Positive end-expiratory pressure-induced, calcium-channel-mediated increases in pulmonary vascular resistance in neonatal lambs
OBJECTIVESa) To study the dose response of the calcium-channel-mediated increases in pulmonary vascular resistance with different levels of positive end-expiratory pressure; b) to study the reversibility of the calcium-channel mediated increases in pulmonary vascular resistance after discontinuation...
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| Veröffentlicht in: | Critical care medicine 1993-07, Vol.21 (7), p.1066-1076 |
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| creator | VENKATARAMAN, SHEKHAR T FUHRMAN, BRADLEY P HOWLAND, DONNA F DEFRANCISIS, MARIA |
| description | OBJECTIVESa) To study the dose response of the calcium-channel-mediated increases in pulmonary vascular resistance with different levels of positive end-expiratory pressure; b) to study the reversibility of the calcium-channel mediated increases in pulmonary vascular resistance after discontinuation of positive end-expiratory pressure; and c) to study the effect of cyclooxygenase and lipoxygenase inhibition on the calcium-channel mediated increases in pulmonary vascular resistance.
DESIGNA prospective, multiexperimental, dose response study.
SETTINGLaboratory setting in a university hospital.
SUBJECTSTwenty-three 4− to 10-day-old neonatal lambs.
INTERVENTIONS AND MEASUREMENTSLungs of neonatal lambs were isolated in situ, and perfused at a constant flow rate, and ventilated at a fixed tidal volume and rate. Mean pulmonary arterial pressure responses to the application and discontinuation of four levels (3.7, 7.4, 11, and 14.7 mm Hg) of positive end-expiratory pressure were studied before and after calcium-channel blockade with verapamil (5 mg) (n = 12). In addition, the mean pulmonary arterial pressure response to 11 mm Hg of positive end-expiratory pressure was studied before and after inhibition of cyclooxygenase with indo-methacin (10 mg/kg) (n = 6) and lipoxygenase with diethylcarbamazine (100 mg/kg) (n = 5).
RESULTSThe magnitude of the calcium-channel-dependent mean pulmonary arterial pressure response 4 mins after the application of positive end-expiratory pressure was dose related (2.1, 3.0,4.1, and 5.5 mm Hg with 3.7,7.4, 11.0, and 14.7 mmHg positive end-expiratory pressure, respectively) and entirely reversible on discontinuation of positive end-expiratory pressure with a time course of 2 to 4 mins. Neither indomethacin nor diethylcarbamazine affected the pulmonary arterial pressure responses to positive end-expiratory pressure. Airway pressure changes with positive end-expiratory pressure were not affected by verapamil indomethacin, or diethylcarbamazine.
CONCLUSIONSThe calcium-channel-mediated pulmonary arterial pressure responses with positive end-expiratory pressure, applied during continuous positive pressure breathing, occur even at low levels of positive end-expiratory pressure, are dose dependent, and are not abolished by treatment with indomethacin or diethylcarbamazine. |
| doi_str_mv | 10.1097/00003246-199307000-00025 |
| format | Article |
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DESIGNA prospective, multiexperimental, dose response study.
SETTINGLaboratory setting in a university hospital.
SUBJECTSTwenty-three 4− to 10-day-old neonatal lambs.
INTERVENTIONS AND MEASUREMENTSLungs of neonatal lambs were isolated in situ, and perfused at a constant flow rate, and ventilated at a fixed tidal volume and rate. Mean pulmonary arterial pressure responses to the application and discontinuation of four levels (3.7, 7.4, 11, and 14.7 mm Hg) of positive end-expiratory pressure were studied before and after calcium-channel blockade with verapamil (5 mg) (n = 12). In addition, the mean pulmonary arterial pressure response to 11 mm Hg of positive end-expiratory pressure was studied before and after inhibition of cyclooxygenase with indo-methacin (10 mg/kg) (n = 6) and lipoxygenase with diethylcarbamazine (100 mg/kg) (n = 5).
