Guidelines for measuring cardiac physiology in mice

Lindsey, Merry L.; Kassiri, Zamaneh; Virag, Jitka A. I.; Brás, Lisandra E. de Castro; Scherrer‐Crosbie, Marielle

doi:10.1152/ajpheart.00339.2017

Cited by 226 publications

(174 citation statements)

References 211 publications

(234 reference statements)

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“…Care was taken to follow the guidelines for measuring cardiac physiology in mice established by the American Physiological Society (Lindsey et al . ). For each analysis, mice were anaesthetized via an isoflurane/O 2 mixture with induction at 4% and maintenance between 1.5% and 3% and the body temperature was maintained at 37°C via a heated surgical pad.…”

Section: Methodsmentioning

confidence: 97%

Effects of living at moderate altitude on pulmonary vascular function and exercise capacity in mice with sickle cell anaemia

Ferguson

Redinius

Yalamanoglu

et al. 2018

The Journal of Physiology

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Exposure to high altitude worsens symptoms and crises in patients with sickle cell disease (SCD). However, it remains unclear whether prolonged exposure to low barometric pressures exacerbates SCD aetiologies or impairs quality of life. We tested the hypothesis that, relative to wild-type (WT) mice, Berkley sickle cell mice (BERK-SS) residing at sea level, mild (1609 m) and moderate (2438 m) altitude would have a higher rate of haemolysis, impaired cardiac function and reduced exercise tolerance, and that the level of altitude would worsen these decrements. Following 3 months of altitude exposure, right ventricular systolic pressure was measured (solid-state transducer). In addition, the adaptive balance between pulmonary vascular endothelial nitric oxide synthase and endothelin was assessed in lung tissue to determine differences in pulmonary vascular adaptation and the speed/duration relationship (critical speed) was used to evaluate treadmill exercise tolerance. At all altitudes, BERK-SS mice had a significantly lower percentage haemocrit and higher total bilirubin and free haemoglobin concentration (P < 0.05 for all). right ventricular systolic pressures in BERK-SS were higher than WT at moderate altitude and also compared to BERK-SS at sea level (P < 0.05, for both). Critical speed was significantly lower in BERK-SS at mild and moderate altitude (P < 0.05). BERK-SS demonstrated exacerbated SCD complications and reduced exercise capacity associated with an increase in altitude. These results suggest that exposure to mild and moderate altitude enhances the progression of SCD in BERK-SS mice compared to healthy WT cohorts and BERK-SS mice at sea level and provides crucial information for the clinical counselling of SCD patients.

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Section: Methodsmentioning

confidence: 97%

Effects of living at moderate altitude on pulmonary vascular function and exercise capacity in mice with sickle cell anaemia

Ferguson

Redinius

Yalamanoglu

et al. 2018

The Journal of Physiology

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“…Of 759 mice, 422 had echocardiography and plasma or gene RT-PCR data at days 0 ( n = 161; 70 F and 91 M), 1 ( n = 38; 15 F and 23 M), 3 ( n = 46; 18 F and 28 M), and 7 ( n = 95; 47 F and 48 M) post-MI. Both MI surgeries and echocardiography were performed according to established guidelines [49, 51]. …”

Section: Materials and Methods (Detailed Methods In Supplemental Matementioning

confidence: 99%

LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling

et al. 2018

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Sex differences in heart failure development following myocardial infarction (MI) are not fully understood. We hypothesized that differential MI signaling could explain variations in outcomes. Analysis of the mouse heart attack research tool 1.0 (422 mice; young = 5.4 ± 0.1; old = 23.3 ± 0.1 months of age) was used to dissect MI signaling pathways, which was validated in a new cohort of mice (4.8 ± 0.2 months of age); and substantiated in humans. Plasma collected at visit 2 from the MI subset of the Jackson Heart Study (JHS; a community-based study consisting of middle aged and older adults of African ancestry) underwent glycoproteomics grouped by outcome: (1) heart failure hospitalization after visit 2 (n = 3 men/12 women) and (2) without hospitalization through 2012 (n = 24 men/21 women). Compared to young male mice, the infarct region of young females had fewer, but more efficient tissue clearing neutrophils with reduced pro-inflammatory gene expression. Apolipoprotein (Apo) F, which acts upstream of the liver X receptors/retinoid X receptor (LXR/RXR) pathway, was elevated in the day 7 infarcts of old mice compared to young controls and was increased in both men and women with heart failure. In vitro, Apo F stimulated CD36 and peroxisome proliferator-activated receptor (PPAR)γ activation in male neutrophils to turn off NF-κB activation and stimulate LXR/RXR signaling to initiate resolution. Female neutrophils were desensitized to Apo F and instead relied on thrombospondin-1 stimulation of CD36 to upregulate AMP-activated protein kinase, resulting in an overall better wound healing strategy. With age, female mice were desensitized to LXR/RXR signaling, resulting in enhanced interleukin-6 activation, a finding replicated in the JHS community cohort. This is the first report to uncover sex differences in post-MI neutrophil signaling that yielded better outcomes in young females and worse outcomes with age.Electronic supplementary materialThe online version of this article (10.1007/s00395-018-0699-5) contains supplementary material, which is available to authorized users.

