Exogenous Hydrogen Sulfide Protects Against Traumatic Hemorrhagic Shock Via Attenuation of Oxidative Stress

2012 ◽  
Vol 176 (1) ◽  
pp. 210-219 ◽  
Author(s):  
Wei Chai ◽  
Yan Wang ◽  
Jia-Yan Lin ◽  
Xu-De Sun ◽  
Li-Nong Yao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Hemorrhagic Shock ◽  
Traumatic Hemorrhagic Shock

scholarly journals The calcilytic drug Calhex-231 ameliorates vascular hyporesponsiveness in traumatic hemorrhagic shock by inhibiting oxidative stress and mitochondrial fission

2020 ◽  
Author(s):  
Yan Lei ◽  
Xiaoyong Peng ◽  
Tao Li ◽  
Liangming Liu ◽  
Guangming Yang
Keyword(s):  
Oxidative Stress ◽  
Hemorrhagic Shock ◽  
Vascular Reactivity ◽  
Mitochondrial Fission ◽  
Blood Perfusion ◽  
Mitochondrial Fusion ◽  
Vital Organ ◽  
Animal Survival ◽  
Traumatic Hemorrhagic Shock ◽  
Mlc Phosphorylation

Abstract Background The calcium-sensing receptor (CaSR) plays a fundamental role in extracellular calcium homeostasis in humans. Surprisingly, CaSR is also expressed in non-homeostatic tissues and is involved in regulating diverse cellular functions. The objective of this study was to determine if Calhex-231 (Cal), a negative modulator of CaSR, may be beneficial in the treatment of traumatic hemorrhagic shock (THS) by improving cardiovascular function, and investigated its relationship to oxidative stress and the mitochondrial fusion-fission pathway. Methods Rats that had been subjected to traumatic hemorrhagic shock were used as models in this study. Hypoxia-treated vascular smooth muscle cells (VSMCs) were also used. The effects of Cal on cardiovascular function, animal survival, hemodynamic parameters, and vital organ function in THS rats were observed, and the relationship to oxidative stress and mitochondrial fusion-fission was investigated. Results Cal significantly improved hemodynamics, elevated blood pressure, increased vital organ blood perfusion and local oxygen supply, and markedly improved the survival outcomes of THS rats. Furthermore, Cal significantly improved vascular reactivity after THS, including the pressor response of THS rats to norepinephrine (NE), and also the contractile response of superior mesenteric arteries, mesenteric arterioles, and isolated VSMCs to NE. Cal also restored the THS-induced decrease in myosin light chain (MLC) phosphorylation, which is the principal mechanism responsible for VSMC contraction and vascular reactivity. Inhibition of MLC phosphorylation antagonized the Cal-induced restoration of vascular reactivity following THS. Cal decreased oxidative stress indexes and increased antioxidant enzyme levels in THS rats, and also reduced reactive oxygen species levels in hypoxic VSMCs. In addition, THS induced expression of mitochondrial fission proteins Drp1 and Fis1, and decreased expression of mitochondrial fusion protein Mfn1 in vascular tissues. Cal reduced expression of Drp1 and Fis1, but did not affect Mfn1 expression. In hypoxic VSMCs, Cal inhibited hypoxia-induced mitochondrial fragmentation and preserved mitochondrial morphology. Conclusions Calhex-231 exhibits outstanding potential for effective therapy of traumatic hemorrhagic shock, due to its ability to improve hemodynamics, increase vital organ blood perfusion, and markedly prolong animal survival. These beneficial effects result from its protection of vascular function via inhibition of oxidative stress and mitochondrial fission.

