title: Treating ischemic left ventricular dysfunction with hypertonic saline administered after coronary occlusion in pigs.
abstract: OBJECTIVE
  The effects of hypertonic saline on ventricular function are controversial, whether it is increasing contractility or preload. There are no data, however, on the influence of hypertonic saline in a stunned myocardium.
  
  
  METHODS
  This study was prospective and randomized in order to analyze the effects of hypertonic saline solution (7.5%) on myocardial function and systemic hemodynamics in a porcine model of ischemia and reperfusion.
  
  
  METHODS
  A university teaching hospital, animal research laboratory.
  
  
  METHODS
  Twelve adult domestic swine.
  
  
  METHODS
  Myocardial stunning was produced by the complete occlusion of the proximal left anterior descending artery for 15 minutes followed by reperfusion. Five minutes after reperfusion, the animals were assigned to receive 4 mL/kg of hypertonic saline (n = 7) or normal saline (n = 5) over 10 minutes. Pressure-tipped catheters were placed in the left ventricular cavity and aorta. The dimensions of the left ventricle were measured with ultrasonic microcrystals. Cardiac output was measured with transit time ultrasound. Data were recorded continuously and compared before the occlusion, 5 minutes after reperfusion, and at the end of the infusion.
  
  
  RESULTS
  Compared with baseline, ventricular function was significantly depressed after left anterior descending artery occlusion. Left ventricular dP/dT and its end-systolic pressure-volume slope decreased (38% and 52%, respectively; p < 0.05), with a concomitant increase in systemic vascular resistance. The administration of hypertonic saline significantly improved left ventricular function (Emax 1,422 +/- 198 mmHg/mL, and dP/dT 3.2 +/- 0.4 mmHg/s v normal saline group values of 1,156 +/- 172 and 2.5 +/- 0.5, respectively; p < 0.05), cardiac output (2.5 +/- 0.5 v 1.84 +/- 0.4 L/min, p < 0.05), and lowered systemic vascular resistance (from 28.8 +/- 2.3 to 23.5 +/- 1.4, p < 0.05), with no significant changes with normal saline administration.
  
  
  CONCLUSIONS
  After transient myocardial ischemia, hypertonic saline administered over a short period of time acts as an inodilator by increasing contractility while simultaneously lowering systemic vascular resistance.
authors.affiliation: Department of Anesthesiology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA. asidi@anest.ufl.edu
authors.forename: Avner
authors.initials: A
authors.lastname: Sidi
authors.forename: Jochen D
authors.initials: JD
authors.lastname: Muehlschlegel
authors.forename: David S
authors.initials: DS
authors.lastname: Kirby
authors.forename: Robert R
authors.initials: RR
authors.lastname: Kirby
authors.forename: Emilio B
authors.initials: EB
authors.lastname: Lobato
mesh_terms: D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D003327:Coronary Disease / Q000150:complications* / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D012462:Saline Solution, Hypertonic / Q000627:therapeutic use*; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D012462:Saline Solution, Hypertonic