The ischemic rat heart releases S100B

Mazzini, Guilherme S.; Schaf, Débora Vigevani; Oliveira, Álvaro Reischak de; Gonçalves, Carlos Alberto; Belló‐Klein, Adriane; Bordignon, Solange; Bruch, Ricardo; Campos, Guilherme F.; Vassallo, Dalton Valentim; Souza, Diogo O.; Portela, Luis Valmor

doi:10.1016/j.lfs.2004.12.035

Cited by 43 publications

(30 citation statements)

References 26 publications

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“…S100B expression was observed in ischemic heart disease [27] . S100B expression was also observed in myocardial infarction and S100B-deficient mice were beneficial to preservation of cardiac function herein [28] .…”

Section: Discussionmentioning

confidence: 98%

RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

Dessing¹,

Pulskens²,

Teske³

et al. 2011

J Innate Immun

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Section: Discussionmentioning

confidence: 98%

RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

Dessing¹,

Pulskens²,

Teske³

et al. 2011

J Innate Immun

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“…Several arguments favor a predominant- ly cerebral origin of the S100B serum levels we found in this pilot study. The isolated ischemic rat heart releases S100B, but only for a maximum of 60 min after myocardial ischemia [39] . As yet no data are available in man.…”

Section: Discussionmentioning

confidence: 97%

Circulating Cerebral S100B Protein Is Associated with Depressive Symptoms following Myocardial Infarction

Tulner¹,

Smith

Jonge

et al. 2009

Neuropsychobiology

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Background: Prevalence of depressive symptoms in the post-myocardial infarction (MI) period varies from 8 to 30%. Cerebral damage after MI, caused by transient ischemia, an inflammatory response or both, may contribute to development of post-MI depression. S100B is an established protein marker of cerebral damage. In a pilot study, the authors assessed whether S100B serum levels are: (1) increased during the week after MI, and (2) related to depressive symptoms during index hospital admission and the year following MI. Methods: This pilot study is a substudy of the Myocardial Infarction and Depression Intervention Trial (MIND-IT). In 48 patients, serum levels of S100B were available at 1, 2, 3, 4 and 8 days following MI. Subsequently, in 27 patients, depressive symptoms were measured at 0, 3, 6, 9 and 12 months following MI with the Beck Depression Inventory (BDI). In 21 of the initial 48 patients, BDI data were lacking due to refusals to fill out BDI forms or missing data. Results: Significant and transient increases in serum S100B were observed in 81.3% of the 48 patients: 37.5% reached S100B serum levels comparable to serum levels found in acute brain injury (>0.20 μg/l) and 43.8% reached mildly elevated S100B serum levels comparable to serum levels found in depressive disorder (0.10–0.20 μg/l). In 18.7%, no S100B was detected in serum. Using non-parametric Spearman rank correlation tests, a trend towards an association was found between serum S100B and depressive symptoms during the post-MI year (ρ values between 0.16 and 0.53) in 27 patients who completed both the S100B serum study and the BDI study. Conclusion: Transiently elevated levels of S100B are suggestive of minor acute cerebral damage in the first days following MI and associated with depressive symptoms in the year following MI. Cerebral damage could be an important mechanism in the pathogenesis in a subtype of post-MI depression.

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“…While S100b is highly expressed in astrocytes, low concentrations of S100b are expressed in heart, gastrointestinal or vesical cells, adipocytes and melanocytes (4)(5)(6)(7). It has been shown that serum S100b levels increase in several cardiac, vascular, neurologic and psychiatric conditions (8)(9)(10). A few number of studies has been carried out in the area of raised S100b protein levels or expressions in antidepressant treatment.…”

mentioning

confidence: 99%

Correlation between Amitriptyline-Induced Cardiotoxic Effects and Cardiac S100b Protein in Isolated Rat Hearts

et al. 2016

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Background:Amitriptyline is an important cause of mortality due to its cardiovascular toxicity. Aims: To investigate the changes in levels of cardiac S100b protein on amitriptyline-induced cardiotoxicity and also to examine the correlation between amitriptyline-induced cardiotoxic effects and cardiac S100b protein in an isolated rat heart model. Study Design: Animal experimentation, isolated heart model. Methods: After a stabilization period, isolated hearts were randomized to two groups (n=5 and n=7). In the control group, isolated hearts were subjected to an infusion of 5% dextrose for 60 minutes. In the amitriptyline group, 5.5×10 -5 M amitriptyline was infused for 60 minutes to achieve amitriptyline toxicity. After the infusion period, heart tissues were removed for histological examination. Results:In comparison to control treatment, amitriptyline infusion decreased left ventricular developed pressure (LVDP), dp/dtmax and heart rate (HR) and significantly prolonged QRS duration (p<0.05). The semiquantitative scores for S100b protein levels in amitriptyline-infused hearts were higher than in the control group (p<0.01). At the end of the experiment, in the amitriptyline-infused group, significant correlations were found between LVDP and S100b protein scores (r=-0.807, p=0.003) and between QRS duration and S100b protein scores (r=0.859, p=0.001). Conclusion:Our results indicate that the S100b protein may be a helpful indicator or biomarker in studying the cardiotoxic effects of amitriptyline.

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The ischemic rat heart releases S100B

Cited by 43 publications

References 26 publications

RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

RAGE Does Not Contribute to Renal Injury and Damage upon Ischemia/Reperfusion-Induced Injury

Circulating Cerebral S100B Protein Is Associated with Depressive Symptoms following Myocardial Infarction

Correlation between Amitriptyline-Induced Cardiotoxic Effects and Cardiac S100b Protein in Isolated Rat Hearts

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