scholarly journals Chemical Ablation Of Purkinje Fibers Diminishes Spontaneous Activity In A Rat Model Of Regional Ischemia And Reperfusion

2009 ◽  
Vol 96 (3) ◽  
pp. 258a-259a
Author(s):  
Matthew W. Kay ◽  
Luther M. Swift ◽  
Huda Asfour ◽  
Craig Forleiter ◽  
Marco A. Mercader ◽  
...  
2006 ◽  
Vol 84 (8-9) ◽  
pp. 903-912 ◽  
Author(s):  
Sarah J. Canyon ◽  
Geoffrey P. Dobson

We have previously shown that an intravenous infusion of adenosine and lidocaine (AL) solution protects against death and severe arrhythmias and reduces infarct size in the in vivo rat model of regional ischemia. The aim of this study was to examine the relative changes of myocardial high-energy phosphates (ATP and PCr) and pH in the left ventricle during ischemia–reperfusion using 31P NMR in AL-treated rats (n = 7) and controls (n = 6). The AL solution (A: 305 μg·(kg body mass)–1·min–1; L: 608 μg·(kg body mass)–1·min–1) was administered intravenously 5 min before and during 30 min coronary artery ligation. Two controls died from ventricular fibrillation; no deaths were recorded in AL-treated rats. In controls that survived, ATP fell to 73% ± 29% of baseline by 30 min ischemia and decreased further to 68% ± 28% during reperfusion followed by a sharp recovery at the end of the reperfusion period. AL-treated rats maintained relatively constant ATP throughout ischemia and reperfusion ranging from 95% ± 6% to 121% ± 10% of baseline. Owing to increased variability in controls, these results were not found to be significant. In contrast, control [PCr] was significantly reduced in controls compared with AL-treated rats during ischemia at 10 min (68% ± 7% vs. 99% ± 6%), at 15 min (68% ± 10% vs. 93% ± 2%), and at 20 min (67% ± 15% vs. 103% ± 5%) and during reperfusion at 10 min (56% ± 22% vs. 99% ± 7%), at 15 min (60% ± 10% vs. 98% ± 7%), and at 35 min (63% ± 14% vs. 120% ± 11%) (p < 0.05). Interestingly, changes in intramyocardial pH between each group were not significantly different during ischemia and fell by about 1 pH unit to 6.6. During reperfusion, pH in AL-treated rats recovered to baseline in 5 min but not in controls, which recovered to only around pH 7.1. There was no significant difference in the heart rate, mean arterial pressure, and rate-pressure product between the controls and AL treatment during ischemia and reperfusion. We conclude that AL cardioprotection appears to be associated with the preservation of myocardial high-energy phosphates, downregulation of the heart at the expense of a high acid-load during ischemia, and with a rapid recovery of myocardial pH during reperfusion.


2006 ◽  
Author(s):  
Rajesh N. Raman ◽  
Christopher D. Pivetti ◽  
Dennis L. Matthews ◽  
Christoph Troppmann ◽  
Stavros G. Demos

Surgery ◽  
2007 ◽  
Vol 142 (5) ◽  
pp. 722-733 ◽  
Author(s):  
Niubel Diaz Padilla ◽  
Arlène K. van Vliet ◽  
Ivo G. Schoots ◽  
Mercedes Valls Seron ◽  
M. Adrie Maas ◽  
...  

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Iyad M Ayoub ◽  
Jeejabai Radhakrishnan ◽  
Raúl J Gazmuri

Objective: We have previously reported in a rat model of VF and closed-chest resuscitation that cytochrome c is released into the bloodstream after resuscitation from cardiac arrest attaining plasma levels inversely proportional to survival. Recent evidence indicates that release of cytochrome c during ischemia and reperfusion may be a manifestation of prolonged opening of the mitochondrial permeability transition pore (mPTP). In this study, we investigated whether cyclosporin A (CsA, an inhibitor of mPTP opening) can prevent post-resuscitation (PR) myocardial dysfunction and improve survival. Methods: VF was electrically induced and left untreated for 10 mins. Resuscitation was attempted by 8 mins of chest compression followed by biphasic waveform defibrillation. Rats were randomized to received a bolus CsA (10 mg/kg) five minutes before inducing VF (n=6), immediately before starting chest compression (n=6), or to receive vehicle control before inducing VF (n=3) or before starting chest compression (n=3). CsA-treated (n=12) and vehicle-treated (n=6) rats were pooled for this analysis after noticing no differences between subgroups. Resuscitated rats were monitored for up to 6 hours. Results: All rats were successfully resuscitated. Treatment with CsA did not improve PR myocardial function (Table ). Survival time was comparable between CsA-treated (321±67 mins) and vehicle-treated (331±67 mins) rats. Conclusions: In our rat model of VF and resuscitation, CsA failed to prevent PR myocardial dysfunction and improve survival. These data contrast with numerous studies demonstrating a protective effect in isolated heart models of ischemia and reperfusion. Two possible explanations are the mPTP does not open in this unique setting of cardiac arrest and resuscitation, and the optimal in vivo dose of CsA needs to be determined as the protective effects of CsA are dose dependent. Hemodynamic and Left Ventricular Function


2020 ◽  
Vol 52 (6) ◽  
pp. 1880-1883
Author(s):  
Kengo Shibata ◽  
Takahiro Hayasaka ◽  
Satsuki Hashimoto ◽  
Kohei Umemoto ◽  
Takahisa Ishikawa ◽  
...  

2019 ◽  
Vol 15 (6) ◽  
pp. 1582-1588 ◽  
Author(s):  
Mustafa Sayhan ◽  
Serhat Oguz ◽  
Ömer Salt ◽  
Nuray Can ◽  
Taner Ozgurtas ◽  
...  

2020 ◽  
Vol 143 (1) ◽  
pp. 9-16
Author(s):  
Adchara Janyou ◽  
Piyawadee Wicha ◽  
Vatcharee Seechamnanturakit ◽  
Kanokkan Bumroongkit ◽  
Chainarong Tocharus ◽  
...  

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