scholarly journals GW27-e0155 Effects of hydrogen sulfide on inflammatory factors in acute myocardial ischemia injury in rats

2016 ◽  
Vol 68 (16) ◽  
pp. C54
Author(s):  
Zhang Jianxin
Keyword(s):  
Hydrogen Sulfide ◽  
Myocardial Ischemia ◽  
Acute Myocardial Ischemia ◽  
Inflammatory Factors

scholarly journals Electroacupuncture Ameliorates Acute Myocardial Ischemia: A Potential Role of the Locus Coeruleus

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Xin Wu ◽  
Kun Wang ◽  
Shuai Cui ◽  
Shengbing Wu ◽  
Guoqi Zhu ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Locus Coeruleus ◽  
Serum Levels ◽  
Acute Myocardial Ischemia ◽  
Inflammatory Factors ◽  
Neuron Activity ◽  
Myocardial Tissue ◽  
Hs Crp

The locus coeruleus (LC) is closely linked with cardiovascular disease. However, whether it mediates the alleviating effect of electroacupuncture (EA) on acute myocardial ischemia (AMI) remains unclear. A rat model of myocardial ischemia was established through occlusion of the left anterior descending coronary artery. Multichannel in vivo recording and other techniques were used to assess neurons in the LC, norepinephrine (NE) and dopamine (DA) levels in central and myocardial tissue, serum levels of inflammatory factors, and cardiac function. After induction of AMI, LC neuron activity increased and the central NE concentrations increased, while those of DA decreased. Moreover, the serum levels of high-sensitivity C-reactive protein (hs-CRP) increased, whereas those of interleukin-10 (IL-10) decreased. However, these effects were reversed by EA. Additionally, LC lesioning affected NE and DA levels in myocardial tissue and weakened the antimyocardial ischemic effect of EA. Collectively, our results indicated that LC is closely related to AMI and plays an important role in the antimyocardial ischemic effect of EA. This mechanism may be related to inhibition of LC neuron activity by EA, which inhibits the release of large amounts of hs-CRP and promotes that of IL-10 in the serum. Besides, after LC lesioning, EA may improve cardiac function by inhibiting the release of large amounts of NE and promoting the release of DA in myocardial tissue.

scholarly journals Effect of hydrogen sulfide on inflammatory cytokines in acute myocardial ischemia injury in rats

2015 ◽  
Vol 9 (3) ◽  
pp. 1068-1074 ◽  
Author(s):  
FANG LIU ◽  
GUANG-JIE LIU ◽  
NA LIU ◽  
GANG ZHANG ◽  
JIAN-XIN ZHANG ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Myocardial Ischemia ◽  
Inflammatory Cytokines ◽  
Acute Myocardial Ischemia

scholarly journals Hydrogen Sulfide Alleviates Acute Myocardial Ischemia Injury by Modulating Autophagy and Inflammation Response under Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Ya-dan Bai ◽  
Yu-rong Yang ◽  
Xue-pan Mu ◽  
Ge Lin ◽  
You-ping Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Myocardial Ischemia ◽  
Cardiac Injury ◽  
Acute Myocardial Ischemia ◽  
Ischemic Myocardium ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Inflammation Response ◽  
Apoptosis And Inflammation

This study aims to investigate the influence of excessive oxidative stress on cardiac injury during acute myocardial ischemia (AMI), with a focus on apoptosis, autophagy, and inflammatory cell infiltration, and to detect the role of hydrogen sulfide (H2S) in this process. We found that SOD1 knockout (KO) mice showed excessive oxidative stress and exacerbated myocardium injury after AMI. Increased apoptosis and inflammation response in the ischemic myocardium contribute to this deterioration, whereas enhanced autophagy plays a protective role. Myocardial inflammation after AMI was much more severe in SOD1 KO mice than in wild-type mice. Pretreatment with the H2S donor NaHS reduced autophagy and apoptosis levels in the ischemic myocardium and alleviated the regional inflammation response in the cardiac tissues of SOD1 KO mice. Moreover, autophagy and apoptosis levels were significantly enhanced in SOD1 knockdown primary neonatal rat cardiomyocytes (NRCMs) under glucose deprivation. Pretreatment with NaHS can partially inhibit this elevation. Taken together, we found that excessive oxidative stress can aggravate cardiac injury during AMI. Exogenous H2S can alleviate cardiac injury during AMI by reducing apoptosis and inflammation response in heart tissues under oxidative stress.

