Sentence examples for both normal and failing from inspiring English sources

Experimental data and the results of numerical modeling accumulated over the past decade show the emerging importance of this late current component for the function of both normal and failing myocardium.

The organization of t-tubules, L-type calcium channels (DHPRs), ryanodine receptors (RyRs) and contractile machinery were examined in fixed ventricular tissue samples from both normal and failing hearts (idiopathic (non-ischemic) dilated cardiomyopathy) using high resolution fluorescent imaging.

These effects were analyzed in both normal and failing heart conditions.

In total, 16 potential active alkaloid components with similar structures in Fuzi were retained on both normal and failing myocardium CMC models.

Interestingly, this is in keeping with previous studies in human myocardium, both normal and failing human heart (37, 38, 45) and rats (17).

Although the presence and proteolytic activity of MMP9 and MMP2 have been confirmed in both normal and failing hearts [ 4] as well as in skeletal muscles [ 5], the formation of HMW complexes containing these 2 major proteases and associated enzymatic activity has not been comprehensively studied in these tissues.

Delayed SR Ca2+ release in cardiomyocytes has been correlated to gaps in the t-tubule system, both in normal and failing ventricular cardiomyocytes (18, 39).

The actions of volatile anesthetics on left ventricular (LV) function in normal and failing hearts have been previously evaluated, but the effects of these agents on left atrial (LA) function in the presence of LV dysfunction are unknown.

This review considers (1) quantitative integration of INaL into the established electrophysiological and Ca2+ regulatory mechanisms in normal and failing cardiomyocytes and (2) a new therapeutic strategy utilizing a selective inhibition of INaL to target both arrhythmias and impaired contractility in HF.

This report presents a detailed analysis of the architecture of cellular structures critical to excitation-contraction coupling in normal and failing human myocardium.

In contrast, the work of Ohler et-al (2009) showed no significant change in the structure of t-system between isolated normal and failing cardiomyocytes by using 2-photon imaging of di-8-ANNEPs labeling [25].