scholarly journals Effects of CoQ10 on the erythrocyte and heart tissue cholinesterase, nitric oxide and malondialdehyde levels in acute organophosphate toxicity

Critical Care ◽  
2011 ◽  
Vol 15 (S1) ◽  
Author(s):  
A Bayır ◽  
H Kara ◽  
Ö Köylü ◽  
R Kocabaş ◽  
A Ak
Keyword(s):  
Nitric Oxide ◽  
Heart Tissue ◽  
Organophosphate Toxicity

Impaired cardiovascular function in male rats with hypo- and hyperthyroidism: Involvement of imbalanced nitric oxide synthase levels

2020 ◽  
Vol 20 ◽  
Author(s):  
Nasibeh Yousefzadeh ◽  
Sajad Jeddi ◽  
Asghar Ghasemi
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Left Ventricular Pressure ◽  
Cardiovascular Function ◽  
Heart Tissue ◽  
Left Ventricular ◽  
Male Rats ◽  
Protein Levels

Background and Objective: All three isoforms of nitric oxide (NO) synthase (NOS) are targets for thyroid hormones in cardiovascular system. The aim of this study was to assess effects of hypoand hyperthyroidism on inducible (iNOS), endothelial (eNOS), and neural (nNOS) NOS levels in aorta and heart tissues of male rats. Methods: Rats were divided into control, hypothyroid, and hyperthyroid groups; hypo- and hyperthyroidism were induced by adding propylthiouracil (500 mg/L) and L-thyroxine (12 mg/L) to drinking water for a period of 21 days, respectively. At day 21, systolic blood pressure, heart rate, left ventricular developed pressure (LVDP), peak rate of positive and negative (±dp/dt) changes in left ventricular pressure as well as NO metabolites (NOx) and iNOS, eNOS, and nNOS protein levels in aorta and heart were measured. Results: Compared to controls, LVDP and ±dp/dt were lower in both hypo- and hyperthyroid rats. Compared to controls, heart rate and systolic blood pressure were lower in hypothyroid and higher in hyperthyroid rats. NOx levels in the heart of hypothyroid rats were lower (53%) whereas in the heart and aorta of hyperthyroid rats were higher (56% and 40%) than controls. Compared to controls, hypothyroid rats had lower levels of eNOS, iNOS, and nNOS in aorta (16%, 34%, and 15%, respectively) and lower iNOS and higher nNOS in heart tissue (27% and 46%). In hyperthyroid rats, eNOS levels were lower (54% and 30%) and iNOS were higher (63%, and 35%) in the aorta and heart while nNOS was lower in the aorta (18%). Conclusion: Hypothyroidism increased while hyperthyroidism decreased ratio of eNOS/iNOS in aorta and heart; these changes of NOS levels were associated with impaired cardiovascular function.

Opening of Ca2+-activated K+ channels triggers early and delayed preconditioning against I/R injury independent of NOS in mice

2004 ◽  
Vol 287 (5) ◽  
pp. H2070-H2077 ◽  
Author(s):  
Xiaoyin Wang ◽  
Chang Yin ◽  
Lei Xi ◽  
Rakesh C. Kukreja
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Western Blot ◽  
Channel Blocker ◽  
Treated Group ◽  
Heart Tissue ◽  
Mouse Heart ◽  
K Channels ◽  
Nos Inhibitor ◽  
Delayed Cardioprotection

Opening of Ca2+-activated K+ (KCa) channels has been shown to confer early cardioprotection. It is unknown whether the opening of these channels also induces delayed cardioprotection. In addition, we determined the involvement of nitric oxide synthases (NOSs), which have been implicated in cardioprotection induced by opening of mitochondrial ATP-sensitive K+ (KATP) channels. Adult male ICR mice were pretreated with the KCa-channel opener NS-1619 either 10 min or 24 h before 30 min of global ischemia and 60 min of reperfusion (I/R) in Langendorff mode. Infusion of NS-1619 (10 μM) for 10 min before I/R led to smaller infarct sizes as compared with the vehicle (DMSO)-treated group ( P < 0.05). This infarct-limiting effect of NS-1619 was associated with improvement in ventricular functional recovery after I/R. The NS-1619-induced protection was abolished by coadministration with the KCa-channel blocker paxilline (1 μM). Similarly, pretreatment with NS-1619 (1 mg/kg ip) induced delayed protection 24 h later ( P < 0.05). Interestingly, the NS-1619-induced late protection was not blocked by the NOS inhibitor Nω-nitro-l-arginine methyl ester (15 mg/kg ip). Unlike diazoxide (the opener of mitochondrial KATP channels), NS-1619 did not increase the expression of inducible or endothelial NOS. Western blot analysis demonstrated the existence of α- and β-subunits of KCa channels in mouse heart tissue. We conclude that opening of KCa channels leads to both early and delayed preconditioning effects through a mechanism that is independent of nitric oxide.

