Post–conditioning reduces infarct size in the isolated rat heart: Role of coronary flow and pressure and the nitric oxide/cGMP pathway

Transient (2 min) acidic (pH 6.6) reperfusion with low [HCO3-] solution suppresses reperfusion-induced ventricular fibrillation (VF) in the isolated rat heart. Using this preparation, we tested whether the effect was mediated by the high [H+] or the low [HCO3-] of perfusate. Left and right coronary beds were independently perfused with HCO3(-)-containing (25.0 mmol/l) solution at pH 7.4. Regional ischemia was then induced by stopping flow to the left coronary bed for 10 min. Hearts were subsequently assigned to four groups (n = 12 hearts/group), and the left coronary bed was reperfused with either HCO3(-)-containing (25.0 or 4.0 mmol/l) or HCO3(-)-free (5.0 mmol/l HEPES) solution, at pH 7.4 throughout (control reperfusion) or at pH 6.6 for the first 2 min and at pH 7.4 from 2 to 5 min (acidic reperfusion). Regardless of the buffer, controls exhibited a high (92 and 100%) incidence of VF; this was reduced to 42% in both of the acidic reperfusion groups (P < 0.05). There were no intergroup differences in heart rate, coronary flow, or size of ischemic zone. Thus high [H+], rather than low [HCO3-], appears to mediate the antifibrillatory effect of transient acidic reperfusion.

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ROLE OF SDF-1α/CXCR4 AXIS TO THE CARDIOPROTECTIVE EFFECT OF ISCHEMIC POST-CONDITIONING IN ISOLATED RAT HEART

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(13)60218-1 ◽

2013 ◽

Vol 61 (10) ◽

pp. E217

Author(s):

Jeong-Su Kim ◽

Ju-Hyun Park ◽

Kook-Jin Chun ◽

Young-Ho Jang ◽

June-Hong Kim ◽

...

Keyword(s):

Rat Heart ◽

Isolated Rat Heart ◽

Cardioprotective Effect ◽

Cxcr4 Axis ◽

Isolated Rat

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Species-dependent hemodynamic effects of adenosine A3-receptor agonists IB-MECA and Cl-IB-MECA

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.276.6.h2076 ◽

1999 ◽

Vol 276 (6) ◽

pp. H2076-H2084 ◽

Cited By ~ 9

Author(s):

Robert D. Lasley ◽

Prakash Narayan ◽

M. Salik Jahania ◽

Elizabeth L. Partin ◽

Kathleen R. Kraft ◽

...

Keyword(s):

Receptor Antagonist ◽

Rat Heart ◽

Coronary Flow ◽

Receptor Activation ◽

Isolated Rat Heart ◽

Pressure Effects ◽

Hemodynamic Effects ◽

Receptor Agonists ◽

Coronary Dilation ◽

Isolated Rat

The purpose of this study was to compare the hemodynamic effects of the adenosine A3-receptor agonists N 6-(3-iodobenzyl)-9-[5-(methylcarbamoyl)-β-d-ribofuranosyl]adenine (IB-MECA) and 2-chloro- N 6-(3-iodobenzyl)-9-[5-(methylcarbamoyl)-β-d-ribofuranosyl]adenine (Cl-IB-MECA) in isolated rat and rabbit hearts and in the intact, open-chest pig. Isolated hearts perfused with Krebs-Henseleit buffer at a constant pressure (70 mmHg) were treated with 50 nM of either IB-MECA or Cl-IB-MECA. Neither IB-MECA nor Cl-IB-MECA altered ventricular function or heart rate in the isolated rat and rabbit hearts, and neither agent altered coronary flow in the rabbit. However, 2 min of IB-MECA treatment in the isolated rat heart increased coronary flow by 25%, an effect that did not exhibit tachyphylaxis. The IB-MECA-induced coronary dilation was only partially attenuated by the adenosine A3-receptor antagonist MRS-1191 (50 nM). IB-MECA-induced coronary dilation was completely blocked by the adenosine A2a-receptor antagonist 7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (Sch-58261, 50 nM). Cl-IB-MECA (50 nM) did not increase coronary flow in the rat, but 100 nM did increase flow by 18%. In pentobarbital sodium-anesthetized pigs IB-MECA (5 μg/kg iv) decreased systemic blood pressure and increased pulmonary artery pressure, effects that did exhibit tachyphylaxis. These results illustrate that adenosine A3-receptor agonists produce species-dependent effects, which in the rat heart appear to be caused by adenosine A2a-receptor activation.

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