Changes in Biomechanical Parameters During Heart Perfusion and After Midazolam Pre-Medication - Experimental Pilot Study

Bartošíková, Lenka; Nečas, Jiří; Bartošík, Tomáš; Fráňa, Petr; Pavlík, Martin

doi:10.5507/bp.2008.012

Cited by 5 publications

(4 citation statements)

References 33 publications

(31 reference statements)

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“…As propofol and midazolam have gained widespread use in cardiac surgery, their cardioprotective effects have been increasingly recognized. Experimental and clinical studies have demonstrated that propofol and midazolam attenuated myocardial ischaemia-reperfusion injury 5-7. However, their underlying mechanisms are not completely understood, and only limited information is available regarding the precise effects of propofol and midazolam on inflammation and oxidative stress 8-10.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Effects of Propofol and Midazolam on Inflammation and Oxidase Stress in Children with Congenital Heart Disease Undergoing Cardiac Surgery

et al. 2011

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PurposeTo investigate and compare the effects of propofol and midazolam on inflammation and oxidase stress in children with congenital heart disease undergoing cardiac surgery.Materials and MethodsThirty-two ASA class I-II children with congenital heart disease undergoing cardiac surgery were randomly divided into two groups: propofol combined with low dose fentanyl (PF group, n = 16) and midazolam combined with low dose fentanyl (MF group, n = 16). Tracheal extubation time and length of Intensive Care Unit (ICU) stay were recorded. Blood samples were taken before operation (T0), at 2 h after release of the aorta cross-clamp (T3) and at 24 h after operation (T4) to measure interleukin 6 (IL-6), IL-8, superoxide dismutase (SOD) and malondialdehyde (MDA) levels. Myocardium samples were collected at 10-20 min after aorta cross-clamp (T1) and at 10-20 min after the release of the aorta cross-clamp (T2) to detect heme oxygenase-1 (HO-1) expression.ResultsTracheal extubation time and length of ICU stay in PF group were significantly shorter than those of the MF group (p < 0.05, respectively). After cardiopulmonary bypass, IL-6, IL-8 and MDA levels were significantly increased, and the SOD level was significantly reduced in both two groups, but PF group exhibited lower IL-6, IL-8 and MDA levels and higher SOD levels than the MF group (p < 0.05, respectively). The HO-1 expression in the PF group was significantly higher than that in MF group at the corresponding time points (p < 0.05, respectively).ConclusionPropofol is superior to midazolam in reducing inflammation and oxidase stress and in improving post-operation recovery in children with congenital heart disease undergoing cardiac surgery.

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Section: Introductionmentioning

confidence: 99%

Comparison of the Effects of Propofol and Midazolam on Inflammation and Oxidase Stress in Children with Congenital Heart Disease Undergoing Cardiac Surgery

et al. 2011

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“…Schedule: stabilization/compound perfusion/reperfusion proceeded at intervals of 10/15/10 min. Left ventricle pressure (LVP), left ventricle end diastolic pressure (LVEDP), and contractility (dP/dtmax) were measured using a ball filled with liquid (8–12 mmHg), inserted through the left atrium into the left ventricle and connected to an analog convertor Isotec HSE, DIF modul HSE (Harvard apparatus GmbH, March-Hugstetten, Germany) [ 16 , 17 ].…”

Section: Methodsmentioning

confidence: 99%

Silymarin Constituent 2,3-Dehydrosilybin Triggers Reserpine-Sensitive Positive Inotropic Effect in Perfused Rat Heart

et al. 2015

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2,3-dehydrosilybin (DHS) is a minor flavonolignan component of Silybum marianum seed extract known for its hepatoprotective activity. Recently we identified DHS as a potentially cardioprotective substance during hypoxia/reoxygenation in isolated neonatal rat cardiomyocytes. This is the first report of positive inotropic effect of DHS on perfused adult rat heart. When applied to perfused adult rat heart, DHS caused a dose-dependent inotropic effect resembling that of catecholamines. The effect was apparent with DHS concentration as low as 10 nM. Suspecting direct interaction with β-adrenergic receptors, we tested whether DHS can trigger β agonist-dependent gene transcription in a model cell line. While DHS alone was unable to trigger β agonist-dependent gene transcription, it enhanced the effect of isoproterenol, a known unspecific β agonist. Further tests confirmed that DHS could not induce cAMP accumulation in isolated neonatal rat cardiomyocytes even though high concentrations (≥ 10 μM) of DHS were capable of decreasing phosphodiesterase activity. Pre-treatment of rats with reserpine, an indole alkaloid which depletes catecholamines from peripheral sympathetic nerve endings, abolished the DHS inotropic effect in perfused hearts. Our data suggest that DHS causes the inotropic effect without acting as a β agonist. Hence we identify DHS as a novel inotropic agent.