REPERFUSION DOES NOT INDUCE OXIDATIVE STRESS BUT SUSTAINED ENDOPLASMIC RETICULUM STRESS IN LIVERS OF RATS SUBJECTED TO TRAUMATIC-HEMORRHAGIC SHOCK

Shock ◽  
2010 ◽  
Vol 33 (3) ◽  
pp. 289-298 ◽  
Author(s):  
Johanna Catharina Duvigneau ◽  
Andrey V. Kozlov ◽  
Clara Zifko ◽  
Astrid Postl ◽  
Romana T. Hartl ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Hemorrhagic Shock ◽  
Traumatic Hemorrhagic Shock

scholarly journals Effects of hydrogen sulfide on hemodynamics, inflammatory response and oxidative stress during resuscitated hemorrhagic shock in rats

Critical Care ◽  
2010 ◽  
Vol 14 (5) ◽  
Author(s):  
Frédérique Ganster ◽  
Mélanie Burban ◽  
Mathilde de la Bourdonnaye ◽  
Lionel Fizanne ◽  
Olivier Douay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Inflammatory Response ◽  
Hemorrhagic Shock ◽  
And Oxidative Stress

scholarly journals The Calcilytic Drug Calhex-231 Ameliorates Vascular Hyporesponsiveness in Traumatic Hemorrhagic Shock by Inhibiting Oxidative Stress and miR-208a-Mediated Mitochondrial Fission

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yan Lei ◽  
Xiaoyong Peng ◽  
Yi Hu ◽  
Mingying Xue ◽  
Tao Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hemorrhagic Shock ◽  
Vascular Reactivity ◽  
Mitochondrial Fission ◽  
Cardiovascular Function ◽  
Mitochondrial Fusion ◽  
Mitochondrial Morphology ◽  
Vital Organ ◽  
Traumatic Hemorrhagic Shock ◽  
Mlc Phosphorylation

Background. The calcium-sensing receptor (CaSR) plays a fundamental role in extracellular calcium homeostasis in humans. Surprisingly, CaSR is also expressed in nonhomeostatic tissues and is involved in regulating diverse cellular functions. The objective of this study was to determine if Calhex-231 (Cal), a negative modulator of CaSR, may be beneficial in the treatment of traumatic hemorrhagic shock (THS) by improving cardiovascular function and investigated the mechanisms. Methods. Rats that had been subjected to THS and hypoxia-treated vascular smooth muscle cells (VSMCs) were used in this study. The effects of Cal on cardiovascular function, animal survival, hemodynamics, and vital organ function in THS rats and the relationship to oxidative stress, mitochondrial fusion-fission, and microRNA (miR-208a) were investigated. Results. Cal significantly improved hemodynamics, elevated blood pressure, increased vital organ blood perfusion and local oxygen supply, and markedly improved the survival outcomes of THS rats. Furthermore, Cal significantly improved vascular reactivity after THS in vivo and in vitro. Cal also restored the THS-induced decrease in myosin light chain (MLC) phosphorylation (the key element for VSMC contraction). Inhibition of MLC phosphorylation antagonized the Cal-induced restoration of vascular reactivity following THS. Cal suppressed oxidative stress in THS rats and hypoxic-VSMCs. Meanwhile, THS induced expression of mitochondrial fission proteins Drp1 and Fis1 and decreased expression of mitochondrial fusion protein Mfn1 in vascular tissues. Cal reduced expression of Drp1 and Fis1. In hypoxic-VSMCs, Cal inhibited mitochondrial fragmentation and preserved mitochondrial morphology. In addition, miR-208a mimic decreased Fis1 expression, and miR-208a inhibitor prevented Cal-induced Fis1 downregulation in hypoxic-VSMCs. Conclusion. Calhex-231 exhibits outstanding potential for effective therapy of traumatic hemorrhagic shock, and the beneficial effects result from its protection of vascular function via inhibition of oxidative stress and miR-208a-mediated mitochondrial fission.

scholarly journals Therapeutic role of atrial natriuretic peptide in early treatment of traumatic hemorrhagic shock

2021 ◽  
Vol 19 ◽  
pp. 205873922110044
Author(s):  
Shou-Yin Jiang ◽  
Ye-Hua Shen ◽  
Tai-Wen Rao ◽  
Xiao-Gang Zhao
Keyword(s):  
Oxidative Stress ◽  
Atrial Natriuretic Peptide ◽  
Hemorrhagic Shock ◽  
Natriuretic Peptide ◽  
Sham Group ◽  
Control Group ◽  
Organ Protection ◽  
Traumatic Hemorrhagic Shock ◽  
And Control ◽  
Atrial Natriuretic

