scholarly journals Nitrosative Stress and Myocardial Sarcoplasmic Endoreticular Calcium Adenosine Triphosphatase Subtype 2a Activity after Lung Resection in Swine

2007 ◽  
Vol 107 (6) ◽  
pp. 954-962 ◽  
Author(s):  
Paul M. Heerdt ◽  
Paul Lane ◽  
Brian Y. Pan ◽  
Ulrich Schaefer ◽  
Mark Crabtree ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adenosine Triphosphatase ◽  
Nitrosative Stress ◽  
Lung Resection ◽  
Force Frequency ◽  
Calcium Cycling ◽  
Biochemical Basis ◽  
Frequency Relation ◽  
Calcium Adenosine Triphosphatase ◽  
Phospholamban Phosphorylation

Background Chronic, disease-associated oxidative stress induces myocardial peroxynitrite formation that may lead to nitrosative inhibition of the calcium cycling protein sarcoplasmic endoreticular calcium adenosine triphosphatase subtype 2a (SERCA2a). The current study was designed to test the hypothesis that the acute oxidative stress associated with lung resection also induces myocardial nitrosative stress and alters SERCA2a activity. Methods Ventricular myocardium from 16 swine was studied; 11 animals had undergone left upper lobectomy (n = 7) or sham thoracotomy (n = 4) 3 days before harvest, and 5 were nonoperated controls. Tissue peroxynitrite was assessed by measurement of 3-nitrotyrosine incorporation into proteins. SERCA2a activity was determined from indo-1 uptake by isolated sarcoplasmic reticular membranes. Expression of SERCA2a and its regulatory protein phospholamban were determined by Western blotting, as was the phospholamban phosphorylation state (when dephosporylated, phospholamban inhibits SERCA2a). Mechanical significance of changes in SERCA2a activity was assessed from the force-frequency relation of isometric myocardial trabeculae. Results Relative to both the control and sham groups, lobectomy animals exhibited a greater than twofold higher myocardial 3-nitrotyrosine incorporation and an approximately 50% lower SERCA2a activity, but no difference in SERCA2a or phospholamban expression or phospholamban phosphorylation. Concomitantly, whereas the trabecular force-frequency relation of control animals was positive, that of lobectomy animals was negative, consistent with impaired calcium cycling. Conclusions These data indicate that oxidative/nitrosative stress associated with lung resection influences SERCA2a activity independent of any influence on protein expression or phospholamban phosphorylation. The findings link an acute event with a subcellular process primarily described for chronic illness and suggest a biochemical basis for perioperative changes in myocardial mechanical reserve.

Force-frequency relation and myofilament Ca2+ sensitivity

2008 ◽  
pp. 39-41
Author(s):  
Regis Lamberts ◽  
Jolanda van der Velden ◽  
Ger Stienen
Keyword(s):  
Force Frequency ◽  
Frequency Relation

Adrenergic Control of the Force-Frequency Relation

Circulation ◽  
1995 ◽  
Vol 92 (8) ◽  
pp. 2327-2332 ◽  
Author(s):  
John Ross ◽  
Toshiro Miura ◽  
Masashi Kambayashi ◽  
Gregory P. Eising ◽  
Kyu-Hyung Ryu
Keyword(s):  
Force Frequency ◽  
Adrenergic Control ◽  
Frequency Relation

scholarly journals Oxygen Is Instrumental for Biological Signaling: An Overview

Oxygen ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 3-15
Author(s):  
John T. Hancock
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Nitrosative Stress ◽  
Redox Status ◽  
Complex Interplay ◽  
Wide Range ◽  
Form Part ◽  
High Concentrations ◽  
And Control ◽  
Signaling Components

Control of cellular function is extremely complex, being reliant on a wide range of components. Several of these are small oxygen-based molecules. Although reactive compounds containing oxygen are usually harmful to cells when accumulated to relatively high concentrations, they are also instrumental in the control of the activity of a myriad of proteins, and control both the upregulation and downregulation of gene expression. The formation of one oxygen-based molecule, such as the superoxide anion, can lead to a cascade of downstream generation of others, such as hydrogen peroxide (H2O2) and the hydroxyl radical (∙OH), each with their own reactivity and effect. Nitrogen-based signaling molecules also contain oxygen, and include nitric oxide (NO) and peroxynitrite, both instrumental among the suite of cell signaling components. These molecules do not act alone, but form part of a complex interplay of reactions, including with several sulfur-based compounds, such as glutathione and hydrogen sulfide (H2S). Overaccumulation of oxygen-based reactive compounds may alter the redox status of the cell and lead to programmed cell death, in processes referred to as oxidative stress, or nitrosative stress (for nitrogen-based molecules). Here, an overview of the main oxygen-based molecules involved, and the ramifications of their production, is given.

Heart rate as a determinant of L-type Ca2+ channel activity: Mechanisms and implication in force-frequency relation

1998 ◽  
Vol 93 (S1) ◽  
pp. s051-s059 ◽  
Author(s):  
S. Lemaire ◽  
C. Piot ◽  
F. Leclercq ◽  
V. Leuranguer ◽  
J. Nargeot ◽  
...  
Keyword(s):  
Heart Rate ◽  
Force Frequency ◽  
Channel Activity ◽  
Frequency Relation

Preeclampsia and calcium adenosine triphosphatase activity of red blood cell ghosts

