The Differential Effects of Prostaglandin E1 and Nitroglycerin on Regional Cerebral Oxygenation in Anesthetized Patients

We evaluated the effects of prostaglandin E1 (PGE1) and nitroglycerin (NTG) on regional tissue oxygenation and use in the brain using near infrared spectroscopy (NIRS).Twenty-four patients who underwent elective cardiac surgery were randomly divided into two groups. The study was performed after the...

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Veröffentlicht in:Anesthesia and analgesia 1997-11, Vol.85 (5), p.1054-1059
Hauptverfasser: Kadoi, Yuji, Saito, Shigeru, Morita, Toshihiro, Imai, Takasuke, Kawahara, Huminori, Fujita, Nao, Goto, Fumio
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container_end_page 1059
container_issue 5
container_start_page 1054
container_title Anesthesia and analgesia
container_volume 85
creator Kadoi, Yuji
Saito, Shigeru
Morita, Toshihiro
Imai, Takasuke
Kawahara, Huminori
Fujita, Nao
Goto, Fumio
description We evaluated the effects of prostaglandin E1 (PGE1) and nitroglycerin (NTG) on regional tissue oxygenation and use in the brain using near infrared spectroscopy (NIRS).Twenty-four patients who underwent elective cardiac surgery were randomly divided into two groups. The study was performed after the induction of anesthesia and before the start of the surgical procedure. After measuring arterial and jugular venous blood gases, cardiovascular hemodynamics, and relative cerebral oxyhemoglobin (HbO2), deoxyhemoglobin, and cytochrome aa3 at the baseline, PGE1 (n = 12) or NTG (n = 12) was infused intravenously at a rate of 0.3 g/kg or 5 g/kg, respectively. Thirty minutes after the start of drug infusion, administration of the drugs was stopped. Both PGE1 and NTG reduced mean arterial pressure to approximately 70% of the baseline value 10, 20, and 30 min after start of drug infusion (P < 0.05). Internal jugular venous pressure increased significantly during NTG but not during PGE1 infusion (P < 0.05). PGE1 increased HbO2 concentration, which was sustained for 30 min after discontinuing the drug. NTG increased HbO2 concentration, but this gradually returned to the baseline level after discontinuation of the drug. Baseline value of jugular oxygen saturation was 64.5% +/- 2.1%, and there was no significant changes during the infusion of PGE1 or NTG. These results demonstrate that both NTG and PGE1 increased cerebral oxygen saturation as measured by NIRS. This may be explained by local cerebral hyperemia without major alteration in flow/metabolism coupling of brain. The onset of this increase was slower and the duration of this effect after discontinuation of the drug was more prolonged with PGE1. These phenomena occurred despite the relatively similar time course of the effect of these two drugs on systemic hemodynamic values. ImplicationsThe cerebrovascular effects of vasodilators used for induced hypotension are not fully understood. In this study, we used near infrared spectrometry and jugular oxygen saturation measurement to assess the effects of prostaglandin E1 and nitroglycerin on cerebral perfusion. We found that nitroglycerin and prostaglandin E1 increase cerebral oxygen saturation as measured by near infrared spectrometry, but with different time courses. This information will hopefully help anesthesiologists to better maintain adequate regional cerebral oxygenation.(Anesth Analg 1997;85:1054-9)
doi_str_mv 10.1097/00000539-199711000-00017
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The study was performed after the induction of anesthesia and before the start of the surgical procedure. After measuring arterial and jugular venous blood gases, cardiovascular hemodynamics, and relative cerebral oxyhemoglobin (HbO2), deoxyhemoglobin, and cytochrome aa3 at the baseline, PGE1 (n = 12) or NTG (n = 12) was infused intravenously at a rate of 0.3 g/kg or 5 g/kg, respectively. Thirty minutes after the start of drug infusion, administration of the drugs was stopped. Both PGE1 and NTG reduced mean arterial pressure to approximately 70% of the baseline value 10, 20, and 30 min after start of drug infusion (P &lt; 0.05). Internal jugular venous pressure increased significantly during NTG but not during PGE1 infusion (P &lt; 0.05). PGE1 increased HbO2 concentration, which was sustained for 30 min after discontinuing the drug. NTG increased HbO2 concentration, but this gradually returned to the baseline level after discontinuation of the drug. Baseline value of jugular oxygen saturation was 64.5% +/- 2.1%, and there was no significant changes during the infusion of PGE1 or NTG. These results demonstrate that both NTG and PGE1 increased cerebral oxygen saturation as measured by NIRS. This may be explained by local cerebral hyperemia without major alteration in flow/metabolism coupling of brain. The onset of this increase was slower and the duration of this effect after discontinuation of the drug was more prolonged with PGE1. These phenomena occurred despite the relatively similar time course of the effect of these two drugs on systemic hemodynamic values. ImplicationsThe cerebrovascular effects of vasodilators used for induced hypotension are not fully understood. In this study, we used near infrared spectrometry and jugular oxygen saturation measurement to assess the effects of prostaglandin E1 and nitroglycerin on cerebral perfusion. We found that nitroglycerin and prostaglandin E1 increase cerebral oxygen saturation as measured by near infrared spectrometry, but with different time courses. 