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“…A 4 mm 1.2 F catheter probe (Transonic) was inserted into the left ventricle via the heart apex and volume measurements were calibrated automatically by admittance from the probe. Measurements were made following the best practice guidelines for invasive hemodynamic measurement in mice [26]. Heart rate was maintained at 450 to 500 beats per minute (bpm) by adjusting anesthesia (1-2% isoflurane) and maintaining body temperature at 37°C.…”

Section: Left Ventricle Hemodynamicsmentioning

confidence: 99%

Exercise Training Promotes Cardiac Hydrogen Sulfide Biosynthesis and Mitigates Pyroptosis to Prevent High-Fat Diet-Induced Diabetic Cardiomyopathy

et al. 2019

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Obesity increases the risk of developing diabetes and subsequently, diabetic cardiomyopathy (DMCM). Reduced cardioprotective antioxidant hydrogen sulfide (H 2 S) and increased inflammatory cell death via pyroptosis contribute to adverse cardiac remodeling and DMCM. Although exercise training (EX) has cardioprotective effects, it is unclear whether EX mitigates obesity-induced DMCM by increasing H 2 S biosynthesis and mitigating pyroptosis in the heart. C57BL6 mice were fed a high-fat diet (HFD) while undergoing treadmill EX for 20 weeks. HFD mice developed obesity, hyperglycemia, and insulin resistance, which were reduced by EX. Left ventricle pressure-volume measurement revealed that obese mice developed reduced diastolic function with preserved ejection fraction, which was improved by EX. Cardiac dysfunction was accompanied by increased cardiac pyroptosis signaling, structural remodeling, and metabolic remodeling, indicated by accumulation of lipid droplets in the heart. Notably, EX increased cardiac H 2 S concentration and expression of H 2 S biosynthesis enzymes. HFD-induced obesity led to features of type 2 diabetes (T2DM), and subsequently DMCM. EX during the HFD regimen prevented the development of DMCM, possibly by promoting H 2 S-mediated cardioprotection and alleviating pyroptosis. This is the first report of EX modulating H 2 S and pyroptotic signaling in the heart. mechanisms induced by EX to ameliorate cardiac dysfunction would lead to novel therapeutic targets for DMCM-especially in patients unable to exercise.Cardiomyocyte cell death is a key molecular event in the progression of DMCM, as the death of terminally differentiated cardiomyocytes leads to loss of contractile units and instigates fibrosis [12]. In metabolic syndrome, the diabetic environment of hyperglycemia, inflammatory cytokines, oxidative damage, and lipotoxicity induces several types of cell death, including non-inflammatory (apoptosis), and inflammatory (pyroptosis) cell death in the heart [13][14][15]. Pyroptosis is an inflammasome-mediated cell death mechanism where activation of the NOD-like receptor protein 3 (NLRP3) inflammasome activates caspase-1 and results in cell lysis and release of the interleukin IL-1β [16]. Hyperglycemia, fatty acids, and oxidative stress activate NLRP3 and caspase-1-mediated inflammasome, and inhibition of NLRP3 mitigates DMCM in diabetic rats [17][18][19]. Furthermore, HFD and obesity lead to inflammasome activation and infiltration of macrophages into adipose tissue, the key player in pyroptosis [18,20]. However, the role of pyroptosis in obesity-induced cardiac remodeling is unclear. Vandanmagsar et al. demonstrated that EX reduces pyroptotic cell death in adipose and liver tissue, however, this effect has not been evaluated in the heart [18].Hydrogen sulfide (H 2 S), a cardioprotective gaseous signaling molecule produced by homocysteine transsulfuration, prevents adverse cardiac remodeling and cell death, including pyroptosis [21]. H 2 S inhibits caspase-1 activity and IL-1β secretion both in vit...

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Guidelines for measuring cardiac physiology in mice

Cited by 226 publications

References 211 publications

Effects of living at moderate altitude on pulmonary vascular function and exercise capacity in mice with sickle cell anaemia

Effects of living at moderate altitude on pulmonary vascular function and exercise capacity in mice with sickle cell anaemia

LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling

Exercise Training Promotes Cardiac Hydrogen Sulfide Biosynthesis and Mitigates Pyroptosis to Prevent High-Fat Diet-Induced Diabetic Cardiomyopathy

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