title: Load dependence of the effective regurgitant orifice area in a sheep model of aortic regurgitation.
abstract: Treatment of patients with aortic regurgitation with vasodilators reduces regurgitant volume, ventricular dilation and left ventricular mass. Although these effects are presumably due to afterload reduction, it is also possible that the aortic regurgitant orifice area is not constant. To test the latter hypothesis, aortic regurgitation was created in 10 open chest sheep by partial resection of the noncoronary leaflet under direct visualization. Regurgitant flow was measured with an aortic supravalvular electromagnetic probe; aortic and left ventricular pressures were measured with catheter-tipped micromanometer pressure transducers. The effective regurgitant orifice area was calculated by a modification of the continuity equation in a manner similar to the Gorlin equation. The regurgitant orifice area was measured three times: after aortic regurgitation was created, after mean arterial pressure was increased by 15 to 25 mm Hg with intravenous dopamine and after mean arterial pressure was reduced by 15 to 25 mm Hg with intravenous sodium nitroprusside. Comparison of regurgitant volumes and areas obtained after creation of aortic regurgitation and at the conclusion of the experiment in the absence of dopamine or sodium nitroprusside demonstrated no significant change over time. Dopamine administration was associated with an 86 +/- 81% increase in regurgitant volume (p less than 0.01) and a 38 +/- 44% increase in regurgitant orifice area (p less than 0.01). Sodium nitroprusside administration resulted in a 51 +/- 14% decrease in regurgitant volume (p less than 0.001) and a 28 +/- 21% reduction in regurgitant orifice area (p = 0.007). In this model of acute aortic regurgitation, the effective regurgitant orifice area was altered by increasing or decreasing the aortic transvalvular pressure gradient.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
authors.forename: S C
authors.initials: SC
authors.lastname: Reimold
authors.forename: J G
authors.initials: JG
authors.lastname: Byrne
authors.forename: E S
authors.initials: ES
authors.lastname: Caguioa
authors.forename: C C
authors.initials: CC
authors.lastname: Lee
authors.forename: R G
authors.initials: RG
authors.lastname: Laurence
authors.forename: P S
authors.initials: PS
authors.lastname: Peigh
authors.forename: L H
authors.initials: LH
authors.lastname: Cohn
authors.forename: R T
authors.initials: RT
authors.lastname: Lee
mesh_terms: D000818:Animals; D001021:Aortic Valve / Q000503:physiopathology; D001022:Aortic Valve Insufficiency / Q000188:drug therapy / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology; D004298:Dopamine / Q000494:pharmacology; D055590:Electromagnetic Phenomena; D009599:Nitroprusside / Q000494:pharmacology; D012212:Rheology; D012756:Sheep; D014160:Transducers, Pressure; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D004298:Dopamine