Chronic Isoproterenol Treatment of Mice: Effects on Catecholamines and Rectal Temperature

McKay, Genie; Ward, Allen; Morse, Luana; Klingman, Gerda I.

doi:10.1002/jps.2600620520

Cited by 8 publications

(3 citation statements)

References 19 publications

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“…In an ischemia reperfusion injury model, female mouse demonstrated higher postischemic contractile function and lesser ATP-depletion [10]. In a chronic isoproterenol model, Klingman et al found elevated heart to body weight ratio in males but not in females [11]. Finally, total norepinephrine levels in parotid and sub-maxillary glands were reduced in males but not in females.…”

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confidence: 99%

Isoproterenol-Induced Heart Failure Mouse Model Using Osmotic Pump Implantation

Chang

Ren

Rau

et al. 2018

Methods in Molecular Biology

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Isoproterenol is used widely for inducing heart failure in mice. Isoproterenol is a nonselective beta-adrenergic agonist. The acute model mimics stress-induced cardiomyopathy. The chronic model mimics advanced heart failure in humans. In this chapter, we describe a protocol that we used to induce heart failure in 100+ strains of inbred mice. Techniques on surgical pump implantation and echocardiography are described in detail. We also discuss the impact of drug dosage, duration, mortality, age, gender, and strain on cardiac remodeling responses. The success of model creation may be assessed by echocardiogram or molecular markers. This chapter may be relevant to those who are interested in using this heart failure model.

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confidence: 99%

Isoproterenol-Induced Heart Failure Mouse Model Using Osmotic Pump Implantation

Chang

Ren

Rau

et al. 2018

Methods in Molecular Biology

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“…Female mice have demonstrated higher post-ischemic contractile function and lesser ATP-depletion in an ischemia reperfusion injury model as compared to male mice 21 . Moreover, in a chronic ISO model, male mice have demonstrated an elevated heart to body weight ratio and reduced total norepinephrine levels in parotid and submaxillary glands as compared to females 22 . The user may need to consider gender-based differences in the observed outcomes when applying this approach to females and males.…”

Section: Discussionmentioning

confidence: 99%

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Ren¹,

Chang²,

Tran³

et al. 2019

JoVE

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Isoproterenol (ISO), is a non-selective beta-adrenergic agonist, that is used widely to induce cardiac injury in mice. While the acute model mimics stress-induced cardiomyopathy, the chronic model, administered through an osmotic pump, mimics advanced heart failure in humans. The purpose of the described protocol is to create the chronic ISO-induced heart failure model in mice using an implanted mini-pump. This protocol has been used to induce heart failure in 100+ strains of inbred mice. Techniques on surgical pump implantation are described in detail and may be relevant to anyone interested in creating a heart failure model in mice. In addition, the weekly cardiac remodeling changes based on echocardiographic parameters for each strain and expected time to model development are presented. In summary, the method is simple and reproducible. Continuous ISO administered via the implanted mini-pump over 3 to 4 weeks is sufficient to induce cardiac remodeling. Finally, the success for ISO model creation may be assessed in vivo by serial echocardiography demonstrating hypertrophy, ventricular dilation, and dysfunction.

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“…Additionally, our chosen model system limits our study to male mice as female mice do not develop consistently increased heart mass and hypertrophy after chronic isoproterenol administration as previously described. 72 Finally, we use a noncontractile cell line for our in vitro studies, which does not fully recapitulate the in vivo physiology of the myocardium.…”

Section: Limitationsmentioning

confidence: 99%

Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy

Pavelec,

Young,

Luviano

et al. 2024

Circulation Research

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BACKGROUND: PANX1 (pannexin 1), a ubiquitously expressed ATP release membrane channel, has been shown to play a role in inflammation, blood pressure regulation, and myocardial infarction. However, the possible role of PANX1 in cardiomyocytes in the progression of heart failure has not yet been investigated. METHOD: We generated a novel mouse line with constitutive deletion of PANX1 in cardiomyocytes (Panx1 MyHC6 ). RESULTS: PANX1 deletion in cardiomyocytes had no effect on unstressed heart function but increased the glycolytic metabolism and resulting glycolytic ATP production, with a concurrent decrease in oxidative phosphorylation, both in vivo and in vitro. In vitro, treatment of H9c2 cardiomyocytes with isoproterenol led to PANX1-dependent release of ATP and Yo-Pro-1 uptake, as assessed by pharmacological blockade with spironolactone and siRNA-mediated knockdown of PANX1. To investigate nonischemic heart failure and the preceding cardiac hypertrophy, we administered isoproterenol, and we demonstrated that Panx1 MyHC6 mice were protected from systolic and diastolic left ventricle volume increases as a result of cardiomyocyte hypertrophy. Moreover, we found that Panx1 MyHC6 mice showed decreased isoproterenol-induced recruitment of immune cells (CD45 + ), particularly neutrophils (CD11b + , Ly6g + ), to the myocardium. CONCLUSIONS: Together, these data demonstrate that PANX1 deficiency in cardiomyocytes increases glycolytic metabolism and protects against cardiac hypertrophy in nonischemic heart failure at least in part by reducing immune cell recruitment. Our study implies PANX1 channel inhibition as a therapeutic approach to ameliorate cardiac dysfunction in patients with heart failure.

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Chronic Isoproterenol Treatment of Mice: Effects on Catecholamines and Rectal Temperature

Cited by 8 publications

References 19 publications

Isoproterenol-Induced Heart Failure Mouse Model Using Osmotic Pump Implantation

Isoproterenol-Induced Heart Failure Mouse Model Using Osmotic Pump Implantation

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy

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