Heart Rate and Electrocardiography Monitoring in Mice

Ho, David; Zhao, Xin; Gao, Shumin; Hong, Chull; Vatner, Dorothy E.; Vatner, Stephen F.

doi:10.1002/9780470942390.mo100159

Cited by 100 publications

(77 citation statements)

References 29 publications

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“…C) that was consistent with the observed myocardial dysfunction in DKO hearts . Upon two‐dimensional echocardiographic evaluation, DKO mice displayed abnormal M‐mode with decreased left ventricular internal diameter (LVID) in diastole as well as in systole (Fig. D).…”

Section: Resultsmentioning

confidence: 68%

Bile acid excess induces cardiomyopathy and metabolic dysfunctions in the heart

et al. 2016

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Cardiac dysfunction in patients with liver cirrhosis is strongly associated with increased serum bile acid concentrations. Here we show that excess bile acids decrease fatty acid oxidation in cardiomyocytes and can cause heart dysfunction, a cardiac syndrome that we term Cholecardia. Fxr; Shp double knockout (DKO) mice, a model for bile acid overload, display cardiac hypertrophy, bradycardia, and exercise intolerance. In addition, DKO mice exhibit an impaired cardiac response to catecholamine challenge. Consistent with this decreased cardiac function, we show that elevated serum bile acids reduce cardiac fatty acid oxidation both in vivo and ex vivo. We find that increased bile acid levels suppress expression of Pgc1α, a key regulator of fatty acid metabolism, and that Pgc1α overexpression in cardiac cells was able to rescue the bile acid-mediated reduction in fatty acid oxidation genes. Importantly, intestinal bile acid sequestration with cholestyramine was sufficient to reverse the observed heart dysfunction in the DKO mice. Conclusions Overall, we propose that decreased Pgc1α expression contributes to the metabolic dysfunction in Cholecardia, and that reducing serum bile acid concentrations will be beneficial against metabolic and pathological changes in the heart.

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Section: Resultsmentioning

confidence: 68%

Bile acid excess induces cardiomyopathy and metabolic dysfunctions in the heart

et al. 2016

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“…We observed an early bradycardia in the initial postoperative and post-implantation phase (Figure 1A), with gradual recovery over the first two to three hours (median time 131 minutes, range 56 to 301 minutes) to a normal range: 500 to 700 bpm (49). We observed a corresponding mild hypothermia after surgery (Figure 1B), with core temperature recovering to normal values, typically after recovery of bradycardia.…”

Section: Resultsmentioning

confidence: 93%

Use of Biotelemetry to Define Physiology-Based Deterioration Thresholds in a Murine Cecal Ligation and Puncture Model of Sepsis

Lewis

Yuan

Zhang

et al. 2016

Critical Care Medicine

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Objective Murine models of critical illness are commonly used to test new therapeutic interventions. However, these interventions are often administered at fixed time intervals after the insult, perhaps ignoring the inherent variability in magnitude and temporality of the host response. We propose to use wireless biotelemetry monitoring to define and validate criteria for acute deterioration and generate a physiology-based murine cecal ligation and puncture (CLP) model that is more similar to the conduct of human trials of sepsis. Design Laboratory and animal research Setting University basic science laboratory Subjects Male C57BL/6 mice Interventions Mice underwent CLP, and an HD-X11 wireless telemetry monitor (DSI) was implanted that enabled continuous, real-time measurement of heart rate, core temperature, and mobility. We performed a population-based analysis to determine threshold criteria that met face validity for acute physiologic deterioration. We assessed construct validity by temporally matching mice that met these acute physiologic deterioration thresholds with mice that had not yet met deterioration threshold. We analyzed matched blood samples for blood gas, inflammatory cytokine concentration, Cystatin C, and alanine aminotransferase. Measurements and Main Results We observed that a 10% reduction in both heart rate and temperature sustained for >=10 minutes defined acute physiologic deterioration. There was significant variability in the time to reach acute deterioration threshold across mice, ranging from 339 to 529 minutes after CLP. We found adequate construct validity, as mice, which met criteria for acute deterioration had significantly worse shock, systemic inflammation (elevated TNFα, p=0.003; IL-6, p=0.01; IL-10, p=0.005), and acute kidney injury when compared to mice that had not yet met acute deterioration criteria. Conclusion We defined a murine threshold for acute physiologic deterioration after CLP that has adequate face and construct validity. This model may enable a more physiology-based model for evaluation of novel therapeutics in critical illness.

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“…793200) subcutaneously under general anesthesia (Ho et al, 2011). Briefly, the three wires were connected to an omnetics connector cemented onto the mouse back and tunneled underneath the skin to reach each of three recording positions (left arm, right arm and right leg).…”

Section: Extended Experimental Proceduresmentioning

confidence: 99%

Collateral Pathways from the Ventromedial Hypothalamus Mediate Defensive Behaviors

Wang

Chen

Lin

2015

Neuron

252

261

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Summary The ventromedial hypothalamus (VMH) was thought to be essential for coping with threat, although its circuit mechanism remains unclear. To investigate this, we optogenetically activated steroidogenic factor 1 (SF1)-expressing neurons in the dorsomedial and central part of VMH (VMHdm/c), and observed a range of context dependent somatomotor and autonomic responses resembling animals' natural defensive behaviors. By activating independent pathways emanating from VMHdm/c, we demonstrated that VMHdm/c projection to the dorsolateral periaqueductal gray (dlPAG) induces inflexible immobility, while the VMHdm/c to anterior hypothalamic nucleus (AHN) pathway promotes avoidance. Furthermore, consistent with the behavior changes induced by VMH to AHN pathway activation, direct activation of the AHN elicited avoidance and escape jumping but not immobility. Finally, retrograde tracing studies revealed that nearly 50% of PAG- projecting VMHdm/c neurons send collateral projection to the AHN and vice versa. Thus, VMHdm/c neurons employ a one-to-many wiring configuration to orchestrate multiple aspects of defensive behaviors.

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Heart Rate and Electrocardiography Monitoring in Mice

Cited by 100 publications

References 29 publications

Bile acid excess induces cardiomyopathy and metabolic dysfunctions in the heart

Bile acid excess induces cardiomyopathy and metabolic dysfunctions in the heart

Use of Biotelemetry to Define Physiology-Based Deterioration Thresholds in a Murine Cecal Ligation and Puncture Model of Sepsis

Collateral Pathways from the Ventromedial Hypothalamus Mediate Defensive Behaviors

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