Effects of the SOD mimetic, M40403, on prostaglandin production in an in vivo model of ischemia and reperfusion in rat heart

2003 ◽  
Vol 52 (0) ◽  
pp. s23-s24 ◽  
Author(s):  
C. Marzocca ◽  
A. Vannacci ◽  
S. Cuzzocrea ◽  
D. Salvemini ◽  
P. F. Mannaioni ◽  
...  
Keyword(s):  
Rat Heart ◽  
In Vivo Model ◽  
Ischemia And Reperfusion ◽  
Prostaglandin Production

scholarly journals Functional cardiac orexin receptors: role of orexin-B/orexin 2 receptor in myocardial protection

2018 ◽  
Vol 132 (24) ◽  
pp. 2547-2564 ◽  
Author(s):  
Vanlata H. Patel ◽  
Emmanouil Karteris ◽  
Jing Chen ◽  
Ioannis Kyrou ◽  
Harman S. Mattu ◽  
...  
Keyword(s):  
Rat Heart ◽  
Troponin I ◽  
Clinical Symptoms ◽  
Human Subjects ◽  
Heart Association ◽  
Significant Negative Correlation ◽  
In Vivo Model ◽  
Rat Cardiomyocytes ◽  
Orexin Receptors

Orexins/hypocretins exert cardiovascular effects which are centrally mediated. In the present study, we tested whether orexins and their receptors may also act in an autocrine/paracrine manner in the heart exerting direct effects. Quantitative reverse transcription-PCR (RT-PCR), immunohistochemical and Western blot analyses revealed that the rat heart expresses orexins and orexin receptors (OXR). In isolated rat cardiomyocytes, only orexin-B (OR-B) caused an increase in contractile shortening, independent of diastolic or systolic calcium levels. A specific orexin receptor-2 (OX2R) agonist ([Ala11, d-Leu15]-Orexin B) exerted similar effects as OR-B, whereas a specific orexin receptor-1 (OX1R) antagonist (SB-408124) did not alter the responsiveness of OR-B. Treatment of the same model with OR-B resulted in a dose-dependent increase in myosin light chain and troponin-I (TnI) phosphorylation. Following ischaemia/reperfusion in the isolated Langendorff perfused rat heart model, OR-B, but not OR-A, exerts a cardioprotective effect; mirrored in an in vivo model as well. Unlike OR-A, OR-B was also able to induce extracellular signal-regulated kinase (ERK) 1/2 (ERK1/2) and Akt phosphorylation in rat myocardial tissue and ERK1/2 phosphorylation in human heart samples. These findings were further corroborated in an in vivo rat model. In human subjects with heart failure, there is a significant negative correlation between the expression of OX2R and the severity of the disease clinical symptoms, as assessed by the New York Heart Association (NYHA) functional classification. Collectively, we provide evidence of a distinct orexin system in the heart that exerts a cardioprotective role via an OR-B/OX2R pathway.

scholarly journals Resistance of Optogenetically Evoked Motor Function to Global Ischemia and Reperfusion in Mouse in Vivo

2013 ◽  
Vol 33 (8) ◽  
pp. 1148-1152 ◽  
Author(s):  
Yicheng Xie ◽  
Shangbin Chen ◽  
Eitan Anenberg ◽  
Timothy H Murphy
Keyword(s):  
Sensory Processing ◽  
Muscle Activity ◽  
Motor Output ◽  
Global Ischemia ◽  
Differential Sensitivity ◽  
In Vivo Model ◽  
Ischemia And Reperfusion ◽  
Motor Systems ◽  
Minute Period

Recently we have shown that despite reperfusion, sensory processing exhibits persistent deficits after global ischemia in a mouse in vivo model. We now address how motor output, specifically cortically evoked muscle activity, stimulated by channelrhodopsin-2 is affected by global ischemia and reperfusion. We find that the light-based optogenetic motor map recovers to 80% within an hour. Moreover, motor output recovers relatively faster and more completely than the sensory processing after 5-minute period of global ischemia. Our results suggest a differential sensitivity of sensory and motor systems to the effects of global ischemia and reperfusion that may have implications for rehabilitation.

Postconditioning fails to prevent radial artery endothelial dysfunction induced by ischemia and reperfusion: evidence from a human in vivo study

2006 ◽  
Vol 84 (6) ◽  
pp. 611-615 ◽  
Author(s):  
Saverio Dragoni ◽  
Giuseppe Di Stolfo ◽  
Silvia Sicuro ◽  
Monica Lisi ◽  
John D. Parker ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Radial Artery ◽  
Tissue Damage ◽  
Animal Studies ◽  
In Vivo Model ◽  
Ischemia And Reperfusion ◽  
Ischemic Tissue ◽  
Before And After ◽  
Dependent Flow

Animal studies have shown that, as compared with unrestricted reperfusion, exposure to brief periods of controlled ischemia (postconditioning) at the end of a prolonged ischemia reduces the extent of tissue damage. We set out to test whether postconditioning can prevent endothelial dysfunction induced by ischemia and reperfusion in a human in vivo model. Ten healthy young non-smoking volunteers were enrolled in this cross-over, controlled, investigator-blinded study. Subjects were exposed to 15 min of forearm ischemia followed by either unrestricted reperfusion or postconditioning (3 periods of 20 s of ischemia separated by 10 s of reperfusion). Endothelium-dependent flow-mediated dilation (FMD) was measured at the level of the radial artery before and after ischemia (with or without postconditioning). Forearm ischemia blunted FMD in both study visits (unrestricted reperfusion visit: before ischemia, 7.7% ± 1.3%; after ischemia, 2.5% ± 1.4%; and postconditioning visit: before, 7.3% ± 1.2%; after, 2.6 ± 1.6%; P < 0.05 for both, P = not significant (NS) between visits). In contrast with data from animal studies, postconditioning (20 s ischemia – 10 s reperfusion repeated 3 times) does not limit post-ischemic endothelial dysfunction in this human in vivo model. Further human studies are necessary to evaluate other reperfusion protocols in an attempt to limit post-ischemic tissue damage.

Establishment of an in vivo model for KCNJ5 dependent hyperaldosteronism

2015 ◽  
Vol 122 (03) ◽  
Author(s):  
U Lichtenauer ◽  
PL Schmid ◽  
A Oßwald ◽  
I Renner-Müller ◽  
M Reincke ◽  
...  
Keyword(s):  
In Vivo Model
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