Preconditioning in cardiac anesthesia…… where are we?

Annachhatre, Ajita Suhrid; Annachhatre, Suhrid

doi:10.4103/aca.aca_116_18

Cited by 8 publications

(5 citation statements)

References 83 publications

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“…Of these, the hypoxic/ischaemic adaptive factors are of greatest interest, because it is likely that the hypoxic component forms the pathogenesis of many diseases and is the main factor in the ischaemic preconditioning effect. In this regard, a study of hypoxic (or ischaemic) preconditioning of the various organs, tissues or the organism as a whole is a high priority [ 1 , 2 , 3 , 4 , 5 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Opposite Pathways of Cholinergic Mechanisms of Hypoxic Preconditioning in the Hippocampus: Participation of Nicotinic α7 Receptors and Their Association with the Baseline Level of Startle Prepulse Inhibition

et al. 2020

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(1) Background. A one-time moderate hypobaric hypoxia (HBH) has a preconditioning effect whose neuronal mechanisms are not studied well. Previously, we found a stable correlation between the HBH efficiency and acoustic startle prepulse inhibition (PPI). This makes it possible to predict the individual efficiency of HBH in animals and to study its potential adaptive mechanisms. We revealed a bi-directional action of nicotinic α7 receptor agonist PNU-282987 and its solvent dimethyl sulfoxide on HBH efficiency with the level of PPI > or < 40%. (2) The aim of the present study was to estimate cholinergic mechanisms of HBH effects in different brain regions. (3) Methods: in rats pretested for PPI, we evaluated the activity of synaptic membrane-bound and water-soluble choline acetyltransferase (ChAT) in the sub-fractions of ‘light’ and ‘heavy’ synaptosomes of the neocortex, hippocampus and caudal brainstem in the intact brain and after HBH. We tested the dose-dependent influence of PNU-282987 on the HBH efficiency. (4) Results: PPI level and ChAT activity correlated negatively in all brain structures of the intact animals, so that the values of the latter were higher in rats with PPI < 40% compared to those with PPI > 40%. After HBH, this ChAT activity difference was leveled in the neocortex and caudal brainstem, while for membrane-bound ChAT in the ‘light’ synaptosomal fraction of hippocampus, it was reversed to the opposite. In addition, a pharmacological study revealed that PNU-282987 in all used doses and its solvent displayed corresponding opposite effects on HBH efficiency in rats with different levels of PPI. (5) Conclusion: We substantiate that in rats with low and high PPI two opposite hippocampal cholinergic mechanisms are involved in hypoxic preconditioning, and both are implemented by forebrain projections via nicotinic α7 receptors. Possible causes of association between general protective adaptation, HBH, PPI, forebrain cholinergic system and hippocampus are discussed.

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Section: Introductionmentioning

confidence: 99%

Opposite Pathways of Cholinergic Mechanisms of Hypoxic Preconditioning in the Hippocampus: Participation of Nicotinic α7 Receptors and Their Association with the Baseline Level of Startle Prepulse Inhibition

et al. 2020

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“…(14) yaptıkları çok merkezli bir çalışmada KABG cerrahisinde volatil anesteziklerin kardiyak troponin değerleri ile belirlenen miyokard hasarını azalttığını göstermişlerdir. KABG cerrahisi geçiren hastalarda volatil anesteziklerin farklı mekanizmalar ile kalbi koruduğu gösterilmiştir (8,9) . Klasik veya erken önkoşullama ile sağlanan korunma tipik olarak uyarının hemen ardından başlamakta, fakat 2-3 saat sonra kaybolmaktadır.…”

Section: Discussionunclassified

“…Volatil anestezikler enerji korunması, disritmilerin azaltılması, kardiyak fonksiyon ve metabolizmanın iyileştirilmesi ile kardiyak korunmaya katkıda bulunurlar (6,7) . Desfluran ve sevofluranın miyokard infarkt alanını azalttığı ve miyokardın önkoşullamasını etkili bir şekilde sağladığı gösterilmiştir (8,9) . Önkoşullama (preconditioning), uzun süreli miyokard iskemi döneminden korunma mekanizmasıdır ve anestezik maddelerin iskemi önkoşullamasına benzer bir mekanizma ile kalbi koruduğu düşünülmektedir.…”

Section: Introductionunclassified

Comparison of Desflurane and Sevoflurane on Myocardial Protection and Inflammation in Coronary Artery Bypass Surgery

