Positive inotropic effect of nicorandil in adult rats in situ

Nakahashi, Kazuhiro; Kitagawa, Yutaka; Itô, Haruo; Kuzumoto, N; Furuya, Hitoshi; Takaki, Miyako

doi:10.1007/s00540-004-0268-y

Cited by 5 publications

(4 citation statements)

References 26 publications

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“…27 In the present study, we infused nicorandil at a dosage of 60 mg/kg/min, and thus the blood concentration of nicorandil may have been 3 times higher than in that report. 27 In the present study, we infused nicorandil at a dosage of 60 mg/kg/min, and thus the blood concentration of nicorandil may have been 3 times higher than in that report.…”

Section: Discussionmentioning

confidence: 54%

Nicorandil Protects Pial Arterioles From Endothelial Dysfunction Induced by Smoking in Rats

Iwata

Iida

et al. 2013

Journal of Neurosurgical Anesthesiology

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Section: Discussionmentioning

confidence: 54%

Nicorandil Protects Pial Arterioles From Endothelial Dysfunction Induced by Smoking in Rats

Iwata

Iida

et al. 2013

Journal of Neurosurgical Anesthesiology

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“…We had proposed that, in in situ hearts, PVA at an appropriate LVV on the curvilinear PVA-V relationship is valuable for evaluating LV mechanoenergetics (4,5,7). In the present study, we calculated mLVV that was the value of [V 0 + (maximum end-systolic volume (ESV) − minimum ESV) on the ESPVR × 1 / 2] from each P-V loop (4,5,7).…”

Section: Data Analysesmentioning

confidence: 96%

“…In the present study, we calculated mLVV that was the value of [V 0 + (maximum end-systolic volume (ESV) − minimum ESV) on the ESPVR × 1 / 2] from each P-V loop (4,5,7). EDPVR values are very close to the volume axis and thus the effect of excluding the EDPVR measure would be small (Fig.…”

Section: Data Analysesmentioning

confidence: 99%

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Effects of a Novel Histone Deacetylase Inhibitor, N-(2-Aminophenyl) Benzamide, on a Reversible Hypertrophy Induced by Isoproterenol in In Situ Rat Hearts

et al. 2007

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Abstract. The aim of the present study was performed to determine whether a novel histone deacetylase (HDAC) inhibitor, N-(2-aminophenyl)-4-{[benzyl(2-hydroxyethyl)amino]methyl} benzamide (K-183), prevents a reversible cardiac hypertrophy induced by isoproterenol and improves left ventricular (LV) dysfunction in rats. Either isoproterenol or vehicle was infused for 3 days by osmotic minipump. One hour prior to the implantation of isoproterenol, K-183 or trichostatin A (TSA) was injected twice a day for 3 days. We recorded continuous LV pressurevolume (P-V) loops of in situ hearts one hour after removal of the osmotic minipump. LV work capability (systolic P-V area at midrange LV volume: PVA mLVV ) and hemodynamics were evaluated. K-183 per se induced neither cardiac hypertrophy nor collagen production. Although K-183 did not prevent the hypertrophy, where PVA mLVV remained decreased, K-183, differently from TSA, significantly attenuated the decrease of cardiac output and the increase of effective arterial elastance in the hypertrophied heart. These results indicate that the novel HDAC inhibitor K-183 has some beneficial effects on hemodynamics, although K-183 has no effects of antihypertrophic modalities.

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A new calpain inhibitor protects left ventricular dysfunction induced by mild ischemia-reperfusion in in situ rat hearts

et al. 2012

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We have previously indicated that a new soluble calpain inhibitor, SNJ-1945 (SNJ), attenuates cardiac dysfunction after cardioplegia arrest-reperfusion by inhibiting the proteolysis of α-fodrin in in vitro study. Nevertheless, the in vivo study design is indispensable to explore realistic therapeutic approaches for clinical use. The aim of the present in situ study was to investigate whether SNJ attenuated left ventricular (LV) dysfunction (stunning) after mild ischemic-reperfusion (mI-R) in rat hearts. SNJ (60 μmol/l, 5 ml i.p.) was injected 30 min before gradual and partial coronary occlusion at proximal left anterior descending artery. To investigate LV function, we obtained curvilinear end-systolic pressure-volume relationship by increasing afterload 60 min after reperfusion. In the mI-R group, specific LV functional indices at midrange LV volume (mLVV), end-systolic pressure (ESP(mLVV)), and pressure-volume area (PVA(mLVV): a total mechanical energy per beat, linearly related to oxygen consumption) significantly decreased, but SNJ reversed these decreases to time control level. Furthermore, SNJ prevented the α-fodrin degradation and attenuated degradation of Ca(2+) handling proteins after mI-R. Our results indicate that improvements in LV function following mI-R injury are associated with inhibition of the proteolysis of α-fodrin in in situ rat hearts. In conclusion, SNJ should be a promising tool to protect the heart from the stunning.

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Positive inotropic effect of nicorandil in adult rats in situ

Abstract: These results suggest that nicorandil exhibited positive inotropic actions on LV function of in situ hearts in adult rats with resultant increased preload (EDV).

Cited by 5 publications

References 26 publications

Nicorandil Protects Pial Arterioles From Endothelial Dysfunction Induced by Smoking in Rats

Nicorandil Protects Pial Arterioles From Endothelial Dysfunction Induced by Smoking in Rats

Effects of a Novel Histone Deacetylase Inhibitor, N-(2-Aminophenyl) Benzamide, on a Reversible Hypertrophy Induced by Isoproterenol in In Situ Rat Hearts

A new calpain inhibitor protects left ventricular dysfunction induced by mild ischemia-reperfusion in in situ rat hearts

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