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

Schwarzl, Michael; Steendijk, Paul; Huber, Stefan; Truschnig-Wilders, M.; Obermayer–Pietsch, Barbara; Maechler, H.; Pieske, Burkert; Post, Heiner

doi:10.1111/j.1748-1716.2011.02332.x

Cited by 31 publications

(43 citation statements)

References 43 publications

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“…Improvement in systolic function with improved myocardial contractility with diastolic function being negatively affected during hypothermia has been reported in an animal model using conductance catheter. 20,21 The temperature-related changes in systolic or diastolic function could not be confirmed by echocardiographic-derived parameters in this study; however, echocardiography may be less sensitive compared with invasive methods.…”

Section: Discussioncontrasting

confidence: 60%

Targeted Temperature Management at 33°C Versus 36°C and Impact on Systemic Vascular Resistance and Myocardial Function After Out-of-Hospital Cardiac Arrest

Bro-Jeppesen

Hassager

Wanscher

et al. 2014

Circ: Cardiovascular Interventions

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emodynamic instability with low cardiac output and low to normal filling pressures is frequent in survivors after out-of-hospital cardiac arrest (OHCA), but may not always be apparent at hospital admission. 1 The hemodynamic profile suggestive of myocardial stunning and vasodilation is part of the postcardiac arrest syndrome, characterized by impaired vasoregulation, reduced cardiac output, and hypotension, which all contribute to decreased organ perfusion.2 Although application of targeted temperature management (TTM) in comatose survivors after OHCA is an established part of postresuscitation care, its effects on central hemodynamics may pose additional challenges to the treating physicians. Our current knowledge of the hemodynamic implications of TTM is limited because most descriptive studies are small or used noninvasive methods for hemodynamic evaluation, 3,4 whereas other studies were primarily designed for evaluating outcome. 5,6 A recent large randomized study, the Target Temperature Management after Cardiac arrest trial (TTM Trial), compared the beneficial effects of a target temperature of 33°C compared with 36°C after OHCA. Both regimens were equally efficacious in terms of mortality (50% versus 48%; P=0.51) and unfavorable neurological outcome (54% versus 52%; P=0.78). 7This study reports the impact on central hemodynamics in survivors after OHCA randomized to a TTM at 33°C or 36°CBackground-Cardiovascular dysfunction is common after out-of-hospital cardiac arrest as part of the postcardiac arrest syndrome, and hypothermia may pose additional impact on hemodynamics. The aim was to investigate systemic vascular resistance index (SVRI), cardiac index, and myocardial performance at a targeted temperature management of 33°C (TTM33) versus 36°C (TTM36

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Section: Discussioncontrasting

confidence: 60%

Targeted Temperature Management at 33°C Versus 36°C and Impact on Systemic Vascular Resistance and Myocardial Function After Out-of-Hospital Cardiac Arrest

Bro-Jeppesen

Hassager

Wanscher

et al. 2014

Circ: Cardiovascular Interventions

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“…The aorta is a large conduit vessel, which usually remains at constant temperature except during certain therapeutic interventions (Schwarzl et al, 2011). Thus, the results obtained cannot easily be extrapolated to the control of peripheral resistance.…”

Section: Endothelium-derived Ach Causes Autocrine No Releasementioning

confidence: 99%

Transient Receptor Potential Channel Opening Releases Endogenous Acetylcholine, which Contributes to Endothelium-Dependent Relaxation Induced by Mild Hypothermia in Spontaneously Hypertensive Rat but Not Wistar-Kyoto Rat Arteries

