The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation

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The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation. / Schwarzl, M; Steendijk, P; Huber, S; Truschnig-Wilders, M; Obermayer-Pietsch, B; Maechler, H; Pieske, B; Post, H.

In: ACTA PHYSIOL, Vol. 203, No. 4, 01.12.2011, p. 409-18.

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Harvard

Schwarzl, M, Steendijk, P, Huber, S, Truschnig-Wilders, M, Obermayer-Pietsch, B, Maechler, H, Pieske, B & Post, H 2011, 'The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation', ACTA PHYSIOL, vol. 203, no. 4, pp. 409-18. https://doi.org/10.1111/j.1748-1716.2011.02332.x

APA

Schwarzl, M., Steendijk, P., Huber, S., Truschnig-Wilders, M., Obermayer-Pietsch, B., Maechler, H., Pieske, B., & Post, H. (2011). The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation. ACTA PHYSIOL, 203(4), 409-18. https://doi.org/10.1111/j.1748-1716.2011.02332.x

Vancouver

Bibtex

@article{b112de748ef544a1ac0a275cae58df6a,
title = "The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation",
abstract = "AIM: Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest.METHODS: In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38°C, n = 8) or MH (33°C, n = 8, intravascular cooling).RESULTS: At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min(-1)) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dt(max) (mmHg s(-1)) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH.CONCLUSION: The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance.",
keywords = "Animals, Cardiac Output, Cardiac Volume, Catecholamines, Diastole, Female, Heart Arrest, Heart Rate, Hypothermia, Induced, Oxygen Consumption, Swine, Systole",
author = "M Schwarzl and P Steendijk and S Huber and M Truschnig-Wilders and B Obermayer-Pietsch and H Maechler and B Pieske and H Post",
note = "{\textcopyright} 2011 The Authors. Acta Physiologica {\textcopyright} 2011 Scandinavian Physiological Society.",
year = "2011",
month = dec,
day = "1",
doi = "10.1111/j.1748-1716.2011.02332.x",
language = "English",
volume = "203",
pages = "409--18",
journal = "ACTA PHYSIOL",
issn = "1748-1708",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

TY - JOUR

T1 - The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation

AU - Schwarzl, M

AU - Steendijk, P

AU - Huber, S

AU - Truschnig-Wilders, M

AU - Obermayer-Pietsch, B

AU - Maechler, H

AU - Pieske, B

AU - Post, H

N1 - © 2011 The Authors. Acta Physiologica © 2011 Scandinavian Physiological Society.

PY - 2011/12/1

Y1 - 2011/12/1

N2 - AIM: Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest.METHODS: In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38°C, n = 8) or MH (33°C, n = 8, intravascular cooling).RESULTS: At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min(-1)) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dt(max) (mmHg s(-1)) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH.CONCLUSION: The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance.

AB - AIM: Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest.METHODS: In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38°C, n = 8) or MH (33°C, n = 8, intravascular cooling).RESULTS: At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min(-1)) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dt(max) (mmHg s(-1)) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH.CONCLUSION: The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance.

KW - Animals

KW - Cardiac Output

KW - Cardiac Volume

KW - Catecholamines

KW - Diastole

KW - Female

KW - Heart Arrest

KW - Heart Rate

KW - Hypothermia, Induced

KW - Oxygen Consumption

KW - Swine

KW - Systole

U2 - 10.1111/j.1748-1716.2011.02332.x

DO - 10.1111/j.1748-1716.2011.02332.x

M3 - SCORING: Journal article

C2 - 21658179

VL - 203

SP - 409

EP - 418

JO - ACTA PHYSIOL

JF - ACTA PHYSIOL

SN - 1748-1708

IS - 4

ER -