title: Prostaglandin synthesis inhibitor prevents hypotension without impairing gut perfusion during normothermic cardiopulmonary bypass.
abstract: Aortic pressure declines during cardiopulmonary bypass (CPB), particularly at normothermia. It has been reported that administering vasoconstrictors during normothermic CPB (NCPB) to restore perfusion pressure might induce hypoperfusion of splanchnic organs. We have reported that prostaglandin (PG), metabolized in the lung but increased during CPB, might have played a substantial role in hypotension, and that a PG synthesis inhibitor (PGSI) could improve hypotension during CPB. This study was designed to examine whether regional perfusion of splanchnic organs was reduced when PGSI restored systemic perfusion pressure during NCPB. NCPB was performed in eight adult goats for 60 minutes (body weight 57.0 +/- 5.9 kg). PGSI was administered in group P (n = 4), while norepinephrine was administered in group C (n = 4), to keep aortic pressure in the range of 50 to 80 mm Hg. The total systemic flow was maintained at approximately 70 ml/kg/min. Tissue blood flow was measured by means of the colored microsphere method before and 30 and 60 minutes after the start of CPB. In group P, gut blood flows after the start of CPB were higher than those before CPB, significantly in the stomach and jejunum at 30 minutes (p < 0.05), whereas gut blood flows in group C were decreased or not changed. In conclusion, PGSI prevents hypotension without impairing gut perfusion during NCPB.
authors.affiliation: Department of Artificial Organs, National Cardiovascular Center Research Institute, Suita, Osaka, Japan.
authors.forename: Koichi
authors.initials: K
authors.lastname: Sato
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Takewa
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Taenaka
authors.forename: Eisuke
authors.initials: E
authors.lastname: Tatsumi
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Nishinaka
authors.forename: Kyoko
authors.initials: K
authors.lastname: Shioya
authors.forename: Toshihide
authors.initials: T
authors.lastname: Fukuda
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ohnishi
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Oshikawa
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Uesho
authors.forename: Hisateru
authors.initials: H
authors.lastname: Takano
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Hayashi
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001831:Body Temperature; D002315:Cardiopulmonary Bypass / Q000379:methods*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D005480:Flurbiprofen / Q000494:pharmacology*; D006041:Goats; D007022:Hypotension / Q000517:prevention & control*; D007583:Jejunum / Q000098:blood supply; D008168:Lung / Q000378:metabolism; D008863:Microspheres; D009638:Norepinephrine / Q000494:pharmacology; D010100:Oxygen / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis*; D013152:Splanchnic Circulation; D013270:Stomach / Q000098:blood supply; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D014662:Vasoconstrictor Agents; D005480:Flurbiprofen; D010100:Oxygen; D009638:Norepinephrine