Sodium thiosulfate mediated cardioprotection against myocardial ischemia-reperfusion injury is defunct in rat heart with co-morbidity of vascular calcification

Ravindran, Sriram; Ramachandran, Kausthubh; Kurian, Gino A.

doi:10.1016/j.biochi.2018.01.004

Cited by 7 publications

(11 citation statements)

References 43 publications

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“…Possible organ-protective effects of STS have been referred to attenuated activation of nuclear transcription factor-κB, hyper-inflammation and oxidative stress ( 2 , 3 ) and reduced apoptosis ( 9 – 11 , 13 ). In addition, we had demonstrated that the marked lung-protective effect of STS in swine with coronary artery disease and, hence, reduced CSE expression coincided with significantly higher tissue glucocorticoid receptor (GR) expression.…”

Section: Discussionmentioning

confidence: 99%

The H2S Donor Sodium Thiosulfate (Na2S2O3) Does Not Improve Inflammation and Organ Damage After Hemorrhagic Shock in Cardiovascular Healthy Swine

Messerer

Gaessler²,

Hoffmann

et al. 2022

Front. Immunol.

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We previously demonstrated marked lung-protective properties of the H2S donor sodium thiosulfate (Na2S2O3, STS) in a blinded, randomized, controlled, long-term, resuscitated porcine model of swine with coronary artery disease, i.e., with decreased expression of the H2S-producing enzyme cystathionine-γ-lyase (CSE). We confirmed these beneficial effects of STS by attenuation of lung, liver and kidney injury in mice with genetic CSE deletion (CSE-ko) undergoing trauma-and-hemorrhage and subsequent intensive care-based resuscitation. However, we had previously also shown that any possible efficacy of a therapeutic intervention in shock states depends both on the severity of shock as well as on the presence or absence of chronic underlying co-morbidity. Therefore, this prospective, randomized, controlled, blinded experimental study investigated the effects of the STS in cardiovascular healthy swine. After anesthesia and surgical instrumentation, 17 adult Bretoncelles-Meishan-Willebrand pigs were subjected to 3 hours of hemorrhage by removal of 30% of the blood volume and titration of the mean arterial pressure (MAP) ≈ 40 ± 5 mmHg. Afterwards, the animals received standardized resuscitation including re-transfusion of shed blood, fluids, and, if needed, continuous i.v. noradrenaline to maintain MAP at pre-shock values. Animals were randomly allocated to either receive Na2S2O3 or vehicle control starting 2 hours after initiation of shock until 24 hours of resuscitation. The administration of Na2S2O3 did not alter survival during the observation period of 68 hours after the initiation of shock. No differences in cardio-circulatory functions were noted despite a significantly higher cardiac output, which coincided with significantly more pronounced lactic acidosis at 24 hours of resuscitation in the Na2S2O3 group. Parameters of liver, lung, and kidney function and injury were similar in both groups. However, urine output was significantly higher in the Na2S2O3 group at 24 hours of treatment. Taken together, this study reports no beneficial effect of Na2S2O3 in a clinically relevant model of hemorrhagic shock-and-resuscitation in animals without underlying chronic cardiovascular co-morbidity.

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Section: Discussionmentioning

confidence: 99%

The H2S Donor Sodium Thiosulfate (Na2S2O3) Does Not Improve Inflammation and Organ Damage After Hemorrhagic Shock in Cardiovascular Healthy Swine

Messerer

Gaessler²,

Hoffmann

et al. 2022

Front. Immunol.

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“…Nicorandil belongs to the adenosine triphosphate K+ channel opening agent and has the effect of dilating coronary artery, relieving coronary spasms, and increasing myocardial blood supply [ 9 ]. According to the study, nicorandil has the function of diastolic blood vessels, increasing coronary blood flow, and is mostly used in the treatment of myocardial ischemia [ 10 ]. Based on this, 104 cases of patients with myocardial ischemia admitted to our hospital from June 2019 to August 2020 were selected as the research objects to explore the clinical effect of nicorandil combined with aspirin in the treatment of patients with myocardial ischemia.…”

Section: Introductionmentioning

confidence: 99%

Clinical Effect of Nicorandil Combined with Aspirin in the Treatment of Myocardial Ischemia