The biological effect of atrial natriuretic peptide (ANP) in traumatic hemorrhagic shock (THS) is unknown. This study was to evaluate whether ANP therapy can show organ protection in THS. Thirty male Sprague-Dawley rats were divided into three groups: ANP group, sham group, and control group. Pressure-controlled THS was induced in rats in ANP group and control group. ANP at a rate of 0.025 μg/kg/min was infused in ANP group during near-80 min of shock. After that, animals were resuscitated for 60 min and observed until 24 h. Hemodynamic parameters during shock and resuscitation were measured. Serum levels of ANP and lactate dehydrogenase, tissue oxidative stress and inflammatory factors, as well as liver and kidney function were determined. Tissue apoptosis was also assessed. There was no statistically significant difference between ANP group and control group in arterial pressure throughout the 150 min monitoring period. Blood urea nitrogen at 90 min and 24 h in ANP group was significantly lower than control group. Alanine transaminase and aspartate aminotransferase activity at 90 min in control group were significantly higher than that in sham group. However, hepatic enzyme activity at 90 min in ANP group was not significantly different compared with sham or control group. After 24 h, myocardial expression of caspase 3 protein in ANP group was significantly reduced compared with control group. Jejunal and hepatic Malondialdehyde was increased following ANP treatment. ANP therapy during early THS has no significant adverse effect on hemodynamics but can exert oxidative stress and certain protective effect on multiple organs. Our study may shed light on the novel therapy of THS with regard to organ protection. The mechanisms underlying the organ protection require further study.

Nitroglycerin Patch in Traumatic Hemorrhagic Shock to Improve Signs of Poor Peripheral Perfusion

2018 ◽  
Vol 86 (6) ◽  
pp. 1253-1261
Author(s):  
MEDHAT S. ALI, M.Sc.; HASSAN I.M. KOTB, M.D. ◽  
ALAA M. AHMED ATIA, M.D.; ABUALAUON M. ABD EL-MOHSEN, M.D.
Keyword(s):  
Hemorrhagic Shock ◽  
Peripheral Perfusion ◽  
Traumatic Hemorrhagic Shock ◽  
Poor Peripheral Perfusion

Protective Effect of Crocin on Liver Function and Survival in Rats With Traumatic Hemorrhagic Shock

2021 ◽  
Vol 261 ◽  
pp. 301-309
Author(s):  
Yang Liu ◽  
Caoyuan Yao ◽  
Yuan Wang ◽  
Xiaolin Liu ◽  
Shanggang Xu ◽  
...  
Keyword(s):  
Liver Function ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Traumatic Hemorrhagic Shock

scholarly journals Fighting Oxidative Stress with Sulfur: Hydrogen Sulfide in the Renal and Cardiovascular Systems

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 373
Author(s):  
Joshua J. Scammahorn ◽  
Isabel T. N. Nguyen ◽  
Eelke M. Bos ◽  
Harry Van Goor ◽  
Jaap A. Joles
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Redox Status ◽  
The Body ◽  
Therapeutic Interventions ◽  
Oxygen Species ◽  
Enzymatic Production ◽  
Age Related ◽  
Anti Oxidant ◽  
Enzymatic Pathways

Hydrogen sulfide (H2S) is an essential gaseous signaling molecule. Research on its role in physiological and pathophysiological processes has greatly expanded. Endogenous enzymatic production through the transsulfuration and cysteine catabolism pathways can occur in the kidneys and blood vessels. Furthermore, non-enzymatic pathways are present throughout the body. In the renal and cardiovascular system, H2S plays an important role in maintaining the redox status at safe levels by promoting scavenging of reactive oxygen species (ROS). H2S also modifies cysteine residues on key signaling molecules such as keap1/Nrf2, NFκB, and HIF-1α, thereby promoting anti-oxidant mechanisms. Depletion of H2S is implicated in many age-related and cardiorenal diseases, all having oxidative stress as a major contributor. Current research suggests potential for H2S-based therapies, however, therapeutic interventions have been limited to studies in animal models. Beyond H2S use as direct treatment, it could improve procedures such as transplantation, stem cell therapy, and the safety and efficacy of drugs including NSAIDs and ACE inhibitors. All in all, H2S is a prime subject for further research with potential for clinical use.

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