scholarly journals The Negative Chronotropic Effect in Rat Heart Stimulated by Ultrasonic Pulses: Role of Sex and Age

2017 ◽  
Vol 36 (4) ◽  
pp. 799-808 ◽  
Author(s):  
Olivia C. Coiado ◽  
William D. O'Brien
2013 ◽  
Vol 12 (5) ◽  
pp. 81-86
Author(s):  
M. G. Glezer ◽  
E. I. Astashkin ◽  
I. N. Sokolova

The study aim was to assess the importance of adequate administration of medications with negative chronotropic effect in the improvement of clinical course and prognosis among patients with coronary heart disease (CHD) and heart failure. The possibility and appropriateness of combination therapy with β-adrenoblockers (β-AB) and an If channel blocker ivabradine is justified. The authors analyse current real-world trends in the administration and dose titration of these medications among ambulatory Russian patients. Russian doctors need to be more active in the treatment of patients with CHD and heart failure and better understand the need for and benefits of dose titration of medications with negative chronotropic effect, as well as the importance of combination therapy for the improvement of clinical course, prognosis, and quality of life. 


2005 ◽  
Vol 288 (3) ◽  
pp. R651-R655 ◽  
Author(s):  
Jiang Xu ◽  
William Kussmaul ◽  
Peter B. Kurnik ◽  
Mohamad Al-Ahdav ◽  
Amir Pelleg

The mechanism of extracellular ATP-triggered vagal depressor reflex was further studied in a closed-chest canine model. Adenosine and ATP were administered individually in equimolar doses (0.01–1.0 μmol/kg) into the right coronary artery (RCA) and left circumflex coronary artery (LCA). When administered into the RCA, adenosine and ATP exerted an identical and relatively small negative chronotropic effect on sinus node automaticity; the time to peak negative chronotropic effect was ≥7 s. When administered into the LCA, adenosine had no effect on sinus node automaticity, whereas ATP markedly suppressed sinus node automaticity. This effect of ATP 1) reached its peak in <2 s after its administration, 2) was short lasting, and 3) was completely abolished by either intravenous administration of the muscarinic cholinergic blocker atropine (0.2 mg/kg) or intra-LCA administration of 2′,3′- O-(2,4,6 -trinitrophenyl)-ATP (TNP-ATP), a potent P2X2/3 purinergic receptor (P2X2/3R) antagonist, but not by diinosine pentaphosphate (Ip5I), a potent inhibitor of P2X1R and P2X3R. Repetitive administrations of ATP were not associated with reduced effects, indicative of receptor desensitization, thereby excluding the involvement of the rapidly desensitized P2X1R in the action of ATP. It was concluded that ATP triggers a cardio-cardiac vagal depressor reflex by activating P2X2/3R located on vagal sensory nerve terminals localized in the left ventricle. Because these terminals mediate vasovagal syncope, these data could suggest a mechanistic role of extracellular ATP in this syndrome and, in addition, give further support to the hypothesis that endogenous ATP released from ischemic myocytes is a mediator of atropine-sensitive bradyarrhythmias associated with left ventricular myocardial infarction.


Pharmacology ◽  
1979 ◽  
Vol 19 (4) ◽  
pp. 202-208 ◽  
Author(s):  
David Hillis ◽  
Shukri F. Khun ◽  
Eugene Braunwald ◽  
Peter R. Maroko

2001 ◽  
Vol 537 (2) ◽  
pp. 467-488 ◽  
Author(s):  
Kageyoshi Ono ◽  
Haruko Masumiya ◽  
Aiji Sakamoto ◽  
Georges Christé ◽  
Toshinori Shijuku ◽  
...  

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