Amitriptyline pharmacologically preconditions rat hearts against cardiac ischemic–reperfusion injury

Lee, S.M.; Hutchinson, Mark R.; Staikopoulos, Vasiliki; Saint, David A.

doi:10.1016/j.ijcard.2015.04.120

Cited by 10 publications

(5 citation statements)

References 38 publications

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“…showed that the application of a TLR4 antagonist could reduce infarct size in rat ischaemic‐reperfused hearts. Similarly, we observed that the administration of amitriptyline (10 μmol/L) before 30 minutes of ischaemia significantly improved left ventricular developed pressure recovery in rat hearts …”

Section: Could Tlr4 Agonists Be Used To Pharmacologically Preconditiosupporting

confidence: 63%

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The role of Toll‐like receptor 4 (TLR4) in cardiac ischaemic‐reperfusion injury, cardioprotection and preconditioning

Lee

Hutchinson

Saint

2016

Clin Exp Pharma Physio

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Cardiac ischaemic-reperfusion injury (IRI) remains the primary cause of mortality throughout the developed world. Molecular mechanisms underlying IRI are complex and are often interlinked with each other driving a synergistic response. Toll-like receptor 4 (TLR4), an immunosurveillance receptor, is known to enhance tissue injury during IRI by enhancing the inflammatory response. The release of endogenous components during IRI bind onto TLR4 leading to the activation of multiple signalling kinases. Once this event occurs these proteins are defined as danger associated molecular patterns molecules (DAMPs) or alarmins. Examples include heat shock proteins, high mobility group box one (HMGB1) and extracellular matrix proteins, all of which are involved in IRI. However, literature in the last two decades suggests that transient stimulation of TLR4 may suppress IRI and thus improve cardiac recovery. Furthermore, it remains to be seen what role TLR4 plays during ischaemic-preconditioning where acute bouts of ischaemia, preceding a harmful bout of ischaemic-reperfusion, is cardioprotective. The other question which also needs to be considered is that if transient TLR4 signalling drives a preconditioning response then what are the ligands which drive this? Hence the second part of this review explores the possible TLR4 ligands which may promote cardioprotection against IRI.

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Section: Could Tlr4 Agonists Be Used To Pharmacologically Preconditiosupporting

confidence: 63%

“…Similarly, we observed that the administration of amitriptyline (10 μmol/L) before 30 minutes of ischaemia significantly improved left ventricular developed pressure recovery in rat hearts. 83…”

Section: Couldtlr4agonistsbeusedto Pharmacologicallyprecondition Hementioning

confidence: 99%

The role of Toll‐like receptor 4 (TLR4) in cardiac ischaemic‐reperfusion injury, cardioprotection and preconditioning

Lee

Hutchinson

Saint

2016

Clin Exp Pharma Physio

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“…However, it is important to highlight that to date no fully powered study has confirmed that anti-depressant (or psycho) therapy improves survival following AMI. Although consistent with the detrimental cardiac impacts of depression, interpretation of the above findings is complicated by pleiotropic cardioprotective effects of such agents [259,260]. Moreover, other agents exhibiting cardioprotective actions also mediate anti-depressant effects (eg.…”

Section: Myocardial Effects Of Anti-depressantsmentioning

confidence: 91%

The heartbreak of depression: ‘Psycho-cardiac’ coupling in myocardial infarction

Headrick

Peart

Budiono

et al. 2017

Journal of Molecular and Cellular Cardiology

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Ample evidence identifies strong links between major depressive disorder (MDD) and both risk of ischemic or coronary heart disease (CHD) and resultant morbidity and mortality. The molecular mechanistic bases of these linkages are poorly defined. Systemic factors linked to MDD, including vascular dysfunction, atherosclerosis, obesity and diabetes, together with associated behavioral changes, all elevate CHD risk. Nonetheless, experimental evidence indicates the myocardium is also directly modified in depression, independently of these factors, impairing infarct tolerance and cardioprotection. It may be that MDD effectively breaks the heart's intrinsic defense mechanisms. Four extrinsic processes are implicated in this psycho-cardiac coupling, presenting potential targets for therapeutic intervention if causally involved: sympathetic over-activity vs. vagal under-activity, together with hypothalamic-pituitary-adrenal (HPA) axis and immuno-inflammatory dysfunctions. However, direct evidence of their involvement remains limited, and whether targeting these upstream mediators is effective (or practical) in limiting the cardiac consequences of MDD is unknown. Detailing myocardial phenotype in MDD can also inform approaches to cardioprotection, yet cardiac molecular changes are similarly ill defined. Studies support myocardial sensitization to ischemic insult in models of MDD, including worsened oxidative and nitrosative damage, apoptosis (with altered Bcl-2 family expression) and infarction. Moreover, depression may de-sensitize hearts to protective conditioning stimuli. The mechanistic underpinnings of these changes await delineation. Such information not only advances our fundamental understanding of psychological determinants of health, but also better informs management of the cardiac consequences of MDD and implementing cardioprotection in this cohort.

