β1-Adrenergic cardiac contractility is increased during early endotoxemic shock: Involvement of cyclooxygenases

Roul, David; Rozec, Bertrand; Ferron, Marine; Erfanian, Morteza; Persello, Antoine; Audigane, Leslie; Grabherr, Amandine; Erraud, Angélique; Merlet, Nolwenn; Guijarro, Damien; Muramatsu, Ikunobu; Lauzier, Benjamin; Gauthier, Chantal

doi:10.1016/j.lfs.2019.116865

Cited by 3 publications

(1 citation statement)

References 43 publications

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“…showed that propranolol and atenolol reduced myocardial contractility by blocking the positive inotropic effects of myocardial β 1 -ARs, thereby decreasing cardiac output and blood pressure (Frishman, 2013;Roul et al, 2019). In addition, there was no significant change in PAP after blocking β 2 -ARs, whereas it increased after hypoxic ventilation in the ICI 118,551 group, indicating that the activation of β 2 -ARs during acute hypoxia can reduce the elevation of PAP.…”

Section: Controlmentioning

confidence: 97%

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

Zhang

Cao

et al. 2020

Experimental Physiology

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New Findings What is the central question of this study?The acute hypoxic compensatory reaction is based on haemodynamic changes, and β‐adrenoceptors are involved in haemodynamic regulation. What is the role of β‐adrenoceptors in haemodynamics during hypoxic exposure? What is the main finding and its importance?Activation of β2‐adrenoceptors attenuates the increase in pulmonary artery pressure during hypoxic exposure. This compensatory reaction activated by β2‐adrenoceptors during hypoxic stress is very important to maintain the activities of normal life. Abstract The acute hypoxic compensatory reaction is accompanied by haemodynamic changes. We monitored the haemodynamic changes in rats undergoing acute hypoxic stress and applied antagonists of β‐adrenoceptor (β‐ARs) subtypes to reveal the regulatory role of β‐ARs on haemodynamics. Sprague–Dawley rats were randomly divided into control, atenolol (β1‐AR antagonist), ICI 118,551 (β2‐AR antagonist) and propranolol (non‐selective β‐AR antagonist) groups. Rats were continuously recorded for changes in haemodynamic indexes for 10 min after administration. Then, a hypoxic ventilation experiment [15% O2, 2200 m a.sl., 582 mmHg (0.765 Pa), PnormalO2 87.3 mmHg; Xining, China] was conducted, and the indexes were monitored for 5 min after induction of hypoxia. Plasma catecholamine concentrations were also measured. We found that, during normoxia, the mean arterial pressure, heart rate, ascending aortic blood flow and pulmonary artery pressure were reduced in the propranolol and atenolol groups. Catecholamine concentrations were increased significantly in the atenolol group compared with the control group. During hypoxia, mean arterial pressure and total peripheral resistance were decreased in the control, propranolol and ICI 118,551 groups. Pulmonary arterial pressure and pulmonary vascular resistance were increased in the propranolol and ICI 118,551 groups. During hypoxia, catecholamine concentrations were increased significantly in the control group, but decreased in β‐AR antagonist groups. In conclusion, the β2‐AR is involved in regulation of pulmonary haemodynamics in the acute hypoxic compensatory reaction, and the activation of β2‐ARs attenuates the increase in pulmonary arterial pressure during hypoxic stress. This compensatory reaction activated by β2‐ARs during hypoxic stress is very important to maintain activities of normal life.

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Section: Controlmentioning

confidence: 97%

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

Zhang

Cao

et al. 2020

Experimental Physiology

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Immune Oxysterol Downregulates the Atrial Inotropic Response to β-Adrenergic Receptor Stimulation: The Role of Liver X Receptors and Lipid Raft Stability

Odnoshivkina

Petrov

2022

J Evol Biochem Phys

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New Approaches to Identify Sepsis Biomarkers: The Importance of Model and Sample Source for Mass Spectrometry

Blangy-Letheule

Persello

Rozec

et al. 2020

Oxidative Medicine and Cellular Longevity

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Septic shock is a systemic inflammatory response syndrome associated with circulatory failure leading to organ failure with a 40% mortality rate. Early diagnosis and prognosis of septic shock are necessary for specific and timely treatment. However, no predictive biomarker is available. In recent years, improvements in proteomics-based mass spectrometry have improved the detection of such biomarkers. This approach can be performed on different samples such as tissue or biological fluids. Working directly from human samples is complicated owing to interindividual variability. Indeed, patients are admitted at different stages of disease development and with signs of varying severity from one patient to another. All of these elements interfere with the identification of early, sensitive, and specific septic shock biomarkers. For these reasons, animal models of sepsis, although imperfect, are used to control the kinetics of the development of the pathology and to standardise experimentation, facilitating the identification of potential biomarkers. These elements underline the importance of the choice of animal model used and the sample to be studied during preclinical studies. The aim of this review is to discuss the relevance of different approaches to enable the identification of biomarkers that could indirectly be relevant to the clinical setting.

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β1-Adrenergic cardiac contractility is increased during early endotoxemic shock: Involvement of cyclooxygenases

Cited by 3 publications

References 43 publications

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

Immune Oxysterol Downregulates the Atrial Inotropic Response to β-Adrenergic Receptor Stimulation: The Role of Liver X Receptors and Lipid Raft Stability

New Approaches to Identify Sepsis Biomarkers: The Importance of Model and Sample Source for Mass Spectrometry

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