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  • 1
    Electronic Resource
    Electronic Resource
    Raman studies of sulfur-containing anions in inorganic polysulfides. Potassium polysulfides (1976)
    s.l. : American Chemical Society
    Inorganic chemistry 15 (1976), S. 1755-1759 
    Details
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ic50162a003
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  • 2
    Electronic Resource
    Electronic Resource
    Raman studies of sulfur-containing anions in inorganic polysulfides. Sodium polysulfides (1976)
    s.l. : American Chemical Society
    Inorganic chemistry 15 (1976), S. 1759-1763 
    Details
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ic50162a004
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  • 3
    Electronic Resource
    Electronic Resource
    Raman studies of sulfur-containing anions in inorganic polysulfides. Barium trisulfide (1976)
    s.l. : American Chemical Society
    Inorganic chemistry 15 (1976), S. 1751-1754 
    Details
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ic50162a002
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  • 4
    Electronic Resource
    Electronic Resource
    EFFECTS OF AMIODARONE AND L8040, NOVEL ANTIANGINAL AND ANTIARRHYTHIC DRUGS, ON CARDIAC AND CORONARY HAEMODYNAMICS AND ON CARDIAC INTRACELLULAR POTENTIALS (1976)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 3 (1976), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects on the coronary and systemic haemodynamics of intravenous and intracoronary injections of two benzfuran derivatives, amiodarone and its brominated analogue (L8040), were studied in open-chest anaesthetized dogs. The effects of L8040 on cardiac intracellular potentials after 6 weeks of 20 mg/kg intraperitoneal injections in rabbits were also investigated.2. Both compounds produced dose-related and quantitatively similar decreases in coronary vascular resistance following their intracoronary administration; threshold effects occurred with about 0.25 mg of each drug and maximal effects with 4 mg. Larger intracoronary doses produced measurable systemic effects.3. Intravenous injections of amiodarone and L8040 (2·5·10 mg/kg) produced dose-related decreases in heart rate and aortic pressure with a fall in total peripheral resistance. The left ventricular output was either unaffected or increased with a consistent augmentation in stroke volume.4. The bradycardia produced by both drugs was associated with prolongation of the P–R interval of the electrocardiogram with no significant effect on the QRS duration or the Q–T interval.5. Each drug produced a decrease in the total peripheral vascular resistance with no change in left ventricular end diastolic pressure except after 10 mg/kg doses which led to an increase in this parameter.6. Cardiac contractile force and peak LV dp/dt were reduced by both drugs in a dose-related manner.7. Chronic intraperitoneal administration of L8040 in rabbits caused a prolongation of the duration of the atrial and ventricular intracellular potential without an effect on the maximal rate of depolarization.8. The effects of amiodarone or L8040 on the coronary circulation and arterial pressure may be attributed to their vasodilator properties but their depressant actions on cardiac contractile force and peak LV dp/dt with an increase in left ventricular end diastolic pressure at high doses, also suggest intrinsic negative inotropic propensity for both compounds.9. It is concluded that the overall effects on coronary and systemic haemodynamics of amiodarone and its brominated analogue are likely to permit a favourable influence on the balance of oxygen supply and demand in myocardial ischaemia; in addition, their actions on sinoatrial and atrio-ventricular conduction as well as those on cardiac repolarization suggest potential antiarrhythmic properties which merit investigation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1976.tb00620.x
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  • 5
    Electronic Resource
    Electronic Resource
    Preconditioning: Markers vs. epiphenomena (1996)
    Springer
    Basic research in cardiology 91 (1996), S. 35-37 
    Details
    ISSN: 1435-1803
    Keywords: Ischemic preconditioning ; adenosine ; ST segment ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788859
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  • 6
    Electronic Resource
    Electronic Resource
    Loss of glycogen during preconditioning is not a prerequisite for protection of the rabbit heart (1996)
    Springer
    Basic research in cardiology 91 (1996), S. 374-381 
    Details
    ISSN: 1435-1803
    Keywords: Glycogen ; preconditioning ; adenosine ; SPT ; bradykinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Depletion of gycogen has been proposed as the mechanism of protection from ischemic preconditioning. The hypothesis was tested by seeing whether pharmacological manipublation of preconditioning causes parallel changes in cardiac glycogen content. Five groups of isolated rabbit hearts were studied. Group 1 experienced 30 min of ischemia only. Group 2 (PC) was preconditioned with 5 min of global ischemia followed by 10 min of reperfusion. Group 3 was preconditioned with 5 min exposure to 400 nM bradykinin followed by a 10 min washout period. Group 4 experienced exposure to 10 μM adenosine followed by a 10 min washout period, and the fifth group was also preconditioned with 5 min ischemia and 10 min reperfusion but 100 μM8-(p-sulfophenyl) theophylline (SPT), which blocks adenosine receptors, was included in the buffer to block preconditioning's protection. Transmural biopsies were taken before treatment, just prior to the 30 min period of global ischemia, and after 30 min of global ischemia. Glycogen in the samples was digested with amyloglucosidase and the resulting glucose was assayed. Baseline glycogen averaged 17.3±0.6 μmol glucose/g wet weight. After preconditioning glycogen decreased to 13.3±1.3 μmol glucose/g wet weight (p〈0.005 vs. baseline). Glycogen was similarly depleted after pharmacological preconditioning with adenosine (14.0±1.0 μmol glucose/g wet weight, p〈0.05 vs. baseline) suggesting a correlation. However, when proconditioning was performed in the pressence of SPT, which blocks protection, glycogen was also depleted by the same amount (13.3±0.7 μmol glucose/g wet weight, p=ns vs. PC). Bradykinin, which also mimics preconditioning, caused no depletion of glycogen (16.3±0.8 μmol glucoseig wet weight, p=ns vs. baseline). Because preconditioning with bradykinin did not deplete glycogen and because glycogen continued to be low when protection from preconditioning was blocked with SPT, we conclude that loss of glycogen per se does not cause the protection of preconditioning.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788717