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“…A careful selection of materials is needed to develop a TEG that can offer exceptional biocompatibility. Although, there is a wide choice of biocompatible materials Epinephrine EPI Expands the coronary blood flow and improves the aortic diastolic pressure [178] Y-27632 Y27 Protects the heart [179] 5,5-Diphenylhydantoin PHT Improves myocardial junction conduction, and in injured cardiac tissue, it shortens the duration of action potential [180] Acetylsalic Acid ASA Cardioprotective agent [181] γ-Aminobutyric acid GABA Decreases blood pressure and involve in the activation of γ-aminobutyric acid receptor to slow down the heart rate [182] Tetraethylthiuram disulfide TET Decreases systolic B.P and augment hypertension markers [183] Amitriptyline hydrochloride AMI Improves cardiac output [184] Phenacetin PHE Enhances hypertension and cardiovascular diseases [185] but important consideration for in vivo biosensing is the device encapsulation, which must be an excellent biocompatible material. The encapsulated TEG-based biosensors are challenging as it makes it difficult for the analyte to reach the TEG active layer to influence the electrical performance of the device.…”

Section: Tetracycline Sensorsmentioning

confidence: 99%

Self‐Powered Active Sensing Based on Triboelectric Generators

Khandelwal

Dahiya

2022

Advanced Materials

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for above concepts. These technological tools require a large number of different types of sensors for real-time monitoring of the parameters of interest, with the aim of increasing efficiency or productivity, enabling predictive actions (e.g., maintenance, monitoring potential hotspots for spread of diseases) and optimizing supply chain and asset traceability while developing a safer and more secure environment. Accordingly, numerous physical, chemical, and biosensors based on different working mechanisms and transducer materials have been reported. [3][4][5][6] Most of these sensors require continuous operation, for which reliable power source is critical.The widely used power source is the batteries that are often bulky, have a limited lifetime, and are difficult to recycle because of toxic chemicals. [7] As a result, they compromise the sensors portability and, in certain cases, also require a complex and costly process to replace after they run out. Coin cells are other alternatives that are now heavily commoditized and usually present a low-cost solution for powering standalone, lightweight, portable, and miniaturized sensors. However, they still require replacement at regular intervals. A self-reliant and sustainable way of powering the sensors to acquire data and send them wirelessly to a data hub, would be ideal. One solution is to combine a small, long-life, energy-storage devices (e.g., a supercapacitor or a rechargeable solid-state battery) with an energy harvester or wireless powering device. [8] There are many ways of harvesting energy from the environment, from solar energy using photovoltaic panels, or heat using thermal electric generators and vibration with piezoelectric and triboelectric generators (TEGs). [9] Herein, we use the term triboelectric generator (TEG), which also covers the triboelectric nanogenerators (TENGs). If the energy budget is balanced correctly, these two components, i.e., energy storage device and the energy harvester, do not need to be large to work for a long time. The availability of ultralow-power electronics and the constantly improving efficiency of energy harvesting devices (e.g., high-efficiency indoor solar cells can provide at least 20 mW cm −2 and the TEGs can provide up to 50 mW cm −2 ) also support such solutions. [9a,10] Further, the sensors and power management integrated components are becoming increasingly less power hungry. [7b] However, this approach The demand for portable and wearable chemical or biosensors and their expeditious development in recent years has created a scientific challenge in terms of their continuous powering. As a result, mechanical energy harvesters such as piezoelectric and triboelectric generators (TEGs) have been explored recently either as sensors or harvesters to store charge in small, but long-life, energy-storage devices to power the sensors. The use of energy harvesters as sensors is particularly interesting, as with such multifunctional operations it is possible to reduce the number devices needed in a system, which a...

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Amitriptyline pharmacologically preconditions rat hearts against cardiac ischemic–reperfusion injury

Cited by 10 publications

References 38 publications

The role of Toll‐like receptor 4 (TLR4) in cardiac ischaemic‐reperfusion injury, cardioprotection and preconditioning

The role of Toll‐like receptor 4 (TLR4) in cardiac ischaemic‐reperfusion injury, cardioprotection and preconditioning

The heartbreak of depression: ‘Psycho-cardiac’ coupling in myocardial infarction

Self‐Powered Active Sensing Based on Triboelectric Generators

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