Method for non-invasively recording electrocardiograms in conscious mice

Chu, Victor; Otero, J; Lopez, Orlando; Morgan, James P.; Amende, Ivo; Hampton, Thomas G.

doi:10.1186/1472-6793-1-6

Cited by 92 publications

(49 citation statements)

References 36 publications

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“…Briefly, individual mice were removed from their home cage and placed on the elevated recording platform of the apparatus a few minutes prior to each data collection time to allow for acclimation. ECG signals were then acquired through disposable footpad electrodes located in the floor of a recording platform (21). Approximately 200 raw ECG signals were analyzed per mouse at each time point using e-MOUSE software (Mouse Specifics, Inc., Boston, MA), which employs processing algorithms for peak detection, digital filtering, and correction of baseline for motion artifacts.…”

Section: Methodsmentioning

confidence: 99%

“…Approximately 200 raw ECG signals were analyzed per mouse at each time point using e-MOUSE software (Mouse Specifics, Inc., Boston, MA), which employs processing algorithms for peak detection, digital filtering, and correction of baseline for motion artifacts. Heart rate (HR) was determined from R-R intervals, and HR variability was calculated as the mean difference in sequential HRs for the entire set of ECG signals analyzed (21, 22). The software also determined cardiac intervals (i.e., PR, QRT, and QTc), which were within the normal ranges for our unoperated and sham mice (21-23).…”

Section: Methodsmentioning

confidence: 99%

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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: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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 QRS interval in untreated MPSVII mice was significantly longer (P Ͻ 0.05) than that from ϩ͞ϩ and treated MPSVII mice. Overall, there was significant correction of ECG indices in the treated MPSVII mice (39,40).…”

Section: Treated Mice Are Partially Repopulated and Functionally Imprmentioning

confidence: 99%

“…ECGs were recorded in conscious mice as described (39,40). Briefly, mice were gently removed from their cages and positioned on a raised ECG recording platform (AnonyMOUSE, Mouse Specifics).…”

Section: Analytical Procedures Prenecropsymentioning

confidence: 99%

Electrocardiographic and other cardiac anomalies in β-glucuronidase-null mice corrected by nonablative neonatal marrow transplantation

Schuldt

Hampton

Chu

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Cardiovascular manifestations of lysosomal storage disease (LSD) are a significant health problem for affected patients. Infantileonset cardiac disease, because of its rapid progression, is usually treated symptomatically. Therapy in older patients includes valve replacement and bone marrow (BM) transplantation, both of which are life threatening in the already debilitated patients. Enzyme replacement therapy has potential benefit but has not yet been demonstrated to provide long-term relief for cardiac disease. Here, we demonstrate prevention of severe cardiac manifestations in ␤-glucuronidase (GUSB) null mice BM-transplanted i.v. as neonates without myeloablative pretreatment. The mice, a model of mucopolysaccharidosis type VII (MPSVII, Sly syndrome), develop progressive LSD unless provided with GUSB early in life. The BM recipients retained GUSB؉ donor cells in the peripheral blood and heart until necropsy at >11 months of age. The enzyme ␤-hexosamindase increased in tissues of GUSB null MPSVII mice was reduced significantly (P ‫؍‬ 0.001) in treated MPSVII hearts. Electrocardiography demonstrated normalization of heart rate, PR, PQ, and QRS intervals in BM recipients. Storage was markedly reduced in the stroma of heart valves, adventitial cells of the aortic root, perivascular and interstitial cells of the myocardium, and interstitial cells of the conduction tissue. Heart͞body weight ratio normalized. The aortic root was still grossly distended, and the conductive myocytes retained storage, suggesting neither plays a major role in ECG normalization. We conclude that transplantation of MPSVII neonates without toxic intervention can prevent many of the cardiovascular manifestations of LSD.

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“…Two-dimensional and M-mode ECGs were performed by using very light sedation (ketamine) (37). ECGs were recorded noninvasively in conscious mice as described (1,38) and analyzed via E-MOUSE (Mouse Specifics, Boston). All other methods were as described, including RBC characterization (22), FPLC plasma fractionation (15,16), gravimetry and MRI analyses (1), and electron microscopy of phosphotungstic acid negatively stained lipoproteins from plasma or FPLC fractions (34).…”

Section: Methodsmentioning

confidence: 99%

Probucol prevents early coronary heart disease and death in the high-density lipoprotein receptor SR-BI/apolipoprotein E double knockout mouse

Braun

Zhang

Miettinen

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

129

142

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Mice with homozygous null mutations in the high-density lipoprotein receptor SR-BI (scavenger receptor class B, type I) and apolipoprotein E genes fed a low-fat diet exhibit a constellation of pathologies shared with human atherosclerotic coronary heart disease (CHD): hypercholesterolemia, occlusive coronary atherosclerosis, myocardial infarctions, cardiac dysfunction (heart enlargement, reduced systolic function and ejection fraction, and ECG abnormalities), and premature death (mean age 6 weeks). They also exhibit a block in RBC maturation and abnormally high plasma unesterified-to-total cholesterol ratio (0.8) with associated abnormal lipoprotein morphology (lamellar͞vesicular and stacked discoidal particles reminiscent of those in lecithin͞cholesterol acyltransferase deficiency and cholestasis). Treatment with the lipid-lowering, antiatherosclerosis, and antioxidation drug probucol extended life to as long as 60 weeks (mean 36 weeks), and at 5-6 weeks of age, virtually completely reversed the cardiac and most RBC pathologies and corrected the unesterified to total cholesterol ratio (0.3) and associated distinctive abnormal lipoprotein morphologies. Manipulation of the timing of administration and withdrawal of probucol could control the onset of death and suggested that critical pathological changes usually occurred in untreated double knockout mice between Ϸ3 (weaning) and 5 weeks of age and that probucol delayed heart failure even after development of substantial CHD. The ability of probucol treatment to modulate pathophysiology in the double knockout mice enhances the potential of this murine system for analysis of the pathophysiology of CHD and preclinical testing of new approaches for the prevention and treatment of cardiovascular disease.atherosclerosis ͉ heart failure ͉ myocardial infarction ͉ unesterified cholesterol C oronary artery atherosclerosis is a major cause of myocardial infarction (MI) and death. We have described a murine model of human coronary heart disease (CHD) (1) that is based on targeted homozygous null mutations in two genes whose products play important roles in normal lipoprotein metabolism and protect mice from atherosclerosis: the high-density lipoprotein (HDL) receptor SR-BI (scavenger receptor class B, type I) (2, 3) and the lipoprotein component apolipoprotein E (apoE) (4-7).Low-fat chow-fed, homozygous null, apoE knockout (KO) mice are hypercholesterolemic (4, 5), develop atherosclerosis between 3 and 4 months of age, and usually live a long life (Ͼ1 year), although older animals can sometimes develop coronary artery occlusions and apparently associated pathology (8, 9). SR-BI controls HDL structure and metabolism and appears to be important for ''reverse cholesterol transport,'' HDL-mediated transport of cholesterol from peripheral tissues (including atherosclerotic plaques) to the liver and then to the bile for excretion (2, 3, 10-16). SR-BI delivers cholesteryl esters and other lipids from HDL to cells via selective lipid uptake (2, 3, 10, 17, 18) and can also mediate un...

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Method for non-invasively recording electrocardiograms in conscious mice

Cited by 92 publications

References 36 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

Electrocardiographic and other cardiac anomalies in β-glucuronidase-null mice corrected by nonablative neonatal marrow transplantation

Probucol prevents early coronary heart disease and death in the high-density lipoprotein receptor SR-BI/apolipoprotein E double knockout mouse

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