RESULTSThe magnitude of the calcium-channel-dependent mean pulmonary arterial pressure response 4 mins after the application of positive end-expiratory pressure was dose related (2.1, 3.0,4.1, and 5.5 mm Hg with 3.7,7.4, 11.0, and 14.7 mmHg positive end-expiratory pressure, respectively) and entirely reversible on discontinuation of positive end-expiratory pressure with a time course of 2 to 4 mins. Neither indomethacin nor diethylcarbamazine affected the pulmonary arterial pressure responses to positive end-expiratory pressure. Airway pressure changes with positive end-expiratory pressure were not affected by verapamil indomethacin, or diethylcarbamazine.
CONCLUSIONSThe calcium-channel-mediated pulmonary arterial pressure responses with positive end-expiratory pressure, applied during continuous positive pressure breathing, occur even at low levels of positive end-expiratory pressure, are dose dependent, and are not abolished by treatment with indomethacin or diethylcarbamazine.</description><identifier>ISSN: 0090-3493</identifier><identifier>EISSN: 1530-0293</identifier><identifier>DOI: 10.1097/00003246-199307000-00025</identifier><identifier>PMID: 8391414</identifier><identifier>CODEN: CCMDC7</identifier><language>eng</language><publisher>Hagerstown, MD: Williams & Wilkins</publisher><subject>Airway Resistance - drug effects ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Animals, Newborn - physiology ; Biological and medical sciences ; Blood Pressure - drug effects ; Calcium Channels - physiology ; Diethylcarbamazine - pharmacology ; Emergency and intensive respiratory care ; Indomethacin - pharmacology ; Intensive care medicine ; Medical sciences ; Positive-Pressure Respiration ; Prospective Studies ; Pulmonary Artery - physiology ; Pulmonary Circulation - drug effects ; Pulmonary Circulation - physiology ; Sheep ; Vascular Resistance - drug effects ; Vascular Resistance - physiology ; Verapamil - pharmacology</subject><ispartof>Critical care medicine, 1993-07, Vol.21 (7), p.1066-1076</ispartof><rights>Williams & Wilkins 1993. All Rights Reserved.</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3845-be3429ccbc3d3b0b81939065063655cf6d32221a3fb3be6f5d161cf022d62f8e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4799141$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8391414$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VENKATARAMAN, SHEKHAR T</creatorcontrib><creatorcontrib>FUHRMAN, BRADLEY P</creatorcontrib><creatorcontrib>HOWLAND, DONNA F</creatorcontrib><creatorcontrib>DEFRANCISIS, MARIA</creatorcontrib><title>Positive end-expiratory pressure-induced, calcium-channel-mediated increases in pulmonary vascular resistance in neonatal lambs</title><title>Critical care medicine</title><addtitle>Crit Care Med</addtitle><description>OBJECTIVESa) To study the dose response of the calcium-channel-mediated increases in pulmonary vascular resistance with different levels of positive end-expiratory pressure; b) to study the reversibility of the calcium-channel mediated increases in pulmonary vascular resistance after discontinuation of positive end-expiratory pressure; and c) to study the effect of cyclooxygenase and lipoxygenase inhibition on the calcium-channel mediated increases in pulmonary vascular resistance.
DESIGNA prospective, multiexperimental, dose response study.
SETTINGLaboratory setting in a university hospital.
SUBJECTSTwenty-three 4− to 10-day-old neonatal lambs.
INTERVENTIONS AND MEASUREMENTSLungs of neonatal lambs were isolated in situ, and perfused at a constant flow rate, and ventilated at a fixed tidal volume and rate. Mean pulmonary arterial pressure responses to the application and discontinuation of four levels (3.7, 7.4, 11, and 14.7 mm Hg) of positive end-expiratory pressure were studied before and after calcium-channel blockade with verapamil (5 mg) (n = 12). In addition, the mean pulmonary arterial pressure response to 11 mm Hg of positive end-expiratory pressure was studied before and after inhibition of cyclooxygenase with indo-methacin (10 mg/kg) (n = 6) and lipoxygenase with diethylcarbamazine (100 mg/kg) (n = 5).
