interventions. Animals in the first group received intravenous BAY 41-8543 (0.6 mg), inhalative BAY 41-8543 (6 mg) or a placebo. In the second group, the dosage of BAY 41-8543 was increased two-fold or combined with inhalation of nitric oxide (iNO). Intravenous and inhaled administration of BAY 41-8543 resulted in a significantly (P<0.05) reduced PVR and increased CO compared with the placebo. Increasing the dosage of BAY 41-8543 or combining it with iNO did not further decrease PVR. The results of the present study indicate that BAY 41-8543 effectively reduces PVR and increases CO in septic shock, through inhaled or intravenous routes of administration.
AB - The effects of inhaled and intravenous application of a guanylate cyclase stimulator (BAY 41-8543) on pulmonary vascular resistance (PVR) and cardiac output (CO) were investigated in an experimental model of septic shock. Following induction of septic shock, anaesthetized pigs (n=31) were randomly place into two groups receiving different interventions. Animals in the first group received intravenous BAY 41-8543 (0.6 mg), inhalative BAY 41-8543 (6 mg) or a placebo. In the second group, the dosage of BAY 41-8543 was increased two-fold or combined with inhalation of nitric oxide (iNO). Intravenous and inhaled administration of BAY 41-8543 resulted in a significantly (P<0.05) reduced PVR and increased CO compared with the placebo. Increasing the dosage of BAY 41-8543 or combining it with iNO did not further decrease PVR. The results of the present study indicate that BAY 41-8543 effectively reduces PVR and increases CO in septic shock, through inhaled or intravenous routes of administration.
U2 - 10.3892/etm.2017.4149
DO - 10.3892/etm.2017.4149
M3 - SCORING: Journal article
C2 - 28413479
VL - 13
SP - 1369
EP - 1375
JO - EXP THER MED
JF - EXP THER MED
SN - 1792-0981
IS - 4
ER -