Microvascular in vivo assessment of reperfusion injury: significance of prostaglandin E1 and I2 in postischemic “no-reflow” and “reflow-paradox”

Tauber, S.; Menger, Michael D.; Lehr, Hans‐Anton

doi:10.1016/s0022-4804(03)00332-9

Cited by 23 publications

(23 citation statements)

References 40 publications

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“…Both drugs were retested for their efficacy in the setting of I/R injury in many experimental studies (Table 3). However, comparative studies of iloprost and alprostadil are infrequent in the literature (6,16,17). The present study compared them and showed that PG analogs iloprost and alprostadil were almost equally effective in preventing I/R injury in skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

“…It also regulates microcirculation by decreasing the levels of proinflammatory cytokines (1). The effects of iloprost on injury caused by I/R in skeletal muscle (6)(7)(8)(9)(10)(11)(12)17) have been well documented, but they are still controversial in the literature. Earlier studies have focused on circulation research.…”

Section: Discussionmentioning

confidence: 99%

“…I/R was induced by a tourniquet in the hindlimb for 3 h/3 h. The IL and AL groups received iloprost (0.5 ng kg -1 min -1 ) and alprostadil (0.05 µg kg -1 min IL-1β, and IL-6) (1). Although the effects of the two are similar, it is thought that PGE 1 is more potent than PGI 2 (6). This difference in modulation of the inflammatory response depends on different prostanoid receptors of individual PG mediators (5).…”

Section: Methodsmentioning

confidence: 99%

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The effects of iloprost and alprostadil on ischemia-reperfusion injury in preventing inflammation, tissue degeneration, and apoptosis in rat skeletal muscle

et al. 2017

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Background/aim: The protective effects of prostaglandin (PG) analogs on ischemia-reperfusion (I/R) have been well documented; however, comparative studies are lacking. The aim of the present study was to determine whether iloprost or alprostadil is more effective in preventing muscle I/R injury.Materials and methods: Thirty-two rats were divided into four groups (n = 8): sham, control, IL (I/R + iloprost), and AL (I/R + alprostadil). I/R was induced by a tourniquet in the hindlimb for 3 h/3 h. The IL and AL groups received iloprost (0.5 ng kg -1 min -1 ) and alprostadil (0.05 µg kg -1 min -1 ) during reperfusion, respectively. After 6 h, blood and muscles were collected for analyses.Results: Serum TNF-α and IL-1β levels were decreased in the IL and AL groups compared with the control group (P < 0.05), whereas IL-6 levels did not change significantly. Tissue malondialdehyde levels were significantly lower in the IL and AL groups (P < 0.05). Tissue catalase levels showed no difference. The histological damage scores and apoptosis scores were both significantly decreased in the IL and AL groups compared with the control group (P< 0.05). Conclusion:The present study indicated that iloprost and alprostadil attenuated I/R injury in skeletal muscle. However, no comparable difference was evident regarding the efficacies of either PG analog.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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The effects of iloprost and alprostadil on ischemia-reperfusion injury in preventing inflammation, tissue degeneration, and apoptosis in rat skeletal muscle

et al. 2017

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“…Similar to NO, PGE1 has cardioprotective effects during IR [67,68], as well as vasodilator effects on the systemic and pulmonary circulation [69]. Fang et al reported that pretreatment of human umbilical vein endothelial cells with PGE1 significantly protected those cells from H 2 O 2 -induced cell death [66].…”

Section: Effect Of Prostaglandin E1mentioning

confidence: 99%

Real-Time Monitoring of Nitric Oxide Dynamics in the Myocardium: Biomedical Application of Nitric Oxide Sensor

Lee¹,

Lee²,

Park³

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Nitric oxide (NO) is an important physiological mediator that regulates a wide range of cellular processes in many tissues. Therefore, the accurate and reliable measurement of physiological NO concentration is essential to the understanding of NO signaling and its biological role. Most methods used for NO detection are indirect including spectroscopic approaches such as the Griess assay for nitrite and detection of methemoglobin after NO reaction with oxyhemoglobin. These methods cannot accurately reflect the changes in NO concentration in vivo and in real time. Therefore, direct methods are necessary for investigating biological process and diseases related to NO in biological conditions. There is a growing interest in the development of electrochemically based sensors for direct, in vivo, and real-time monitoring of NO. Electrochemical methods offer simplicity, good sensitivity, high selectivity, fast response times, and long-term calibration stability compared to other techniques including electron paramagnetic resonance, chemiluminescence, and fluorescence. In this article, we present real-time NO dynamics in the myocardium during myocardial ischemia-reperfusion (IR) utilizing electrochemical NO microsensor. And applications of electrochemical NO sensor for the evaluation of cardioprotective effects of therapeutic treatments such as drug administration and ischemic preconditioning are reviewed.

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“…PGE 1 has vasodilator effects on the systemic and pulmonary circulation [5] and cardio-protective effects during ischemia and reoxygenation [6] . In addition, beneficial effects on angiogenesis, platelet aggregation, blood viscosity and fibrinolysis have been observed [7][8][9][10][11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Protective effects of prostaglandin E1 on human umbilical vein endothelial cell injury induced by hydrogen peroxide

Fang

Zhou

2010

Acta Pharmacol Sin

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Aim: To investigate the protective effects of prostaglandin E 1 (PGE 1 ) against H 2 O 2 -induced oxidative damage on human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were pretreated with PGE 1 (0.25, 0.50, and 1.00 µmol/L) for 24 h and exposed to H 2 O 2 (200 µmol/L) for 12 h, and cell viability was measured by the MTT assay. LDH, NO, SOD, GSH-Px, MDA, ROS, and apoptotic percentage were determined. eNOS expression was measured by Western blotting and real-time PCR. Results: PGE 1 (0.25−1.00 µmol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H 2 O 2 . PGE 1 also suppressed the production of lipid peroxides, such as MDA, restored the activities of endogenous antioxidants including SOD and GSH-Px, and inhibited cell apoptosis. In addition, PGE 1 significantly increased NO content, eNOS protein, and mRNA expression. Conclusion: PGE 1 effectively protected endothelial cells against oxidative stress induced by H 2 O 2 , an activity that might depend on the up-regulation of NO expression.

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Microvascular in vivo assessment of reperfusion injury: significance of prostaglandin E1 and I2 in postischemic “no-reflow” and “reflow-paradox”

Cited by 23 publications

References 40 publications

The effects of iloprost and alprostadil on ischemia-reperfusion injury in preventing inflammation, tissue degeneration, and apoptosis in rat skeletal muscle

The effects of iloprost and alprostadil on ischemia-reperfusion injury in preventing inflammation, tissue degeneration, and apoptosis in rat skeletal muscle

Real-Time Monitoring of Nitric Oxide Dynamics in the Myocardium: Biomedical Application of Nitric Oxide Sensor

Protective effects of prostaglandin E1 on human umbilical vein endothelial cell injury induced by hydrogen peroxide

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