Heart rate limitation and cardiac unloading in sevoflurane post‐conditioning

Larsen, Jens Rolighed; Sivesgaard, Kim; Christensen, Steffen; Honge, Jesper L.; Hasenkam, J. Michael

doi:10.1111/j.1399-6576.2011.02580.x

Cited by 5 publications

(5 citation statements)

References 29 publications

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“…ischemia-reperfusion (I/R) injury, is also initiated 1 . The volatile anesthetic sevoflurane emerged as an important cardioprotective agent in I/R injury of rats, mice 2 , rabbits 3 , pigs 4 and in coronary artery disease 5 of human beings. Sevoflurane produces anesthesia of excellent quality, possesses little systemic toxicity, and undergoes limited biotransformation 6 .…”

mentioning

confidence: 99%

Sevoflurane Postconditioning Protects Rat Hearts against Ischemia-Reperfusion Injury via the Activation of PI3K/AKT/mTOR Signaling

Zhang

Wang

et al. 2014

Sci Rep

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Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway plays a key role in myocardial ischemia-reperfusion (I/R) injury. Mammalian target of rapamycin (mTOR), a downstream target of PI3K/AKT signaling, is necessary and sufficient to protect the heart from I/R injury. Inhaled anesthetic sevoflurane is widely used in cardiac surgeries because its induction and recovery are faster and smoother than other inhaled anesthetics. Sevoflurane proved capable of inducing postconditioning effects in the myocardium. However, the underlying molecular mechanisms for sevoflurane-induced postconditioning (SPC) were largely unclear. In the present study, we demonstrated that SPC protects myocardium from I/R injury with narrowed cardiac infarct focus, increased ATP content, and decreased cardiomyocyte apoptosis, which are mainly due to the activation of PI3K/AKT/mTOR signaling and the protection of mitochondrial energy metabolism. Application of dactolisib (BEZ235), a PI3K/mTOR dual inhibitor, abolishes the up-regulation of pho-AKT, pho-GSK, pho-mTOR, and pho-p70s6k induced by SPC, hence abrogating the anti-apoptotic effect of sevoflurane and reducing SPC-mediated protection of heart from I/R injury. As such, this study proved that PI3K/AKT/mTOR pathway plays an important role in SPC induced cardiac protection against I/R injury.

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mentioning

confidence: 99%

Sevoflurane Postconditioning Protects Rat Hearts against Ischemia-Reperfusion Injury via the Activation of PI3K/AKT/mTOR Signaling

Zhang

Wang

et al. 2014

Sci Rep

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“…Reimer and Jennings [ 26 ] were also able to achieve an improvement in myocardium salvage through the administration of propranolol in dogs after circumflex coronary artery ligation. More than three decades later the paradigm “slow the heart rate to preserve myocardium viability” has remained valid, as showed by recent studies in which the administration of drugs able to reduce heart rate and oxygen consumption were able to improve myocardial salvage in animal models of reperfused myocardial infarction [ 6 , 27 ]. Heart rate reduction by Ivabradine appears to have a positive effect on coronary collateral function in patients with chronic stable coronary artery disease [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

“…It is important to better understand the determinants of progression of necrotic wave [ 1 ] to develop new reperfusion strategies able to maximize the salvaged area and improve clinical parameters and prognosis [ 2 , 3 ]. In last year's, several studies have been carried out in animals demonstrating that higher heart rates during the acute phase of STEMI were associated with larger myocardial damage, regardless of the time of coronary occlusion [ 4 , 5 , 6 ]. Nevertheless, still there is a lack of evidence in humans, since for a long time, histological examination has been the only existing technique to quantify the amount of salvaged myocardium.…”

Section: Introductionmentioning

confidence: 99%

Impact of Heart Rate on Myocardial Salvage in Timely Reperfused Patients with ST-Segment Elevation Myocardial Infarction: New Insights from Cardiovascular Magnetic Resonance