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  • 7
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Ischemic preconditioning ; Na+/H+ exchange ; 5-(N-ethyl-N-isopropyl)amiloride (EIPA) ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6±2.8% of the risk zone to infarct in untreated Krebs buffer-perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4±2.0% and 7.0±1.0%, respectively (p〈0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1±1.5% infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50μM polymyxin B, a PKC inhibitor, or 1μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischemia caused 51.0±2.9% infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4±3.1% (p〈0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8±2.1% (p〈0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction in infarction was seen (23.8±3.5% infarction). To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia-induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which is quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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  • 8
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Key words Ischemic preconditioning – Na+/H+ exchange – 5-(N-ethyl-N-isopropyl)amiloride (EIPA) – protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6 ± 2.8 % of the risk zone to infarct in untreated Krebs buffer perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4 ± 2.0 % and 7.0 ± 1.0 %, respectively (p 〉 0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1 ± 1.5 % infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50 μM polymyxin B, a PKC inhibitor, or 1 μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischmia caused 51.0 ± 2,9 % infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4 ± 3.1 % (p 〉 0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8 ± 2.1 % (p 〉 0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction was seen (23.8 ± 3,5 % infarction) To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which ist quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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  • 9
    Electronic Resource
    Electronic Resource
    Attenuation of S-T Segment elevation during repetitive coronary occlusions truly reflects the protection of Ischemic preconditioning and is not an epiphenomenon (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 426-434 
    Details
    ISSN: 1435-1803
    Keywords: Ischemia ; preconditioning ; 8-(p-sulfophenyl)theophylline ; ST segments ; tyramine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Attenuation of S-T segment elevation between the first and subsequent balloon inflations of a coronary angioplasty procedure has been assumed to indicate a transition to a preconditioned state, but there has been no validation of this assumption. Open-chest rabbits were instrumented with a coronary snare and epicardial electrode. The coronary artery was occluded twice for 5 min with each occlusion followed by 10 min of reflow before a final 30 min occlusion. The evolving S-T elevation was quantitated as the voltage-time integral. For the first coronary occlusion total S-T segment elevation averaged 40.8±5.4 mV·min, significantly antly greater than 26.2±4.6 mV·min for the second occlusion (p〈0.001). There was no further change during the initial 5 min of the third occlusion (24.5±4.5 mV·min). When the protection of ischemic preconditioning was blocked by intravenous infusion of 8-(p-sulfophenyl)theophylline, an adenosine receptor antagonist, attenuation of S-T segment elevation was no longer apparent. When preconditioning was pharmacologically triggered by tyramine rather than ischemia, there also was no alteration in S-T segment elevation among the 3 occlusions. Therefore, S-T elevation was diminished during the second episode of ischemia only when a transition occurred from non-preconditioned to preconditioned state between occlusions. An attenuated S-T segment is a valid marker for the presence of the preconditioned state.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00796217
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  • 10
    Electronic Resource
    Electronic Resource
    Arguments in favor of protein kinase C playing an important role in ischemic preconditioning (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 37-39 
    Details
    ISSN: 1435-1803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion In light of the above we believe that the PKC hypothesis is alive and well. Why then do PKC inhibitors fail to block protection in pig and perhaps dog heart? Those observations argue against PKC playing a universal role in all models of preconditioning. The receptor pathway for preconditioning in the rabbit heart has been found to be highly redundant with no less than 4 substances including adenosine (12), bradykinin (8), opioids (15), and free radicals (5) contributing in parallel to the protection. Preconditioning appears to be very important to the heart. It is not inconceivable, then, that alternative pathways have also developed around PKC in some species to further insure that the ischemic heart would become preconditioned. Whatever the case, it should be remembered that the available human data still support the PKC hypothesis in that rather important species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00797205
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