Zhang

Leung

Vanhoutte

2015

J Pharmacol Exp Ther

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Mild hypothermia causes endothelium-dependent relaxations, which are reduced by the muscarinic receptor antagonist atropine. The present study investigated whether endothelial endogenous acetylcholine contributes to these relaxations. Aortic rings of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats were contracted with prostaglandin F 2a and exposed to progressive mild hypothermia (from 37 to 31°C). Hypothermia induced endotheliumdependent, Nv-nitro-L-arginine methyl ester-sensitive relaxations, which were reduced by atropine, but not by mecamylamine, in SHR but not in WKY rat aortae. The responses in SHR aortae were also reduced by acetylcholinesterase (the enzyme responsible for acetylcholine degradation), bromoacetylcholine (inhibitor of acetylcholine synthesis), hemicholinium-3 (inhibitor of choline uptake), and vesamicol (inhibitor of acetylcholine release). The mild hypothermia-induced relaxations in both SHR and WKY rat aortae were inhibited by AMTB [N-(3-aminopropyl)-2-[(3-methylphenyl)methoxy]-N-(2-thienylmethyl)-benzamide; the transient receptor potential (TRP) M8 inhibitor]; only those in SHR aortae were inhibited by HC-067047 [2-methyl-1-[3-(4-morpholinyl)propyl]-5-phenyl-N-[3-(trifluoromethyl)phenyl]-1H-pyrrole-3-carboxamide; TRPV4 antagonist] while those in WKY rat aortae were reduced by HC-030031 [2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl) acetamide; TRPA1 antagonist]. The endothelial uptake of extracellular choline and release of cyclic guanosine monophosphate was enhanced by mild hypothermia and inhibited by HC-067047 in SHR but not in WKY rat aortae. Compared with WKY rats, the SHR preparations expressed similar levels of acetylcholinesterase and choline acetyltransferase, but a lesser amount of vesicular acetylcholine transporter, located mainly in the endothelium. Thus, mild hypothermia causes nitric oxide-dependent relaxations by opening TRPA1 channels in WKY rat aortae. By contrast, in SHR aortae, TRPV4 channels are opened, resulting in endothelial production of acetylcholine, which, in an autocrine manner, activates muscarinic receptors on neighboring cells to elicit endothelium-dependent relaxations in response to mild hypothermia.

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“…Cooling in vivo also induced LV diastolic dysfunction, as evidenced by slowed active LV relaxation (10,11) and a leftward shift of the end-diastolic pressure-volume relationship (10). However, such diastolic dysfunction was compensated by spontaneous bradycardia (10,12,13). The hypometabolic state induced by MH reduced systemic oxygen demand and improved SvO 2 during experimental myocardial infarction and cardiogenic shock in pigs (13,14).…”

mentioning

confidence: 94%

“…MH increased force development in isolated myocardial muscle strips from failing (7) and nonfailing (8) human hearts and increased left ventricular (LV) contractility in isolated rat hearts (9) and in healthy pigs (10) and dogs (11) in vivo. In resuscitated pigs, MH improved systolic LV function and systemic vascular resistance without an increase of sympathetic tone (12). Cooling in vivo also induced LV diastolic dysfunction, as evidenced by slowed active LV relaxation (10,11) and a leftward shift of the end-diastolic pressure-volume relationship (10).…”

mentioning

confidence: 98%

Mild Hypothermia Attenuates Circulatory and Pulmonary Dysfunction During Experimental Endotoxemia*

Schwarzl

Seiler

Wallner

et al. 2013

Critical Care Medicine

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

Abstract: 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.

Cited by 31 publications

References 43 publications

Targeted Temperature Management at 33°C Versus 36°C and Impact on Systemic Vascular Resistance and Myocardial Function After Out-of-Hospital Cardiac Arrest

Targeted Temperature Management at 33°C Versus 36°C and Impact on Systemic Vascular Resistance and Myocardial Function After Out-of-Hospital Cardiac Arrest

Transient Receptor Potential Channel Opening Releases Endogenous Acetylcholine, which Contributes to Endothelium-Dependent Relaxation Induced by Mild Hypothermia in Spontaneously Hypertensive Rat but Not Wistar-Kyoto Rat Arteries

Mild Hypothermia Attenuates Circulatory and Pulmonary Dysfunction During Experimental Endotoxemia*

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