ArticleNaunyn-Schmiedeberg's archives of pharmacology2005
Reduction of myocardial infarct size by SM-198110, a novel Na+/H+ exchange inhibitor, in rabbits.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 5 citations in OpenAlex.
- Protection against myocardial ischemia/reperfusion injury by short-term diabetes: enhancement of VEGF formation, capillary density, and activation of cell survival signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2006Article
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7 authors at 1 institution in 1 country.
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Abstract
The effects of 3-[2-({[amino(imino)methyl]amino}carbonyl)-4-chloro-1H-indol-1-yl]-1-propanesulphonic acid monohydrate (SM-198110), a novel potent Na+/H+ exchange inhibitor, and cariporide (Hoe642), another Na+/H+ exchange inhibitor, were studied in a myocardial ischaemia and reperfusion injury model. Anaesthetized rabbits were subjected to occlusion of the coronary artery for 30 min followed by reperfusion for 5 h. SM-198110 or cariporide was administered before ischaemia and before reperfusion. We also assessed the anti-necrotic effect of SM-198110 when given before reperfusion, both alone and together with glibenclamide, a K(ATP) channel blocker, 5-hydroxydecanoate (5-HD), a mitochondrial K(ATP) channel-selective blocker and 8-(p-sulphophenyl)-theophylline (8-SPT), an adenosine receptor blocker. The infarct size was reduced dose-dependently by i.v. administration of SM-198110 before ischaemia, with a significant reduction in serum creatine phosphokinase activity. Infarct sizes, normalized to the size of the area-at-risk (means+/-SE) were: vehicle 56.6+/-3.7%; low-dose SM-198110 39.2+/-6.3%; mid-dose 32.8+/-7.4% (P < 0.05); high-dose 22.1+/-6.7% (P < 0.01). This anti-necrotic effect of SM-198110 was achieved without significant haemodynamic changes. Cariporide given before ischaemia also reduced infarct size significantly and dose-dependently. SM-198110 administered before reperfusion also resulted in a dose-dependent reduction in the infarct size. Infarct sizes were: vehicle 56.6+/-3.7%; low-dose SM-198110 44.5+/-5.7%; mid-dose 36.3+/-6.6% (P < 0.01); high-dose 34.7+/-3.8% (P < 0.01). In contrast, cariporide given before reperfusion did not reduce infarct sizes significantly. The anti-necrotic effect of SM-198110 was observed even when given 10 min after the beginning of reperfusion. Glibenclamide and 5-HD abolished the anti-necrotic effect of treatment before reperfusion with SM-198110. However, the co-administration of 8-SPT with SM-198110 did not affect infarct size. These results suggest that, in addition to Na+/H+ exchange inhibition, mitochondrial and/or sarcolemmal K(ATP) channels contribute to the anti-necrotic effect of SM-198110 when the latter is given before reperfusion.
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