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Drug treatments ; Spectroscopy, Near-Infrared ; Thoracic Surgical Procedures ; Vasodilator Agents - therapeutic use ; Vasodilator agents. 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The study was performed after the induction of anesthesia and before the start of the surgical procedure. After measuring arterial and jugular venous blood gases, cardiovascular hemodynamics, and relative cerebral oxyhemoglobin (HbO2), deoxyhemoglobin, and cytochrome aa3 at the baseline, PGE1 (n = 12) or NTG (n = 12) was infused intravenously at a rate of 0.3 g/kg or 5 g/kg, respectively. Thirty minutes after the start of drug infusion, administration of the drugs was stopped. Both PGE1 and NTG reduced mean arterial pressure to approximately 70% of the baseline value 10, 20, and 30 min after start of drug infusion (P &lt; 0.05). Internal jugular venous pressure increased significantly during NTG but not during PGE1 infusion (P &lt; 0.05). PGE1 increased HbO2 concentration, which was sustained for 30 min after discontinuing the drug. NTG increased HbO2 concentration, but this gradually returned to the baseline level after discontinuation of the drug. Baseline value of jugular oxygen saturation was 64.5% +/- 2.1%, and there was no significant changes during the infusion of PGE1 or NTG. These results demonstrate that both NTG and PGE1 increased cerebral oxygen saturation as measured by NIRS. This may be explained by local cerebral hyperemia without major alteration in flow/metabolism coupling of brain. The onset of this increase was slower and the duration of this effect after discontinuation of the drug was more prolonged with PGE1. These phenomena occurred despite the relatively similar time course of the effect of these two drugs on systemic hemodynamic values. ImplicationsThe cerebrovascular effects of vasodilators used for induced hypotension are not fully understood. In this study, we used near infrared spectrometry and jugular oxygen saturation measurement to assess the effects of prostaglandin E1 and nitroglycerin on cerebral perfusion. We found that nitroglycerin and prostaglandin E1 increase cerebral oxygen saturation as measured by near infrared spectrometry, but with different time courses. This information will hopefully help anesthesiologists to better maintain adequate regional cerebral oxygenation.(Anesth Analg 1997;85:1054-9)</description><subject>Aged</subject><subject>Alprostadil - therapeutic use</subject><subject>Anesthesia, General - methods</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Brain - blood supply</subject><subject>Brain - metabolism</subject><subject>Cardiovascular system</subject><subject>Electron Transport Complex IV - metabolism</subject><subject>Hemoglobins - metabolism</subject><subject>Humans</subject><subject>Infusions, Intravenous</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nitroglycerin - therapeutic use</subject><subject>Oxygen Consumption - drug effects</subject><subject>Oxyhemoglobins - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Spectroscopy, Near-Infrared</subject><subject>Thoracic Surgical Procedures</subject><subject>Vasodilator Agents - therapeutic use</subject><subject>Vasodilator agents. Cerebral vasodilators</subject><issn>0003-2999</issn><issn>1526-7598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1UU2P0zAQtRBoKQs_AckHxC1gx7GdOa5K-ZBW7AotZ8txxq0hTRY71W759Uxp6Q1Llsdv3pvxPDPGpXgnBdj34rC0gkoCWCnpUtGW9glbSF2bympon7IFYaqqAeA5e1HKjwNFtOaCXYDSRgAs2OPdBvmHFCNmHOfkB76iOMyFT5Hf5qnMfj34sU8jX0lOAf-a5jyth33ATOA08m-4TtNIyiXV6DIFN4_7NY5-JpgT52rEMm9wTr-x57cEU6fykj2Lfij46nResu8fV3fLz9X1zacvy6vrKqgWbBVBmx50Z7UwAoMADAhdwNiC6tpG9R2iUQp7a6xsvK5V39YCY60646UEdcneHuve5-nXjh7itqkEHGgonHbFWVDWKCOJ2B6JgaYuGaO7z2nr895J4Q6mu3-mu7Pp7q_pJH196rHrttifhSeXKf_mlPcl-CFmP4ZUzrS61XUDDdGaI-1hGmbM5eewe8DsNuiHeeP-9-XqD94LmnE</recordid><startdate>199711</startdate><enddate>199711</enddate><creator>Kadoi, Yuji</creator><creator>Saito, Shigeru</creator><creator>Morita, Toshihiro</creator><creator>Imai, Takasuke</creator><creator>Kawahara, Huminori</creator><creator>Fujita, Nao</creator><creator>Goto, Fumio</creator><general>International Anesthesia Research Society</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>199711</creationdate><title>The Differential Effects of Prostaglandin E1 and Nitroglycerin on Regional Cerebral Oxygenation in Anesthetized Patients</title><author>Kadoi, Yuji ; Saito, Shigeru ; Morita, Toshihiro ; Imai, Takasuke ; Kawahara, Huminori ; Fujita, Nao ; Goto, Fumio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3897-f956d95b75060ec09ece9bcef893b843dbee633ed76714a523d820ef23b6a1193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Aged</topic><topic>Alprostadil - therapeutic use</topic><topic>Anesthesia, General - methods</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Brain - blood