Effects of antiarrhythmic drugs on the extraneuronal accumulation of isoprenaline in perfused rat hearts

1986 ◽  
Vol 334 (2) ◽  
pp. 145-148 ◽  
Author(s):  
Kazumi Sono ◽  
Yoshinobu Akimoto ◽  
Kazuyoshi Kurahashi ◽  
Motohatsu Fujiwara
Keyword(s):  
Antiarrhythmic Drugs ◽  
Rat Hearts ◽  
Perfused Rat Hearts

scholarly journals Effects of antiarrhythmic drugs on the extraneuronal accumulation of isoprenaline in perfused rat hearts.

1985 ◽  
Vol 39 ◽  
pp. 141
Author(s):  
Kazumi Sono ◽  
Yoshinobu Akimoto ◽  
Kazuyoshi Kurahashi ◽  
Motohatsu Fujiwara
Keyword(s):  
Antiarrhythmic Drugs ◽  
Rat Hearts ◽  
Perfused Rat Hearts

Translocation of G-Protein β3 subunit from the cytosol pool to the membrane pool by β1-Adrenergic receptor stimulation in perfused rat hearts

1999 ◽  
Vol 58 (9) ◽  
pp. 1497-1500 ◽  
Author(s):  
Ken Kageyama ◽  
Takeshi Murakami ◽  
Kenji Iizuka ◽  
Kumi Sato ◽  
Kazuo Ichihara ◽  
...  
Keyword(s):  
G Protein ◽  
Adrenergic Receptor ◽  
Receptor Stimulation ◽  
Rat Hearts ◽  
Perfused Rat Hearts

Tm(DOTP)5−: A23Na+ shift agent for perfused rat hearts

1990 ◽  
Vol 15 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Douglas C. Buster ◽  
M. Margarida C. A. Castro ◽  
Carlos F. G. C. Geraldes ◽  
Craig R. Malloy ◽  
A. Dean Sherry ◽  
...  
Keyword(s):  
Rat Hearts ◽  
Perfused Rat Hearts

scholarly journals Activity of phosphorylase in total global ischaemia in the rat heart A phosphorus-31 nuclear-magnetic-resonance study

1981 ◽  
Vol 196 (1) ◽  
pp. 171-178 ◽  
Author(s):  
I A Bailey ◽  
S R Williams ◽  
G K Radda ◽  
D G Gadian
Keyword(s):  
Inhibitory Effect ◽  
Heart Tissue ◽  
Nuclear Magnetic Resonance Study ◽  
Cytosolic Ph ◽  
Global Ischaemia ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Tissue Acidosis ◽  
Good Agreement

1. The uptake and subsequent phosphorylation of deoxyglucose into perfused rat hearts was monitored by 31P n.m.r. 2. The accumulated deoxyglucose 6-phosphate provided (a) an independent method for measuring cytosolic pH in the normoxic and ischaemic heart tissue and (b) a way of studying the activity of phosphorylase during ischaemia. 3. The cytosolic pH measured from the 31P n.m.r. resonance position of deoxyglucose 6-phosphate is in good agreement under all conditions studied with that obtained previously from the Pi resonances. This eliminates any possible doubts about the use of Pi for measuring intracellular pH. 4. Deoxyglucose 6-phosphate in vitro inhibits phosphorylase b but not phosphorylase a. Its inhibitory effect on glycogenolysis during ischaemia is monitored by measuring tissue acidosis by n.m.r. In the initial stages of ischaemia phosphorylase activity is not inhibited, whereas after about 5 min approx. 50% of the activity is inhibited. These observations are interpreted in terms of the relative contributions of phosphorylase a and the AMP-dependent phosphorylase b activities during ischaemia.

Fasudil prevents KATP channel-induced improvement in postischemic functional recovery

2005 ◽  
Vol 288 (6) ◽  
pp. H3011-H3015 ◽  
Author(s):  
Kenya Nishizawa ◽  
Paul E. Wolkowicz ◽  
Tadashi Yamagishi ◽  
Ling-Ling Guo ◽  
Martin M. Pike
Keyword(s):  
Diastolic Pressure ◽  
Rho Kinase ◽  
High Energy ◽  
Left Ventricular ◽  
High Energy Phosphate ◽  
Cellular Processes ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Rock Activity ◽  
Mechanical Recovery

Whereas activation of ATP-dependent potassium (KATP) channels greatly improves postischemic myocardial recovery, the final effector mechanism for KATP channel-induced cardioprotection remains elusive. RhoA is a GTPase that regulates a variety of cellular processes known to be involved with KATP channel cardioprotection. Our goal was to determine whether the activity of a key rhoA effector, rho kinase (ROCK), is required for KATP channel-induced cardioprotection. Four groups of perfused rat hearts were subjected to 36 min of zero-flow ischemia and 44 min of reperfusion with continuous measurements of mechanical function and 31P NMR high-energy phosphate data: 1) untreated, 2) pinacidil (10 μM) to activate KATP channels, 3) fasudil (15 μM) to inhibit ROCK, and 4) both fasudil and pinacidil. Pinacidil significantly improved postischemic mechanical recovery [39 ± 16 vs. 108 ± 4 mmHg left ventricular diastolic pressure (LVDP), untreated and pinacidil, respectively]. Fasudil did not affect reperfusion LVDP (41 ± 13 mmHg) but completely blocked the marked improvement in mechanical recovery that occurred with pinacidil treatment (54 ± 15 mmHg). Substantial attenuation of the postischemic energetic recovery was also observed. These data support the hypothesis that ROCK activity plays a role in KATP channel-induced cardioprotection.

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