Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock
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 p...
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| Veröffentlicht in: | Experimental and therapeutic medicine 2017-04, Vol.13 (4), p.1369-1375 |
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| creator | Kronas, Nils Peters, Birte Richter, Hans Peter Goetz, Alwin Eduard Kubitz, Jens Christian |
| description | 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 |
| doi_str_mv | 10.3892/etm.2017.4149 |
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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.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2017.4149</identifier><identifier>PMID: 28413479</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Analysis ; Blood pressure ; Care and treatment ; Catheters ; Guanylate cyclase ; Heart failure ; Nitric oxide ; Pulmonary hypertension ; Risk factors ; Sepsis ; Septic shock ; Vascular resistance ; Veins & arteries</subject><ispartof>Experimental and therapeutic medicine, 2017-04, Vol.13 (4), p.1369-1375</ispartof><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright © 2017, Spandidos Publications 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-c9a01e9c59eb4f6a25589b1b3c1276bd60a2a5767a088cc0ff733aaae962c4a3</citedby><cites>FETCH-LOGICAL-c482t-c9a01e9c59eb4f6a25589b1b3c1276bd60a2a5767a088cc0ff733aaae962c4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377276/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377276/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28413479$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kronas, Nils</creatorcontrib><creatorcontrib>Peters, Birte</creatorcontrib><creatorcontrib>Richter, Hans Peter</creatorcontrib><creatorcontrib>Goetz, Alwin Eduard</creatorcontrib><creatorcontrib>Kubitz, Jens Christian</creatorcontrib><title>Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>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.</description><subject>Analysis</subject><subject>Blood pressure</subject><subject>Care and treatment</subject><subject>Catheters</subject><subject>Guanylate cyclase</subject><subject>Heart failure</subject><subject>Nitric oxide</subject><subject>Pulmonary hypertension</subject><subject>Risk factors</subject><subject>Sepsis</subject><subject>Septic shock</subject><subject>Vascular resistance</subject><subject>Veins & arteries</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptUktv1DAQjhCIVqVHrsgSFy672IkT2xekquJRqRKX3q2JM9l1Sezgx4r-nv5RHHVbKMI-2PL3GM_oq6q3jG4bqeqPmOZtTZnYcsbVi-qUCVVvGGXty-OdKslOqvMYb2lZbcekbF9XJ7XkrOFCnVb3V24PEyR7QAJuINalAAd0PkcSk53zinlH_Eiin3I_IdllcHflGYm5MxNEJAGHbDCSJU-zdxDuyAGiKdJQoGhjAmce7U3AIonEQBgsGOJzWnIqAMFfCwY7o0swkYhLsobEvTc_3lSvRpginh_Ps-rmy-eby2-b6-9fry4vrjeGyzptjALKUJlWYc_HDuq2lapnfWNYLbp-6CjU0IpOAJXSGDqOomkAAFVXGw7NWfXpwXbJ_YyDwXUUk17Kn0pL2oPVzxFn93rnD7pthCgVisGHo0HwPzPGpGcbDU4TOCzz1GX4UnWio3Whvv-HeutzcKU7zZTiijIlmz-sHUyorRt9qWtWU33BVcO5ZEwU1vY_rLIHnK3xDkdb3p8JNg8CE3yMAcenHhnVa650yZVec6XXXBX-u78H88R-TFHzG8wvzb0</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>Kronas, Nils</creator><creator>Peters, Birte</creator><creator>Richter, Hans Peter</creator><creator>Goetz, Alwin Eduard</creator><creator>Kubitz, Jens Christian</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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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.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>28413479</pmid><doi>10.3892/etm.2017.4149</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Blood pressure Care and treatment Catheters Guanylate cyclase Heart failure Nitric oxide Pulmonary hypertension Risk factors Sepsis Septic shock Vascular resistance Veins & arteries |
| title | Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock |
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