supply</topic><topic>Brain - metabolism</topic><topic>Cardiovascular system</topic><topic>Electron Transport Complex IV - metabolism</topic><topic>Hemoglobins - metabolism</topic><topic>Humans</topic><topic>Infusions, Intravenous</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nitroglycerin - therapeutic use</topic><topic>Oxygen Consumption - drug effects</topic><topic>Oxyhemoglobins - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Spectroscopy, Near-Infrared</topic><topic>Thoracic Surgical Procedures</topic><topic>Vasodilator Agents - therapeutic use</topic><topic>Vasodilator agents. Cerebral vasodilators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kadoi, Yuji</creatorcontrib><creatorcontrib>Saito, Shigeru</creatorcontrib><creatorcontrib>Morita, Toshihiro</creatorcontrib><creatorcontrib>Imai, Takasuke</creatorcontrib><creatorcontrib>Kawahara, Huminori</creatorcontrib><creatorcontrib>Fujita, Nao</creatorcontrib><creatorcontrib>Goto, Fumio</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>Anesthesia and analgesia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kadoi, Yuji</au><au>Saito, Shigeru</au><au>Morita, Toshihiro</au><au>Imai, Takasuke</au><au>Kawahara, Huminori</au><au>Fujita, Nao</au><au>Goto, Fumio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Differential Effects of Prostaglandin E1 and Nitroglycerin on Regional Cerebral Oxygenation in Anesthetized Patients</atitle><jtitle>Anesthesia and analgesia</jtitle><addtitle>Anesth Analg</addtitle><date>1997-11</date><risdate>1997</risdate><volume>85</volume><issue>5</issue><spage>1054</spage><epage>1059</epage><pages>1054-1059</pages><issn>0003-2999</issn><eissn>1526-7598</eissn><coden>AACRAT</coden><abstract>We evaluated the effects of prostaglandin E1 (PGE1) and nitroglycerin (NTG) on regional tissue oxygenation and use in the brain using near infrared spectroscopy (NIRS).Twenty-four patients who underwent elective cardiac surgery were randomly divided into two groups. The study was performed after the induction of anesthesia and before the start of the surgical procedure. After measuring arterial and jugular venous blood gases, cardiovascular hemodynamics, and relative cerebral oxyhemoglobin (HbO2), deoxyhemoglobin, and cytochrome aa3 at the baseline, PGE1 (n = 12) or NTG (n = 12) was infused intravenously at a rate of 0.3 g/kg or 5 g/kg, respectively. Thirty minutes after the start of drug infusion, administration of the drugs was stopped. Both PGE1 and NTG reduced mean arterial pressure to approximately 70% of the baseline value 10, 20, and 30 min after start of drug infusion (P &lt; 0.05). Internal jugular venous pressure increased significantly during NTG but not during PGE1 infusion (P &lt; 0.05). PGE1 increased HbO2 concentration, which was sustained for 30 min after discontinuing the drug. NTG increased HbO2 concentration, but this gradually returned to the baseline level after discontinuation of the drug. Baseline value of jugular oxygen saturation was 64.5% +/- 2.1%, and there was no significant changes during the infusion of PGE1 or NTG. These results demonstrate that both NTG and PGE1 increased cerebral oxygen saturation as measured by NIRS. This may be explained by local cerebral hyperemia without major alteration in flow/metabolism coupling of brain. The onset of this increase was slower and the duration of this effect after discontinuation of the drug was more prolonged with PGE1. These phenomena occurred despite the relatively similar time course of the effect of these two drugs on systemic hemodynamic values. ImplicationsThe cerebrovascular effects of vasodilators used for induced hypotension are not fully understood. In this study, we used near infrared spectrometry and jugular oxygen saturation measurement to assess the effects of prostaglandin E1 and nitroglycerin on cerebral perfusion. We found that nitroglycerin and prostaglandin E1 increase cerebral oxygen saturation as measured by near infrared spectrometry, but with different time courses. This information will hopefully help anesthesiologists to better maintain adequate regional cerebral oxygenation.(Anesth Analg 1997;85:1054-9)</abstract><cop>Hagerstown, MD</cop><pub>International Anesthesia Research Society</pub><pmid>9356099</pmid><doi>10.1097/00000539-199711000-00017</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Journals@Ovid LWW Legacy Archive; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals
subjects Aged
Alprostadil - therapeutic use
Anesthesia, General - methods
Biological and medical sciences
Blood Pressure - drug effects
Brain - blood supply
Brain - metabolism
Cardiovascular system
Electron Transport Complex IV - metabolism
Hemoglobins - metabolism
Humans
Infusions, Intravenous
Medical sciences
Middle Aged
Nitroglycerin - therapeutic use
Oxygen Consumption - drug effects
Oxyhemoglobins - metabolism
Pharmacology. Drug treatments
Spectroscopy, Near-Infrared
Thoracic Surgical Procedures
Vasodilator Agents - therapeutic use
Vasodilator agents. Cerebral vasodilators
title The Differential Effects of Prostaglandin E1 and Nitroglycerin on Regional Cerebral Oxygenation in Anesthetized Patients
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