et al. 2015

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BackgroundPrevious studies evaluating the progression of the necrotic wave in relation to heart rate were carried out only in animal models of ST-elevated myocardial infarction (STEMI). Aim of the study was to investigate changes of myocardial salvage in relation to different heart rates at hospital admission in timely reperfused patients with STEMI by using cardiovascular magnetic resonance (CMR).MethodsOne hundred-eighty-seven patients with STEMI successfully and timely treated with primary coronary angioplasty underwent CMR five days after hospital admission. According to the heart rate at presentation, patients were subcategorized into 5 quintiles: <55 bpm (group I, n = 44), 55–64 bpm (group II, n = 35), 65–74 bpm (group III, n = 35), 75–84 bpm (group IV, n = 37), ≥85 bpm (group V, n = 36). Area at risk, infarct size, microvascular obstruction (MVO) and myocardium salvaged index (MSI) were assessed by CMR using standard sequences.ResultsLower heart rates at presentation were associated with a bigger amount of myocardial salvage after reperfusion. MSI progressively decreased as the heart rates increased (0.54 group I, 0.46 group II, 0.38 group III, 0.34 group IV, 0.32 group V, p<0.001). Stepwise multivariable analysis showed heart rate, peak troponin and the presence of MVO were independent predictor of myocardial salvage. No changes related to heart rate were observed in relation to area at risk and infarct size.ConclusionsHigh heart rates registered before performing coronary angioplasty in timely reperfused patients with STEMI are associated with a reduction in salvaged myocardium. In particular, salvaged myocardium significantly reduced when heart rate at presentation is ≥85 bpm.

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“…This medication quickly enters blood through lungs and leaves blood with the same speed, therefore has a rapid anesthesia and anesthesia return. Minimum alveolar concentration (MAC) is 4.1% in elderly and 3.3% in children (Larsen et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Also, Rivenes et al (2001) found out that halothane causes a significant reduction in the average pressure of ejection fraction and the heart index. Moreover, in a study done by Larsen et al (2012) it became evident that Sevoflurane reduces regional area of infarction and improves hemodynamics in patients. Findings of a research conducted by Hasani et al (2011) (Hasani et al, 2013) indicated that compared with propofol, sevoflurane could have similar and safe effects in non-relaxant intubation in children undergoing surgery (Moshiri et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Comparison of Inhaled Anesthesia with Sevoflurane and Intravenous Anesthetics with Propofol in Children under Flexible Bronchoscopy

Maleki

Takzare

Goudarzi

et al. 2020

BRAIN

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Objective: Bronchoscopy is a diagnostic procedure. Due to lack of cooperation of children, pediatric bronchoscopy is necessarily accompanied by anesthesia. The most prevailing method of anesthesia in children is inhaled anesthesia, but since duration of anesthesia is long and there is involuntary respiration in this method, the amount of dispersed gas is high. The objective of this review is comparing inhaled anesthesia with sevoflurane and intravenous anesthetics with propofol in children under flexible bronchoscopy, in order to do a more appropriate and safe bronchoscopy and also to improve recovery after general anesthesia in children. Methodology: 80 children under the age of 10 who were going under flexible bronchoscopy, were randomly divided into two groups of 40 individuals. For anesthesia of one group inhaled sevoflurane was given, and for the second group intravenous propofol was given; then in both groups changes in blood pressure, heart rate, O2 saturation t, and recovery time were recorded and compared. Findings: There is no significant difference in three times measurement of both anesthetics. In other words the average blood pressure shows no difference after anesthesia, start of bronchoscopy, and end of bronchoscopy in both anesthetics (P-value=0.771). Moreover, no significant difference was observed in three times measurement of both anesthetics. This means that the average heart rate shows no difference after anesthesia, start of bronchoscopy, and end of bronchoscopy in both anesthetics. Furthermore, the average o2sat is different after anesthesia, start of bronchoscopy, and end of bronchoscopy in both anesthetics (P-value>0.001).

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Heart rate limitation and cardiac unloading in sevoflurane post‐conditioning

Abstract: SePost (1.5-3%) reduced infarct size after regional myocardial ischemia in vivo and reduced cardiac work was significantly correlated to myocardial salvage.

Cited by 5 publications

References 29 publications

Sevoflurane Postconditioning Protects Rat Hearts against Ischemia-Reperfusion Injury via the Activation of PI3K/AKT/mTOR Signaling

Sevoflurane Postconditioning Protects Rat Hearts against Ischemia-Reperfusion Injury via the Activation of PI3K/AKT/mTOR Signaling

Impact of Heart Rate on Myocardial Salvage in Timely Reperfused Patients with ST-Segment Elevation Myocardial Infarction: New Insights from Cardiovascular Magnetic Resonance

Comparison of Inhaled Anesthesia with Sevoflurane and Intravenous Anesthetics with Propofol in Children under Flexible Bronchoscopy

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