RESULTSThe magnitude of the calcium-channel-dependent mean pulmonary arterial pressure response 4 mins after the application of positive end-expiratory pressure was dose related (2.1, 3.0,4.1, and 5.5 mm Hg with 3.7,7.4, 11.0, and 14.7 mmHg positive end-expiratory pressure, respectively) and entirely reversible on discontinuation of positive end-expiratory pressure with a time course of 2 to 4 mins. Neither indomethacin nor diethylcarbamazine affected the pulmonary arterial pressure responses to positive end-expiratory pressure. Airway pressure changes with positive end-expiratory pressure were not affected by verapamil indomethacin, or diethylcarbamazine.
CONCLUSIONSThe calcium-channel-mediated pulmonary arterial pressure responses with positive end-expiratory pressure, applied during continuous positive pressure breathing, occur even at low levels of positive end-expiratory pressure, are dose dependent, and are not abolished by treatment with indomethacin or diethylcarbamazine.</description><subject>Airway Resistance - drug effects</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Animals, Newborn - physiology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Calcium Channels - physiology</subject><subject>Diethylcarbamazine - pharmacology</subject><subject>Emergency and intensive respiratory care</subject><subject>Indomethacin - pharmacology</subject><subject>Intensive care medicine</subject><subject>Medical sciences</subject><subject>Positive-Pressure Respiration</subject><subject>Prospective Studies</subject><subject>Pulmonary Artery - physiology</subject><subject>Pulmonary Circulation - drug effects</subject><subject>Pulmonary Circulation - physiology</subject><subject>Sheep</subject><subject>Vascular Resistance - drug effects</subject><subject>Vascular Resistance - physiology</subject><subject>Verapamil - pharmacology</subject><issn>0090-3493</issn><issn>1530-0293</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU2PFCEQQInRrLOrP8GkD8aTKFDQ3RzNZnVNNtGDngkN1RmU_hCaXT3512WccW6SEKjUqwIehDScveFMd29ZHSBkS7nWwLoa0TqFekR2XEENhIbHZMeYZhSkhqfkMudvjHGpOrggFz1oLrnckd-flxy2cI8Nzp7izzUkuy3pV7MmzLkkpGH2xaF_3TgbXSgTdXs7zxjphD7YDX0TZpfQZsx116wlTstsa4d7m12JNjW1U8ibnR0egBlrerOxiXYa8jPyZLQx4_PTekW-vr_5cn1L7z59-Hj97o466KWiA4IU2rnBgYeBDT3XoFmrWAutUm5sPQghuIVxgAHbUXnecjcyIXwrxh7hirw69l3T8qNg3swUssMYbb1PyaZTPa92ugr2R9ClJeeEo1lTmOp7DGfm4N78c2_O7s1f97X0xemMMlQ558KT7Jp_ecpXMzaOqSoJ-YzJTh-4iskj9rDEDVP-HssDJrNHG7e9-d_Pwx_rnJ4d</recordid><startdate>199307</startdate><enddate>199307</enddate><creator>VENKATARAMAN, SHEKHAR T</creator><creator>FUHRMAN, BRADLEY P</creator><creator>HOWLAND, DONNA F</creator><creator>DEFRANCISIS, MARIA</creator><general>Williams & Wilkins</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199307</creationdate><title>Positive end-expiratory pressure-induced, calcium-channel-mediated increases in pulmonary vascular resistance in neonatal lambs</title><author>VENKATARAMAN, SHEKHAR T ; FUHRMAN, BRADLEY P ; HOWLAND, DONNA F ; DEFRANCISIS, MARIA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3845-be3429ccbc3d3b0b81939065063655cf6d32221a3fb3be6f5d161cf022d62f8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Airway Resistance - drug effects</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Animals, Newborn - physiology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Calcium Channels - physiology</topic><topic>Diethylcarbamazine - pharmacology</topic><topic>Emergency and intensive respiratory care</topic><topic>Indomethacin - pharmacology</topic><topic>Intensive care medicine</topic><topic>Medical sciences</topic><topic>Positive-Pressure Respiration</topic><topic>Prospective Studies</topic><topic>Pulmonary Artery - physiology</topic><topic>Pulmonary Circulation - drug effects</topic><topic>Pulmonary Circulation - physiology</topic><topic>Sheep</topic><topic>Vascular Resistance - drug effects</topic><topic>Vascular Resistance - physiology</topic><topic>Verapamil - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VENKATARAMAN, SHEKHAR T</creatorcontrib><creatorcontrib>FUHRMAN, BRADLEY P</creatorcontrib><creatorcontrib>HOWLAND, DONNA