2-(4-(dimethylamino)styryl)-1-methylpyridinium and Coronary-Disease

ip DSPM 5 mg/kg 1 or 4 h before excision of the heart was found to prevent damage to the heart due to global myocardial ischemia. Compared with the controls, the heart rate, coronary resistance, contractile force and edema of the heart were all greatly improved during the 60 min reflow after 25 min of no-flow, especially the heart pretreated with DSPM 4 h prior to excision. In addition, DSPM 1.5, 6 mg/kg markedly reduced the myocardial Ca2+ content measured by isoproterenol in mice. DSPM at higher dosage also lowered the normal myocardial Ca2+ content. These results suggest that DSPM may have a protective effect on myocardial ischemia which might be associated with its calcium antagonistic action.

Topics: Animals; Calcium; Calcium Channel Blockers; Coronary Circulation; Coronary Disease; Female; Heart Rate; In Vitro Techniques; Isoproterenol; Male; Mice; Myocardium; Pyridinium Compounds; Rats; Verapamil

Topics: Animals; Aorta; Coronary Disease; Fluorescent Dyes; Heart; In Vitro Techniques; Membrane Potentials; Mitochondria, Heart; Muscle, Smooth; Myocardial Reperfusion; Pyridinium Compounds; Rats; Spectrometry, Fluorescence

In perfused rat hearts alterations of aortic flow and mitochondrial membrane potential resulting from uncoupling of oxidative phosphorylation, hypoxia and treatment with a cardioprotective drug (2-mercaptopropionylglycine (MPG) have been studied. Mitochondrial membrane potential was followed by surface fluorimetry on DASPMI stained hearts. This fluorochrome specifically stains mitochondria in living cells; fluorescence intensity is related to the electrochemical gradient. Aortic flow turned out to be a much more sensitive indicator of heart function than ventricular pressure or mitochondrial membrane potential. No direct relationship exists between mitochondrial membrane potential and ATP production under the different metabolic conditions. Two phases of hypoxic mitochondrial damage have been deduced: the first results in derangement of ATP synthases while membrane potential is maintained, the second in irreversible damage of mitochondrial membranes with loss of membrane potential.

Topics: Adenosine Triphosphate; Animals; Coronary Disease; Female; Fluorescent Dyes; Heart; Hypoxia; In Vitro Techniques; Perfusion; Pyridinium Compounds; Rats; Rats, Inbred Strains; Tiopronin; Uncoupling Agents