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Updated: Jul 14, 2026
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Treating ischemic left ventricular dysfunction with hypertonic saline administered after coronary occlusion in pigs
Avner Sidi1, Jochen D Muehlschlegel, David S Kirby
1Department of Anesthesiology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA. asidi@anest.ufl.edu
Insights
Hypertonic saline improved cardiac function in stunned pig hearts, acting as an inodilator by boosting contractility and reducing vascular resistance after ischemia and reperfusion.
Area of Science:
- Cardiology
- Cardiovascular Research
- Pharmacology
Background:
- The effects of hypertonic saline on ventricular function remain debated, with no data on its use in stunned myocardium.
- Myocardial stunning, induced by ischemia and reperfusion, significantly impairs cardiac function.
Purpose of the Study:
- To investigate the effects of hypertonic saline (7.5%) on myocardial function and systemic hemodynamics.
- To determine if hypertonic saline can improve cardiac performance in a porcine model of myocardial stunning.
Main Methods:
- Prospective, randomized study in a porcine model.
- Myocardial stunning induced by left anterior descending artery occlusion and reperfusion.
- Animals received either hypertonic saline (4 mL/kg) or normal saline post-reperfusion.
Main Results:
- Hypertonic saline significantly improved left ventricular function (Emax, dP/dT) compared to normal saline.
- Cardiac output increased, and systemic vascular resistance decreased significantly with hypertonic saline.
- Normal saline administration showed no significant changes in cardiac function or hemodynamics.
Conclusions:
- Hypertonic saline acts as an inodilator in stunned myocardium.
- It enhances contractility and reduces systemic vascular resistance shortly after transient ischemia.
Objective(S):
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.
Design:
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.
Setting:
A university teaching hospital, animal research laboratory.
Participants:
Twelve adult domestic swine.
Interventions:
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.
Measurements And Main 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.