F</creatorcontrib><creatorcontrib>DEFRANCISIS, MARIA</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VENKATARAMAN, SHEKHAR T</au><au>FUHRMAN, BRADLEY P</au><au>HOWLAND, DONNA F</au><au>DEFRANCISIS, MARIA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Positive end-expiratory pressure-induced, calcium-channel-mediated increases in pulmonary vascular resistance in neonatal lambs</atitle><jtitle>Critical care medicine</jtitle><addtitle>Crit Care Med</addtitle><date>1993-07</date><risdate>1993</risdate><volume>21</volume><issue>7</issue><spage>1066</spage><epage>1076</epage><pages>1066-1076</pages><issn>0090-3493</issn><eissn>1530-0293</eissn><coden>CCMDC7</coden><abstract>OBJECTIVESa) To study the dose response of the calcium-channel-mediated increases in pulmonary vascular resistance with different levels of positive end-expiratory pressure; b) to study the reversibility of the calcium-channel mediated increases in pulmonary vascular resistance after discontinuation of positive end-expiratory pressure; and c) to study the effect of cyclooxygenase and lipoxygenase inhibition on the calcium-channel mediated increases in pulmonary vascular resistance.
DESIGNA prospective, multiexperimental, dose response study.
SETTINGLaboratory setting in a university hospital.
SUBJECTSTwenty-three 4− to 10-day-old neonatal lambs.
INTERVENTIONS AND MEASUREMENTSLungs of neonatal lambs were isolated in situ, and perfused at a constant flow rate, and ventilated at a fixed tidal volume and rate. Mean pulmonary arterial pressure responses to the application and discontinuation of four levels (3.7, 7.4, 11, and 14.7 mm Hg) of positive end-expiratory pressure were studied before and after calcium-channel blockade with verapamil (5 mg) (n = 12). In addition, the mean pulmonary arterial pressure response to 11 mm Hg of positive end-expiratory pressure was studied before and after inhibition of cyclooxygenase with indo-methacin (10 mg/kg) (n = 6) and lipoxygenase with diethylcarbamazine (100 mg/kg) (n = 5).
RESULTSThe magnitude of the calcium-channel-dependent mean pulmonary arterial pressure response 4 mins after the application of positive end-expiratory pressure was dose related (2.1, 3.0,4.1, and 5.5 mm Hg with 3.7,7.4, 11.0, and 14.7 mmHg positive end-expiratory pressure, respectively) and entirely reversible on discontinuation of positive end-expiratory pressure with a time course of 2 to 4 mins. Neither indomethacin nor diethylcarbamazine affected the pulmonary arterial pressure responses to positive end-expiratory pressure. Airway pressure changes with positive end-expiratory pressure were not affected by verapamil indomethacin, or diethylcarbamazine.
CONCLUSIONSThe calcium-channel-mediated pulmonary arterial pressure responses with positive end-expiratory pressure, applied during continuous positive pressure breathing, occur even at low levels of positive end-expiratory pressure, are dose dependent, and are not abolished by treatment with indomethacin or diethylcarbamazine.</abstract><cop>Hagerstown, MD</cop><pub>Williams & Wilkins</pub><pmid>8391414</pmid><doi>10.1097/00003246-199307000-00025</doi><tpages>11</tpages></addata></record> |
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| ispartof | Critical care medicine, 1993-07, Vol.21 (7), p.1066-1076 |
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| subjects | Airway Resistance - drug effects Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Animals, Newborn - physiology Biological and medical sciences Blood Pressure - drug effects Calcium Channels - physiology Diethylcarbamazine - pharmacology Emergency and intensive respiratory care Indomethacin - pharmacology Intensive care medicine Medical sciences Positive-Pressure Respiration Prospective Studies Pulmonary Artery - physiology Pulmonary Circulation - drug effects Pulmonary Circulation - physiology Sheep Vascular Resistance - drug effects Vascular Resistance - physiology Verapamil - pharmacology |
| title | Positive end-expiratory pressure-induced, calcium-channel-mediated increases in pulmonary vascular resistance in neonatal lambs |
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