Heparin from Intestine and Lung Source Administered in Large Dose to Dogs with Acute Myocardial Ischemia

1978 ◽  
Vol 40 (02) ◽  
pp. 407-417
Author(s):  
Michael J Saliba ◽  
Richard J Pavalec
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Adenosine Triphosphate ◽  
Intestinal Mucosa ◽  
Large Dose ◽  
Acute Myocardial Ischemia ◽  
Ischemic Myocardium ◽  
Atp Levels ◽  
Initial Control ◽  
The Difference

SummaryIntestinal mucosa heparin (IMH) and beef lung heparin (BLH) were infused into dogs subjected to myocardial ischemia by intermittent coronary artery occlusions. The IMH was from a mixture of beef, sheep, and pig intestinal mucosa. Initial control occlusion and recovery was followed by a second occlusion with 60,000 units of IMH or BLH added. Electrocardiographic S-T segment elevations (ST) were measured acutely. There were no significant differences in ST in non-ischemic myocardium before occlusions or with occlusions. In ischemic myocardium, IMH significantly lowered control ST 84% in amount (t = 6.1 p <0.00005), and 76% in number (t = 11.6 p <0.00001). BLH lowered control ST a significant, lesser, 36% in amount (t = 3.6 p <0.008), and 35% in number (t = 3.2 p <0.01). The difference between IMH and BLH in ischemic myocardium was a significant 48% in amount (t = 4.0 p <0.0007), and 41% in number (t = 2.0 p <0.06). Myocardial adenosine triphosphate (ATP) levels were assayed after 90 min. ATP levels were 31% higher in both ischemic and non-ischemic myocardium in IMH-treated dogs than in BLH- treated. It was concluded that IMH and BLH are functionally different, and IMH was significantly more effective.

In Vivo MRI Visualization of Acute Myocardial Ischemia and Reperfusion in Ferrets by the Persistent Action of the Contrast Agent Gd(BME-DTTA)

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3549-3559 ◽  
Author(s):  
Tamás Simor ◽  
Wen-Jang Chu ◽  
Lynne Johnson ◽  
Andras Safranko ◽  
Mark Doyle ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Contrast Agent ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

scholarly journals IP3R1 regulates Ca2+ transport and pyroptosis through the NLRP3/Caspase-1 pathway in myocardial ischemia/reperfusion injury

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Guixi Mo ◽  
Xin Liu ◽  
Yiyue Zhong ◽  
Jian Mo ◽  
Zhiyi Li ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Inflammatory Factors ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Caspase 1 ◽  
Intracellular Ca ◽  
Myocardial Ischemia Reperfusion

AbstractIntracellular ion channel inositol 1,4,5-triphosphate receptor (IP3R1) releases Ca2+ from endoplasmic reticulum. The disturbance of IP3R1 is related to several neurodegenerative diseases. This study investigated the mechanism of IP3R1 in myocardial ischemia/reperfusion (MI/R). After MI/R modeling, IP3R1 expression was silenced in myocardium of MI/R rats to explore its role in the concentration of myocardial enzymes, infarct area, Ca2+ level, NLRP3/Caspase-1, and pyroptosis markers and inflammatory factors. The adult rat cardiomyocytes were isolated and cultured to establish hypoxia/reperfusion (H/R) cell model. The expression of IP3R1 was downregulated or ERP44 was overexpressed in H/R-induced cells. Nifedipine D6 was added to H/R-induced cells to block Ca2+ channel or Nigericin was added to activate NLRP3. IP3R1 was highly expressed in myocardium of MI/R rats, and silencing IP3R1 alleviated MI/R injury, reduced Ca2+ overload, inflammation and pyroptosis in MI/R rats, and H/R-induced cells. The binding of ERP44 to IP3R1 inhibited Ca2+ overload, alleviated cardiomyocyte inflammation, and pyroptosis. The increase of intracellular Ca2+ level caused H/R-induced cardiomyocyte pyroptosis through the NLRP3/Caspase-1 pathway. Activation of NLRP3 pathway reversed the protection of IP3R1 inhibition/ERP44 overexpression/Nifedipine D6 on H/R-induced cells. Overall, ERP44 binding to IP3R1 inhibits Ca2+ overload, thus alleviating pyroptosis and MI/R injury.

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