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Updated: Jun 16, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Cardiac function during mild hypothermia in pigs: increased inotropy at the expense of diastolic dysfunction
H Post1, J D Schmitto, P Steendijk
1Department of Cardiology, Medical University of Graz, Graz, Austria. heiner.post@meduni-graz.at
Aim:
The induction of mild hypothermia (MH; 33 degrees C) has become the guideline therapy to attenuate hypoxic brain injury after out-of-hospital cardiopulmonary resuscitation. While MH exerts a positive inotropic effect in vitro, MH reduces cardiac output in vivo and is thus discussed critically when severe cardiac dysfunction is present in patients. We thus assessed the effect of MH on the function of the normal heart in an in vivo model closely mimicking the clinical setting.
Methods:
Ten anaesthetized, female human-sized pigs were acutely catheterized for measurement of pressure-volume loops (conductance catheter), cardiac output (Swan-Ganz catheter) and for vena cava inferior occlusion. Controlled MH (from 37 to 33 degrees C) was induced by a vena cava inferior cooling catheter.
Results:
With MH, heart rate (HR) and whole body oxygen consumption decreased, while lactate levels remained normal. Cardiac output, left ventricular (LV) volumes, peak systolic and end-diastolic pressure and dP/dt(max) did not change significantly. Changes in dP/dt(min) and the time constant of isovolumetric relaxation demonstrated impaired active relaxation. In addition, MH prolonged the systolic and shortened the diastolic time interval. Pressure-volume analysis revealed increased end-systolic and end-diastolic stiffness, indicating positive inotropy and reduced end-diastolic distensibility. Positive inotropy was preserved during pacing, while LV end-diastolic pressure increased and diastolic filling was substantially impaired due to delayed LV relaxation.
Conclusion:
MH negatively affects diastolic function, which, however, is compensated for by decreased spontaneous HR. Positive inotropy and a decrease in whole body oxygen consumption warrant further studies addressing the potential benefit of MH on the acutely failing heart.
Insights
Mild hypothermia (MH) impairs diastolic heart function but preserves positive inotropy. This study investigated MH
Area of Science:
- Cardiovascular Physiology
- Thermoregulation
- Critical Care Medicine
Background:
- Mild hypothermia (MH) is a guideline therapy for hypoxic brain injury post-cardiopulmonary resuscitation.
- MH has shown in vitro positive inotropic effects but in vivo cardiac output reduction.
- The impact of MH on normal heart function in vivo requires further investigation.
Purpose of the Study:
- To assess the effects of mild hypothermia (33°C) on normal heart function in an in vivo model.
- To evaluate cardiac output, contractility, and relaxation under MH conditions.
Main Methods:
- Utilized an in vivo animal model (human-sized pigs) under anesthesia.
- Measured pressure-volume loops, cardiac output, and performed vena cava occlusion.
- Induced controlled mild hypothermia using a cooling catheter.
Main Results:
- Mild hypothermia decreased heart rate and whole-body oxygen consumption; lactate levels remained normal.
- Cardiac output and left ventricular volumes were unchanged, but active relaxation was impaired.
- Increased ventricular stiffness and impaired diastolic filling were observed, despite preserved positive inotropy.
Conclusions:
- Mild hypothermia negatively impacts diastolic function, compensated by reduced heart rate.
- Preserved positive inotropy and reduced oxygen consumption suggest potential benefits for failing hearts.
- Further research is warranted to explore MH's benefits in acutely failing cardiac conditions.
