Article: Dose-dependent protection of cardiac function by propofol during ischemia and early reperfusion in rats: Effects on 15-F2t-isoprostane formation
| Title | Dose-dependent protection of cardiac function by propofol during ischemia and early reperfusion in rats: Effects on 15-F2t-isoprostane formation |
|---|---|
| Authors | Xia, Z1 Godin, DV1 Chang, TKH1 Ansley, DM1 |
| Issue Date | 2003 |
| Publisher | N R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp |
| Citation | Canadian Journal Of Physiology And Pharmacology, 2003, v. 81 n. 1, p. 14-21 [How to Cite?] DOI: http://dx.doi.org/10.1139/y02-170 |
| Abstract | We examined the effects of propofol (2,6-diisopropylphenol) on functional recovery and 15-F2t-isoprostane generation during ischemia-reperfusion in Langendorff-perfused rat hearts. Before the induction of 40 min of global ischemia, hearts were perfused (10 min) with propofol at 5 (lo-P) or 12 μg/mL (hi-P) in saline or with saline only (control). During ischemia, saline, lo-P, or hi-P was perfused through the aorta at 60 μL/min. During the first 15 min of reperfusion, propofol (5 or 12 μg/mL) was continued, followed by perfusion with 5 μg/mL propofol for 75 min in both propofol-treated groups. After 90 min of reperfusion (Rep-90), heart tissues were harvested for assessment of antioxidant status. In hi-P, we observed increased latency to and greater reduction of ischemic contracture relative to the lo-P or control groups. 15-F2t-Isoprostane concentrations increased during ischemia and were significantly lower in hi-P and lo-P than in control (P < 0.01). At Rep-90, myocardial functional recovery was greater in both propofol-treated groups relative to control, and it correlated positively with tissue antioxidant capacity preservation. Tissue antioxidant capacity was better preserved in hi-P than in lo-P treatment (P < 0.05). We conclude that oxidant injury occurs during ischemia and reperfusion, and propofol provides dose-dependent protection primarily by enhancing tissue antioxidant capacity and reducing lipid peroxidation. |
| ISSN | 0008-4212 2011 Impact Factor: 1.953 2011 SCImago Journal Rankings: 0.149 |
| DOI | http://dx.doi.org/10.1139/y02-170 |
| ISI Accession Number ID | WOS:000181344200003 |
| References | References in Scopus |
| dc.contributor.author | Xia, Z |
|---|---|
| dc.contributor.author | Godin, DV |
| dc.contributor.author | Chang, TKH |
| dc.contributor.author | Ansley, DM |
| dc.date.accessioned | 2012-05-29T06:00:43Z |
| dc.date.available | 2012-05-29T06:00:43Z |
| dc.date.issued | 2003 |
| dc.description.abstract | We examined the effects of propofol (2,6-diisopropylphenol) on functional recovery and 15-F2t-isoprostane generation during ischemia-reperfusion in Langendorff-perfused rat hearts. Before the induction of 40 min of global ischemia, hearts were perfused (10 min) with propofol at 5 (lo-P) or 12 μg/mL (hi-P) in saline or with saline only (control). During ischemia, saline, lo-P, or hi-P was perfused through the aorta at 60 μL/min. During the first 15 min of reperfusion, propofol (5 or 12 μg/mL) was continued, followed by perfusion with 5 μg/mL propofol for 75 min in both propofol-treated groups. After 90 min of reperfusion (Rep-90), heart tissues were harvested for assessment of antioxidant status. In hi-P, we observed increased latency to and greater reduction of ischemic contracture relative to the lo-P or control groups. 15-F2t-Isoprostane concentrations increased during ischemia and were significantly lower in hi-P and lo-P than in control (P < 0.01). At Rep-90, myocardial functional recovery was greater in both propofol-treated groups relative to control, and it correlated positively with tissue antioxidant capacity preservation. Tissue antioxidant capacity was better preserved in hi-P than in lo-P treatment (P < 0.05). We conclude that oxidant injury occurs during ischemia and reperfusion, and propofol provides dose-dependent protection primarily by enhancing tissue antioxidant capacity and reducing lipid peroxidation. |
| dc.description.nature | Link_to_subscribed_fulltext |
| dc.identifier.citation | Canadian Journal Of Physiology And Pharmacology, 2003, v. 81 n. 1, p. 14-21 [How to Cite?] DOI: http://dx.doi.org/10.1139/y02-170 |
| dc.identifier.doi | http://dx.doi.org/10.1139/y02-170 |
| dc.identifier.epage | 21 |
| dc.identifier.isi | WOS:000181344200003 |
| dc.identifier.issn | 0008-4212 2011 Impact Factor: 1.953 2011 SCImago Journal Rankings: 0.149 |
| dc.identifier.issue | 1 |
| dc.identifier.pmid | 12665253 |
| dc.identifier.scopus | eid_2-s2.0-0037247879 |
| dc.identifier.spage | 14 |
| dc.identifier.uri | http://hdl.handle.net/10722/147197 |
| dc.identifier.volume | 81 |
| dc.language | eng |
| dc.publisher | N R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp |
| dc.publisher.place | Canada |
| dc.relation.ispartof | Canadian Journal of Physiology and Pharmacology |
| dc.relation.references | References in Scopus |
| dc.subject.mesh | Anesthetics, Intravenous - Administration & Dosage - Pharmacology |
| dc.subject.mesh | Animals |
| dc.subject.mesh | Antioxidants - Metabolism |
| dc.subject.mesh | Dinoprost - Analogs & Derivatives |
| dc.subject.mesh | Dose-Response Relationship, Drug |
| dc.subject.mesh | F2-Isoprostanes - Biosynthesis |
| dc.subject.mesh | Heart - Drug Effects - Physiopathology |
| dc.subject.mesh | Lipid Peroxidation |
| dc.subject.mesh | Male |
| dc.subject.mesh | Myocardial Ischemia - Metabolism - Physiopathology - Prevention & Control |
| dc.subject.mesh | Myocardial Reperfusion Injury - Metabolism - Physiopathology - Prevention & Control |
| dc.subject.mesh | Propofol - Administration & Dosage - Pharmacology |
| dc.subject.mesh | Rats |
| dc.subject.mesh | Rats, Sprague-Dawley |
| dc.subject.mesh | Ventricular Function, Left - Drug Effects |
| dc.title | Dose-dependent protection of cardiac function by propofol during ischemia and early reperfusion in rats: Effects on 15-F2t-isoprostane formation |
| dc.type | Article |
Author Affiliations
- The University of British Columbia