1994 ◽  
Vol 171 (5) ◽  
pp. 1361-1365 ◽  
Author(s):  
Gianfranco Nardulli ◽  
Fulgencio Proverbio ◽  
Flor G. Limongi ◽  
Reinaldo Marín ◽  
Teresa Proverbio
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Adenosine Triphosphatase ◽  
Adenosine Triphosphatase Activity ◽  
Calcium Adenosine Triphosphatase

scholarly journals The role of oxidative and nitrosative stress in the pathology of osteoarthritis: Novel candidate biomarkers for quantification of degenerative changes in the knee joint

2018 ◽  
Vol 10 (2) ◽  
Author(s):  
Alexander Franz ◽  
Laura Joseph ◽  
Constantin Mayer ◽  
Jan-Frieder Harmsen ◽  
Holger Schrumpf ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Synovial Fluid ◽  
Knee Joint ◽  
Human Serum ◽  
Synovial Membrane ◽  
Nitrosative Stress ◽  
Control Groups ◽  
Oxidative And Nitrosative Stress ◽  
And Oxidative Stress

Osteoarthritis (OA) is the most frequently diagnosed joint disorder worldwide with increasing prevalence and crucial impact on the quality of life of affected patients through chronic pain, decreasing mobility and invalidity. Although some risk factors, such as age, obesity and previous joint injury are well established, the exact pathogenesis of OA on a cellular and molecular level remains less understood. Today, the role of nitrosative and oxidative stress has not been investigated conclusively in the pathogenesis of OA yet. Therefore, the objective of this study was to identify biological substances for oxidative and nitrosative stress, which mirror the degenerative processes in an osteoarthritic joint. 69 patients suffering from a diagnosed knee pain participated in this study. Based on the orthopedic diagnosis, patients were classified into an osteoarthritis group (OAG, n=24) or in one of two control groups (meniscopathy, CG1, n=11; anterior cruciate ligament rupture, CG2, n=34). Independently from the study protocol, all patients underwent an invasive surgical intervention which was used to collect samples from the synovial membrane, synovial fluid and human serum. Synovial biopsies were analyzed histopathologically for synovitis (Krenn-Score) and immunohistochemically for detection of end products of oxidative (8-isoprostane F2α) and nitrosative (3-nitrotyrosine) stress. Additionally, the fluid samples were analyzed for 8-isoprostane F2α and 3-nitrotyrosine by competitive ELISA method. The analyzation of inflammation in synovial biopsies revealed a slight synovitis in all three investigated groups. Detectable concentrations of 3-nitrotyrosine were reported in all three investigated groups without showing any significant differences between the synovial biopsies, fluid or human serum. In contrast, significant increased concentrations of 8-isoprostane F2α were detected in OAG compared to both control groups. Furthermore, our data showed a significant correlation between the histopathological synovitis and oxidative stress in OAG (r=0.728, P<0.01). There were no significant differences between the concentrations of 8-isoprostane F2α in synovial fluid and human serum. The findings of the current study support the hypothesis that oxidative and nitrosative stress are components of the multi-factory pathophysiological formation of OA. It seems reasonable that an inflammatory process in the synovial membrane triggers the generation of oxidative and nitrosative acting substances which can lead to a further degradation of the articular cartilage. Based on correlations between the observed degree of inflammation and investigated biomarkers, especially 8-isoprostane F2α seems to be a novel candidate biomarker for OA. However, due to the finding that also both control groups showed increased concentrations of selected biomarkers, future studies have to validate the diagnostic potential of these biomarkers in OA and in related conditions of the knee joint.

scholarly journals Dynamic control of maximal ventricular elastance via the baroreflex and force-frequency relation in awake dogs before and after pacing-induced heart failure

2010 ◽  
Vol 299 (1) ◽  
pp. H62-H69 ◽  
Author(s):  
Xiaoxiao Chen ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Masashi Ichinose ◽  
Soroor Soltani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transfer Function ◽  
Transfer Functions ◽  
Dynamic Properties ◽  
System Response ◽  
Force Frequency ◽  
Arterial Baroreflex ◽  
Ventricular Elastance ◽  
Arterial Blood ◽  
Frequency Relation

We investigated to what extent maximal ventricular elastance ( Emax) is dynamically controlled by the arterial baroreflex and force-frequency relation in conscious dogs and to what extent these mechanisms are attenuated after the induction of heart failure (HF). We mathematically analyzed spontaneous beat-to-beat hemodynamic variability. First, we estimated Emax for each beat during a baseline period using the ventricular unstressed volume determined with the traditional multiple beat method during vena cava occlusion. We then jointly identified the transfer functions (system gain value and time delay per frequency) relating beat-to-beat fluctuations in arterial blood pressure (ABP) to Emax (ABP→ Emax) and beat-to-beat fluctuations in heart rate (HR) to Emax (HR→ Emax) to characterize the dynamic properties of the arterial baroreflex and force-frequency relation, respectively. During the control condition, the ABP→ Emax transfer function revealed that ABP perturbations caused opposite direction Emax changes with a gain value of −0.023 ± 0.012 ml−1, whereas the HR→ Emax transfer function indicated that HR alterations caused same direction Emax changes with a gain value of 0.013 ± 0.005 mmHg·ml−1·(beats/min)−1. Both transfer functions behaved as low-pass filters. However, the ABP→ Emax transfer function was more sluggish than the HR→ Emax transfer function with overall time constants (indicator of full system response time to a sudden input change) of 11.2 ± 2.8 and 1.7 ± 0.5 s ( P < 0.05), respectively. During the HF condition, the ABP→ Emax and HR→ Emax transfer functions were markedly depressed with gain values reduced to −0.0002 ± 0.007 ml−1 and −0.001 ± 0.004 mmHg·ml−1·(beats/min)−1 ( P < 0.1). Emax is rapidly and significantly controlled at rest, but this modulation is virtually abolished in HF.

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