scholarly journals Inducible Nitric Oxide Synthase in Heart Tissue and Nitric Oxide in Serum of Trypanosoma cruzi-Infected Rhesus Monkeys: Association with Heart Injury

2012 ◽  
Vol 6 (5) ◽  
pp. e1644 ◽  
Author(s):  
Cristiano Marcelo Espinola Carvalho ◽  
Jaline Coutinho Silverio ◽  
Andrea Alice da Silva ◽  
Isabela Resende Pereira ◽  
Janice Mery Chicarino Coelho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Trypanosoma Cruzi ◽  
Inducible Nitric Oxide Synthase ◽  
Rhesus Monkeys ◽  
Heart Tissue ◽  
Heart Injury ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Light and Electron Microscopic localization of inducible nitric oxide synthase in the heart of rats with myocarditis

1995 ◽  
Vol 53 ◽  
pp. 708-709
Author(s):  
T. Nishikawa ◽  
S. Ishiyama ◽  
K. Takeda ◽  
T. Shimojo ◽  
M. Hiroe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Tissue Injury ◽  
Cell Damage ◽  
Acute Myocarditis ◽  
Inflammatory Cells ◽  
Heart Tissue ◽  
Electron Microscopic ◽  
Autoimmune Myocarditis ◽  
Oxide Synthase

Nitric oxide synthase (NOS) is an enzyme involved in the synthesis of nitric oxide (NO). The inducible form of NOS (iNOS) is induced in the presence of cytokines and produces massive amounts of NO which may be harmful to living tissue. In acute myocarditis, a serious disease which can be fatal, extensive myocardial cell damage associated with massive inflammatory cell infiltration is usually observed and large amounts of cytokines are released from inflammatory cells. However, the mechanism of the heart tissue injury is still unclear. In this study, we investigated the role of iNOS in the myocardial tissue injury in acute myocarditis.The heart tissue specimens were taken from Lewis rats with experimentally induced autoimmune myocarditis. An immunohistochemical study was performed using iNOS antibody raised in New Zealand white rabbits immunized with synthetic peptides (17 amino acids) corresponding to the C-terminal of macrophage iNOS. The specificity of the antibody was confirmed by Western blot analysis. Immunoelectron microscopic studies were carried out by the gold-labeled IgG method using ultrathin sections of LR white resin-embedded material.

The Role of Superoxide and Nitric Oxide in the Development of Myocardial Injury in Rat Myocarditis.

2000 ◽  
Vol 6 (S2) ◽  
pp. 488-489
Author(s):  
T. Nishikawa ◽  
S. Ishiyama ◽  
A. Suzuki ◽  
A. Masuda ◽  
T. Kasajima
Keyword(s):  
Nitric Oxide ◽  
Myocardial Injury ◽  
Histochemical Study ◽  
Myocardial Damage ◽  
Heart Tissue ◽  
Complex Method ◽  
Paraffin Sections ◽  
Tissue Specimens ◽  
The Relationship

The mechanism of myocardial injury in myocarditis is still unclear. Recently, nitric oxide (NO), massively produced in the inflammation, has been suggested to be harmful for tissue at excess amount as well as superoxide. However, it is still unclear the relationship between production of NO with superoxide and myocardial damage in myocarditis. In this study, we investigated whether NO and/or superoxide play an important role in the pathogenesis of myocardial injury in myocarditis.The heart tissue specimens were taken from Lewis rats with experimentally induced myocarditis. Immunohistochemical staining was performed using polyclonal antibody for inducible NO synthase by avidin-biotin peroxidase complex method in paraffin sections of the tissue. Histochemical study for ultrastructural H2O2-producing site in the heart tissue was carried out by Brigg’ s method using CeCl3; briefly, the heart tissues were incubated in 0.1M Tris-malate buffer with ImM CeCl3 and 10mM aminotriazole. Then tissues were fixed in 2% glutaraldehyde, postfixed with 1% OsO4 and embedded in resin for electron microscopy.

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