Physiology and analysis of the electrocardiographic <scp>T</scp> wave in mice

Speerschneider, Tobias; Thomsen, Morten B.

doi:10.1111/apha.12172

Cited by 61 publications

(83 citation statements)

References 23 publications

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“…Previous studies have demonstrated that this dose or less causes a significant tachycardia in normal mice (21, 24-26). Serial ECGs were recorded from CLP mice at 25 h post-surgery before and after administration of isoproterenol.…”

Section: Resultsmentioning

confidence: 86%

Impaired Heart Rate Regulation and Depression of Cardiac Chronotropic and Dromotropic Function in Polymicrobial Sepsis

Hoover

Ozment²,

Wondergem³

et al. 2015

Shock

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The scope of cardiac pathophysiology in sepsis has not been fully defined. Accordingly, we evaluated the effects of sepsis on heart rate (HR), HR variability, and conduction parameters in a murine model of sepsis. Electrocardiograms were recorded non-invasively from conscious mice before and after cecal ligation and puncture (CLP) or sham surgery. Responses of isolated atria to tyramine and isoproterenol were quantified to assess the functional state of sympathetic nerves and postjunctional sensitivity to adrenergic stimulation. CLP mice had lower HR compared to sham at 16-18 h post-surgery (Sham: 741±7 beats per min, CLP: 557±31 beats per min, n=6/group, P<0.001), and there was significant prolongation of the PR, QRS and QTc intervals. Slowing of HR and conduction developed within 4-6 h after CLP and were preceded by a decrease in HR variability. Treatment of CLP mice with isoproterenol (5 mg/kg, i.p.) at 25 h post-surgery failed to increase HR or decrease conduction intervals. The lack of in vivo response to isoproterenol cannot be attributed to hypothermia since robust chronotropic and inotropic responses to isoproterenol were evoked from isolated atria at 25 and 30° C. These findings demonstrate that impaired regulation of HR (i.e, reduced HR variability) develops before the onset of overt cardiac rate and conduction changes in septic mice. Subsequent time-dependent decreases in HR and cardiac conduction can be attributed to hypothermia and would contribute to decreased cardiac output and organ perfusion. Since isolated atria from septic mice showed normal responsiveness to adrenergic stimulation, we conclude that impaired effectiveness of isoproterenol in vivo can be attributed to reversible effects of systemic factors on adrenergic receptors and/or post-receptor signaling.

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Section: Resultsmentioning

confidence: 86%

Impaired Heart Rate Regulation and Depression of Cardiac Chronotropic and Dromotropic Function in Polymicrobial Sepsis

Hoover

Ozment²,

Wondergem³

et al. 2015

Shock

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“…5B)in a manner similar to those described previously in mice[ 40]. In an attempt to quantify the magnitude of ECG alternans, we estimated the T-wave alternans ratio using the method described previously [40,41]. We found that the T -wave alternans ratio was significantly higher in RyR2 -SOF mice than that in RyR2-WT mice (Fig.…”

Section: Resultsmentioning

confidence: 69%

“…To test this possibility, we performed telemetric ECG recordings on conscious RyR2-WT and RyR2-SOF mutant mice at rest and after the injection of isoproterenol (ISO), which was used to induce alternans[ 40,41]. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

Suppression of ryanodine receptor function prolongs Ca2+ release refractoriness and promotes cardiac alternans in intact hearts

Zhong

Sun

Vallmitjana

et al. 2016

Biochemical Journal

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Beat-to-beat alternations in the amplitude of the cytosolic Ca2+ transient (Ca 2+ alternans) are thought to be the primary cause of cardiac alternans that can lead to cardiac arrhythmias and sudden death. Despite its important role in arrhythmogenesis, the mechanism underlying Ca 2+ alternans remains poorly understood. Here we investigated the role of cardiac ryanodine receptor (RyR2), the major Ca2+ release channel responsible forcytosolic Ca2+ transients, in cardiac alternans. Using a unique mouse model harboring a suppression -of-function (SOF) RyR2 mutation (E4872Q), we assessed the effect of genetically suppressing RyR2 function on Ca 2+ and action potential duration (APD)alternans in intact hearts , and electrocardiogram (ECG) alternans in vivo. We found that RyR2-SOF hearts displayed prolonged sarcoplasmic reticulum Ca2+ release refractoriness and enhanced propensity for Ca2+ al ternans. RyR2-SOF hearts/mice also exhibited increased propensity for APD and ECG alternans. Caffeine, which enhances RyR2 activity and the propensity for catecholaminergic polymorphic ventricular tachycardia ( CPVT), suppressed Ca2+ alternans in RyR2 -SOF hearts, whereas carvedilol, a beta-blocker that suppresses RyR2 activity and CPVT, promoted Ca2+ alternans in these hearts. Thus, RyR2 function is an important determinant of Ca2+ , APD, and ECG alternans. Our data also indicate that the activity of RyR2 influences the propensity for cardiac alternans and CPVT in an opposite manner. Therefore, overly suppressing or enhancing RyR2 function is pro-arrhythmic.

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“…It should be noted that inhaled isoflurane anesthesia reduces heart rate, and therefore increases QT-intervals. However, amplitude of recovery T-waves remains unaffected 18 .…”

Section: Representative Resultsmentioning

confidence: 99%

Confirmation of Myocardial Ischemia and Reperfusion Injury in Mice Using Surface Pad Electrocardiography

Scofield

Singh

2016

JoVE

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Many animal models have been established for the study of myocardial remodeling and heart failure due to its status as the number one cause of mortality worldwide. In humans, a pathologic occlusion forms in a coronary artery and reperfusion of that occluded artery is considered essential to maintain viability of the myocardium at risk. Although essential for myocardial recovery, reperfusion of the ischemic myocardium creates its own tissue injury. The physiologic response and healing of an ischemia/reperfusion injury is different from a chronic occlusion injury. Myocardial ischemia/reperfusion injury is gaining recognition as a clinically relevant model for myocardial infarction studies. For this reason, parallel animal models of ischemia/reperfusion are vital in advancing the knowledge base regarding myocardial injury. Typically, ischemia of the mouse heart after left anterior descending (LAD) coronary artery occlusion is confirmed by visible pallor of the myocardium below the occlusion (ligature). However, this offers only a subjective way of confirming correct or consistent ligature placement, as there are multiple major arteries that could cause pallor in different myocardial regions. A method of recording electrocardiographic changes to assess correct ligature placement and resultant ischemia as well as reperfusion, to supplement observed myocardial pallor, would help yield consistent infarct sizes in mouse models. In turn, this would help decrease the number of mice used. Additionally, electrocardiographic changes can continue to be recorded non-invasively in a time-dependent fashion after the surgery. This article will demonstrate a method of electrocardiographically confirming myocardial ischemia and reperfusion in real time.

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Physiology and analysis of the electrocardiographic T wave in mice

Abstract: The end of the T wave is readily available from conscious and anaesthetized mice. Heart rate correction of QT interval duration in the anaesthetized mouse is not recommended.

Cited by 61 publications

References 23 publications

Impaired Heart Rate Regulation and Depression of Cardiac Chronotropic and Dromotropic Function in Polymicrobial Sepsis

Impaired Heart Rate Regulation and Depression of Cardiac Chronotropic and Dromotropic Function in Polymicrobial Sepsis

Suppression of ryanodine receptor function prolongs Ca2+ release refractoriness and promotes cardiac alternans in intact hearts

Confirmation of Myocardial Ischemia and Reperfusion Injury in Mice Using Surface Pad Electrocardiography

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