Doğan¹,

Kurtipek²

2021

JARSS

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Çalışmamızda koroner arter bypass greftleme cerrahisi geçirecek hastalarda intraoperatif miyokard iskemisi açısından desfluran ve sevofluran anestezi uygulamalarının ST-segmenti, kardiyak enzim ve TNF-α düzeyleri üzerine etkilerini karşılaştırmayı amaçladık. Yöntem: Elektif koroner arter bypass greftleme cerrahisi planlanan toplam 31 olgu iki gruba randomize edildi ve Grup D'ye desfluran, Grup S'de yer alan hastalara sevofluran anestezik ajan olarak kullanıldı. İntraoperatif dönemde hemodinamik parametreler, ST-segment değişiklikleri, kalp debisi ve kullanılan volatil ajanların minimum alveolar konsantrasyon değerleri takip edildi. Anestezi indüksiyonu öncesi, intraoperatif ve postoperatif belirli dönemlerde alınan kan örneklerinden kardiyak enzim ve tümör nekrotizan faktör-α (TNF-α) ölçümleri yapıldı. Bulgular: Her iki grup arasında kaydedilen hemodinamik parametreler, ST-segment değişikliği ve kalp debisi değerleri arasında farklılık gözlenmedi. Kreatin kinaz-MB ve troponin-T değerlerinde gruplar arasında farklılık bulunmadı. Grup D'de postoperatif 2. saatte ölçülen TNF-α düzeyleri Grup S'ye göre anlamlı olarak daha düşük tespit edildi. Grup S'de cilt kapatıldıktan sonraki ve postoperatif 24. saatte ölçülen TNF-α değerleri Grup D'ye göre daha düşüktü. Sonuç: Desfluran ve sevofluran koroner arter bypass greftleme cerrahisi anestezisinde ST-segment değişikliği, kreatin kinaz-MB ve troponin-T ile belirlenebilen miyokard korunmasını benzer oranda sağlar. Erken postoperatif dönemde desfluran, geç postoperatif dönemde sevofluran TNF-α düzeyleri ile gösterilen inflamasyon yanıtını daha fazla baskılamaktadır. Desfluranın koroner arter bypass greftleme cerrahisinde stabil hemodinami ve miyokard korunması sağlaması ve antiinflamatuar etkileri nedeniyle güvenilir bir volatil anestezik ajan olarak kullanılabileceğini düşünüyoruz.

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“…The concept of preconditioning was conceived some time ago [50]. For example, in cardiac surgery, it is now well known that a period of moderate ischemia can cause preconditioning and thereby enhancing resistance to a subsequent period of ischemia over a longer period [51]. It has also been shown that ischemic preconditioning is effective not only in the heart [52] but also in the nervous system [53], skeletal muscle [54], and liver [55].…”

Section: Discussionmentioning

confidence: 99%

Conflicting Actions of Inhalational Anesthetics, Neurotoxicity and Neuroprotection, Mediated by the Unfolded Protein Response

Kokubun

Jin

Komita

et al. 2020

IJMS

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Preclinical studies have shown that exposure of the developing brain to inhalational anesthetics can cause neurotoxicity. However, other studies have claimed that anesthetics can exert neuroprotective effects. We investigated the mechanisms associated with the neurotoxic and neuroprotective effects exerted by inhalational anesthetics. Neuroblastoma cells were exposed to sevoflurane and then cultured in 1% oxygen. We evaluated the expression of proteins related to the unfolded protein response (UPR). Next, we exposed adult mice in which binding immunoglobulin protein (BiP) had been mutated, and wild-type mice, to sevoflurane, and evaluated their cognitive function. We compared our results to those from our previous study in which mice were exposed to sevoflurane at the fetal stage. Pre-exposure to sevoflurane reduced the expression of CHOP in neuroblastoma cells exposed to hypoxia. Anesthetic pre-exposure also significantly improved the cognitive function of adult wild-type mice, but not the mutant mice. In contrast, mice exposed to anesthetics during the fetal stage showed cognitive impairment. Our data indicate that exposure to inhalational anesthetics causes endoplasmic reticulum (ER) stress, and subsequently leads to an adaptive response, the UPR. This response may enhance the capacity of cells to adapt to injuries and improve neuronal function in adult mice, but not in developing mice.

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Preconditioning in cardiac anesthesia…… where are we?

Cited by 8 publications

References 83 publications

Opposite Pathways of Cholinergic Mechanisms of Hypoxic Preconditioning in the Hippocampus: Participation of Nicotinic α7 Receptors and Their Association with the Baseline Level of Startle Prepulse Inhibition

Opposite Pathways of Cholinergic Mechanisms of Hypoxic Preconditioning in the Hippocampus: Participation of Nicotinic α7 Receptors and Their Association with the Baseline Level of Startle Prepulse Inhibition

Comparison of Desflurane and Sevoflurane on Myocardial Protection and Inflammation in Coronary Artery Bypass Surgery

Conflicting Actions of Inhalational Anesthetics, Neurotoxicity and Neuroprotection, Mediated by the Unfolded Protein Response

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