A new concept of the isolated perfused heart preparation with on-line computerized data evaluation

Krzemiński, Tadeusz F.; Kurcok, A; Kapustecki, Janusz; Kowaliński, Jerzy; Slowiński, Zbigniew; Brus, Ryszard

doi:10.1016/0160-5402(91)90001-l

Cited by 8 publications

(1 citation statement)

References 17 publications

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“…In addition, studying the effects of M-2 in two different models of working heart ischemia (low-flow and regional), we confirmed that it improved coronary flow in both models, while favorably maintaining aortic pressure parameters [ 35 ]. Moreover, it provided outstanding protection against deleterious effects of calcium overload (induced by veratridine in the Langendorff heart) by significant prevention of the left ventricular diastolic pressure rise and coronary flow decrease [ 36 , 37 ].…”

Section: Introductionmentioning

confidence: 99%

Dihydropyridines’ metabolites-induced early apoptosis after myocardial infarction in rats; new outlook on preclinical study with M-2 and M-3

et al. 2015

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Our previous studies established cardio-protective effects of furnidipine and its active metabolites called M-2 and M-3. The aim of current research was to compare the effects of single oral pretreatment with 20 mg kg−1 of M-2 and M-3 on mortality, different forms of arrhythmias, blood pressures parameters and ST-segment changes during occlusion (for 90 min) and reperfusion in the model of myocardial infarction in rats evoked by left anterior descending coronary artery occlusion. Additionally, the development of programmed cell death and biochemical parameters in blood serum were studied at 4th day after infarction. Furnidipines’ metabolites effectively reduced mortality index while did not markedly influence on blood pressures parameters, arrhythmias, ST-segment changes as well as biochemical parameters. Intriguingly, programmed cell death study (TUNEL) showed distinct increase in the amount of apoptotic nuclei in post-infarcted myocardium, granulation tissue and what is more in arteriolar walls after M-2 and M-3 application. Moreover, M-2 turned out to be more powerful in stimulation of apoptosis in granulation tissue surrounding infarcted area whereas M-3 presented balanced profile in this matter. Taking into account that programmed cell death plays positive role in post-infarcted heart healing, M-2 presents itself as more attractive agent for oral pretreatment in early stages of ischemia by non-stable individuals due to its more specific action in stimulation repairing processes in granulation tissue as well as in arteriolar walls. While M-2 and M-3 are common metabolites present in degradation pathways of many widely used dihydropyridines in clinic, this key fact put the new outlook on understanding additional mechanism and effects of not only furnidipines’ metabolites but also other dihydropyridines.

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Section: Introductionmentioning

confidence: 99%