Chen

Xiong

et al. 2022

BioMed Research International

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Objective. To investigate the clinical effect of nicorandil combined with aspirin in the treatment of myocardial ischemia. Methods. A total of 104 patients with myocardial ischemia were admitted to our hospital from June 2019 to August 2020. These patients were selected as the research objects and randomly divided into two groups: the control group and the observation group. The control group was given asilin, and the observation group was given nicorandil tablets based on the control group. Both groups were given continuous treatment for 3 months. The curative effect, cardiac function indexes, dynamic electrocardiogram, and the occurrence of adverse reactions were observed in the two groups. Results. The total effective rate of the observation group was 96.15% (50/52), which was higher than that of the control group (61.54%, 32/52), and the difference was statistically significant ( P < 0.05 ). After treatment, left ventricular ejection fraction (LVEF) and peak early/late diastolic flow velocity (E/A) were increased ( P < 0.05 ), while peak early diastolic flow velocity to peak mitral annular root movement velocity (E/Ea) was decreased ( P < 0.05 ). After treatment, LVEF and E/A in the observation group were higher than those in the control group, while E/Ea was lower than that in the control group ( P < 0.05 ). The frequency, duration of ST segment, and a total load of myocardial ischemia in the ST segment within 24 h after treatment were decreased compared with those before treatment ( P < 0.05 ). The frequency and duration of ST segment decreased, and the total load of myocardial ischemia in the observation group was lower than those in the control group within 24 h after treatment ( P < 0.05 ). After treatment, the total occurrence of adverse reactions in the observation group was lower than that in the control group ( P < 0.05 ). Conclusion. Nicorandil combined with aspirin in the treatment of patients with myocardial ischemia has a significant effect, which can effectively improve the electrocardiogram and cardiac function indicators of patients and reduce the incidence of adverse reactions and is worthy of clinical application.

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“…Complex I activity was increased (Ravindran et al, 2017) to compensate for the decrease in ATP synthase activity. Disruption of the cristae (Cui et al, 2017; Kim et al, 2012) of the mitochondrial inner membrane and mitochondrial swelling (Ravindran et al, 2018, 2017) were also reported. In addition, PGC‐1α and its downstream target gene, SIRT3, were reduced, demonstrating impaired mitochondrial biogenesis in CKD rats (Feng et al, 2019).…”

Section: Roles Of Mitochondrial Function In Vc In Ckd Models: Reports...mentioning

confidence: 99%

“…Since impaired mitochondrial function is a mechanism which is at least partly responsible for VC in CKD, nicorandil has been investigated to alleviate VC in a CKD rat model. In adenine‐induced CKD rats, nicorandil administration reversed mitochondrial function by improving mitochondrial depolarization, increasing mitochondrial respiration capacity, mitochondrial Krebs cycle enzymes (SDH, MDH) (Ravindran et al, 2018, 2017), and ATP synthase activity (Ravindran et al, 2017), and attenuating Ca‐induced mitochondrial swelling (Ravindran et al, 2018, 2017). Furthermore, nicorandil was shown to induce antioxidant activity and suppress ROS production, as evidenced by an increase in GSH, GR (Ravindran et al, 2018, 2017), GPx, SOD, and CAT (Ravindran et al, 2018), and a decrease in TBARS, MDA (Ravindran et al, 2018, 2017), and superoxide anion (Ravindran et al, 2017), leading to a reduction in aortic calcification (Ravindran et al, 2018, 2017).…”

Section: Effect Of Interventions On Mitochondrial Function Against Vc...mentioning

confidence: 99%

“…STS is an antioxidant and a direct calcium chelating agent that is generally used for the treatment of calciphylaxis (Peng et al, 2018). In adenine‐induced CKD rats, STS reduced VC, but did not either preserve mitochondrial function or suppress oxidative stress (Ravindran et al, 2018). However, the combination of STS and nicorandil successfully restored mitochondrial function, activated antioxidant capability, and suppressed ROS production, leading to further attenuation of VC than following treatment with STS alone (Ravindran et al, 2018).…”

Section: Effect Of Interventions On Mitochondrial Function Against Vc...mentioning

confidence: 99%

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Mitochondria and vascular calcification in chronic kidney disease: Lessons learned from the past to improve future therapy

Pongsuwan

Kusirisin

Narongkiattikhun

et al. 2022

Journal Cellular Physiology

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Chronic kidney disease-mineral and bone disorders (CKD-MBD) is a common complication of CKD Stages 3-5. Hyperphosphatemia is one of the major metabolic components of CKD-MBD, frequently resulting in vascular calcification (VC) in advanced-stage patients. Also, a long duration of renal replacement therapy can cause the worsening of VC, leading to increased cardiovascular morbidity and mortality. Vascular smooth muscle cells play an important role in the development of VC through osteochondrogenic transformation and the apoptotic process. It has been shown that mitochondrial dysfunction is involved with CKD progression, and excessive oxidative stress can aggravate osteoblastic transformation and VC. Currently, novel interventions targeting mitochondrial function and dynamics, in addition to mitochondrial antioxidants, have been studied with the aim of attenuating VC. This review aims to comprehensively summarize and discuss the experimental and clinical reports concerning mitochondrial studies, along with the purpose of interventions that can improve the outcomes of VC among CKD patients.

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Sodium thiosulfate mediated cardioprotection against myocardial ischemia-reperfusion injury is defunct in rat heart with co-morbidity of vascular calcification

Cited by 7 publications

References 43 publications

The H2S Donor Sodium Thiosulfate (Na2S2O3) Does Not Improve Inflammation and Organ Damage After Hemorrhagic Shock in Cardiovascular Healthy Swine

The H2S Donor Sodium Thiosulfate (Na2S2O3) Does Not Improve Inflammation and Organ Damage After Hemorrhagic Shock in Cardiovascular Healthy Swine

Clinical Effect of Nicorandil Combined with Aspirin in the Treatment of Myocardial Ischemia

Mitochondria and vascular calcification in chronic kidney disease: Lessons learned from the past to improve future therapy

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