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“…Midazolam has gained widespread use in cardiac surgery; its cardioprotective effects have been increasingly recognized. Experimental and clinical studies have demonstrated that midazolam attenuated myocardial ischemia-reperfusion injury [16]. Although midazolam has more beneficial effects than other currently used sedative drugs [17], its effects on chondrocytes have not been investigated at the cellular or molecular levels.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of midazolam on MMP-9, MMP-1 and MMP-13 expression in PMA-stimulated human chondrocytes via recovery of NF-κB signaling

Wang

Huan²,

Hsieh³

et al. 2013

aoms

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IntroductionMidazolam, a benzodiazepine, has a hypnotic effect and is widely used as an intravenous sedative. Past studies have clearly established that midazolam has beneficial effects in attenuating ischemia-reperfusion injury more than other currently used sedative drugs. However, the role of midazolam on chondroprotection via inhibition of matrix metalloproteinases (MMPs) is warrant investigation. The aim of this study was to examine the mechanisms of action of midazolam on MMP expression via nuclear factor κB (NF-κB) signaling in activated chondrosarcoma cells maintained in vitro.Material and methodsChondrocytes, SW1353 cells, were stimulated with phorbol 12-myristate 13-acetate (PMA) in the absence or presence of various concentrations of midazolam (5-20 µM). Release of MMP-9 into the culture media was determined by gelatin zymography. The expressions of MMP-1, MMP-9 and MMP-13, phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinases and degradation of IκB-α were determined by western blotting assay.ResultsMidazolam significantly down-regulated PMA-induced MMP-9 protein expression at concentrations of 5, 10 and 20 µM, the values were 1.95 ±0.09 (p < 0.01), 1.71 ±0.12 (p < 0.01) and 1.35 ±0.20 (p < 0.001), respectively. At concentrations of 5, 10 and 20 µM, it was significantly inhibited the PMA-induced expressions of MMP-1 (2.27 ±0.10, 1.98 ±0.11 and 1.56 ±0.15; p < 0.001) and MMP-13 (0.89 ±0.04, 0.81 ±0.07, and 0.74 ±0.09; p < 0.001), respectively. Midazolam at concentrations of 10 and 20 µM for 15 min significantly reversed the rate of degradation (0.895 ±0.051; p < 0.05 and 0.926 ±0.060; p < 0.01, respectively) of IκB-α in PMA-chondrocyte cells. In addition, this sedative drug inhibited PMA-induced levels of phos-ERK (1.243 ±0.12, 1.108 ±0.16 and 0.903 ±0.19, respectively) and phos-p38 (1.146 ±0.10, 1.063 ±0.13 and 0.946 ±0.18, at concentrations of (5, 10 and 20 µM), respectively.ConclusionsThese results are important for understanding the mechanism of midazolam in inhibiting PMA-induced MMP expression through the signaling pathways of either NF-κB or ERK/p38 MAPKs down-regulation.

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Changes in Biomechanical Parameters During Heart Perfusion and After Midazolam Pre-Medication - Experimental Pilot Study

Cited by 5 publications

References 33 publications

Comparison of the Effects of Propofol and Midazolam on Inflammation and Oxidase Stress in Children with Congenital Heart Disease Undergoing Cardiac Surgery

Comparison of the Effects of Propofol and Midazolam on Inflammation and Oxidase Stress in Children with Congenital Heart Disease Undergoing Cardiac Surgery

Silymarin Constituent 2,3-Dehydrosilybin Triggers Reserpine-Sensitive Positive Inotropic Effect in Perfused Rat Heart

Inhibitory effect of midazolam on MMP-9, MMP-1 and MMP-13 expression in PMA-stimulated human chondrocytes via recovery of NF-κB signaling

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