Anesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation

Soh, Sarah; Song, Jong Wook; Choi, Nakcheol; Shim, Jæ Kwang

doi:10.17085/apm.2018.13.1.1

Cited by 4 publications

(12 citation statements)

References 49 publications

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“…This attenuates excessive ROS generation and mitochondrial calcium accumulation that provides the optimal medium for ATP production and inhibits mPTP pore opening. This channel is a direct target of volatile anesthetics [34,35].…”

Section: Enzyme Mechanisms Of Myocardial Conditioningmentioning

confidence: 99%

“…Numerous subsequent studies have addressed anesthetic preconditioning effects on the myocardium using enflurane, isoflurane, sevoflurane, and desflurane, aiming to also elucidate the underlying mechanisms for such effects. Thus far, evidence suggests that anesthetic preconditioning shares fundamental characteristics with ischemic preconditioning, providing early and delayed windows of myocardial protection [35][36][37].…”

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

“…In addition, anesthetic and ischemic preconditioning share many of the same molecular processes involved in myocardial protection, such as G-protein-coupled cell membrane receptors, mediation via multiple protein kinases, and the opening of K ATP channels [24,35,38].…”

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

“…This pathway is considered the main pro-survival kinase cascade and is a combination of two parallel cascades: the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt pathway, which prevents pro-inflammatory and apoptotic events through the exchange of signals with nuclear factor kappa B (NF-kB) and glycogen synthase kinase 3β (GSK3β), and the MAP kinase 1 MEK1/ERK1/2 pathway [30]. In brief, cardioprotective signaling by volatile anesthetics is mainly initiated by G-protein-coupled cell-membrane receptors, which include β1and β2-adrenergic receptors and adenosine-A1 receptor [35]. Volatile anesthetics prime the activation of the sarcolemma and mitochondria K ATP channels, the putative end-effectors of preconditioning, by stimulation of adenosine receptors and subsequent activation of protein kinase C (PKC) and by increased formation of NO and ROS.…”

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

“…Experimental investigations suggest that the ability of volatile anesthetics to protect the myocardium by anesthetic preconditioning significantly increases from isoflurane to sevoflurane to desflurane. Not only the type of volatile anesthetic but also the duration and frequency of exposure to the volatile anesthetic before ischemia have been shown to be of potential relevance in in-vitro experiments [35].…”

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

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Heart Failure after Cardiac Surgery: The Role of Halogenated Agents, Myocardial Conditioning and Oxidative Stress

Guerrero-Orriach

Carmona

Gonzalez-Alvarez

2022

IJMS

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Heart disease requires a surgical approach sometimes. Cardiac-surgery patients develop heart failure associated with ischemia induced during extracorporeal circulation. This complication could be decreased with anesthetic drugs. The cardioprotective effects of halogenated agents are based on pre- and postconditioning (sevoflurane, desflurane, or isoflurane) compared to intravenous hypnotics (propofol). We tried to put light on the shadows walking through the line of the halogenated anesthetic drugs’ effects in several enzymatic routes and oxidative stress, waiting for the final results of the ACDHUVV-16 clinical trial regarding the genetic modulation of this kind of drugs.

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Section: Enzyme Mechanisms Of Myocardial Conditioningmentioning

confidence: 99%

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

Section: Anesthetic Preconditioning Induced By Volatile Anestheticsmentioning

confidence: 99%

See 3 more Smart Citations

Heart Failure after Cardiac Surgery: The Role of Halogenated Agents, Myocardial Conditioning and Oxidative Stress

Guerrero-Orriach

Carmona

Gonzalez-Alvarez

2022

IJMS

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Volatile Anesthetics and O2 Activate TASK-1/3 by Weak H-Bonding with X-Gate Uncharged Arg-245: The Major Molecular Mechanism for Carotid Body Hypoxic Sensitivity and Further Insights into Fighter Pilot +Gz-Induced LOC

DUNCAN¹

2023

Preprint

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Hypoxic conditions are rapidly sensed by the carotid body initiating the hypoxic ventilatory response (HVR) pathways. TASK-1/3 K+ channels are responsible for this and a decrease in PO2 causes them to rapidly close, depolarizing the cell and initiating synaptic transmission. Adequate O2 pressures and Volatile Anesthetics (VA) activate these channels preventing the HVR. After years of research, the precise molecular mechanisms for hypoxic effects are still poorly understood. The exact VA binding site and mechanism of action is also unknown. Here it is shown, with the use of molecular electrostatic potentials (MEP), that O2 and VA weakly H-bond to an uncharged Arginine guanidinium group (Arg-245) within the X-gate, breaking other H-bonds and forming δ-charges in the hydrophobic region which opens the pore allowing K+ to flow out. The current flow for a number of channel activators, including VA and O2, is highly correlated with H-bond strength and resulting δ-charge magnitude (R2 = 0.998). The sequence of molecular changes is explored in detail explaining the significance of current outflow "flickering" from open to closed. O2 modulates these channels directly.The role of H2S in this and other related systems is explored. VA and O2 share a number of mutual sites of action, shedding additional light on jet fighter pilot rapid +Gz loss-of-consciousness and subsequent convulsive episodes - also poorly understood after years of research.

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Coronary Artery Occlusion with Sharp Blood Pressure Drop during General Anesthesia Induction: A Case Report

Ji,

Seo,

Jung

et al. 2024

Medicina

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Most anesthetics reduce cardiac functions and lower blood pressure (BP), potentially causing excessive BP reduction in dehydrated patients or those with heart conditions, such as coronary artery disease (CAD). Considering the increased prevalence of cardiovascular disease with age, anesthesiologists must be cautious about BP reduction during general anesthesia in older adults. In the present case, a 76-year-old male patient with undiagnosed CAD in a hypovolemic state experienced a significant drop in systolic BP to the fifties during propofol and sevoflurane anesthesia. Despite the use of vasopressors, excessive hypotension persisted, leading to anesthesia suspension. Subsequent cardiac examinations, including computed tomography heart angio and calcium score, and coronary angiogram, revealed a near total occlusion of the proximal left anterior descending coronary artery (pLAD) and the formation of collateral circulation. After 5 days of hydration and anticoagulation medications and confirmation of normovolemic state, general anesthesia was attempted again and successfully induced; a normal BP was maintained throughout the surgery. Thus, it is important to conduct a thorough cardiac evaluation and maintain normovolemia for general anesthesia in older adults.

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Anesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation

Cited by 4 publications

References 49 publications

Heart Failure after Cardiac Surgery: The Role of Halogenated Agents, Myocardial Conditioning and Oxidative Stress

Heart Failure after Cardiac Surgery: The Role of Halogenated Agents, Myocardial Conditioning and Oxidative Stress

Volatile Anesthetics and O2 Activate TASK-1/3 by Weak H-Bonding with X-Gate Uncharged Arg-245: The Major Molecular Mechanism for Carotid Body Hypoxic Sensitivity and Further Insights into Fighter Pilot +Gz-Induced LOC

Coronary Artery Occlusion with Sharp Blood Pressure Drop during General Anesthesia Induction: A Case Report

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