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1 was completely preserved because of greater cardiac contraction.
2 ynaptic transmission, neural plasticity, and cardiac contraction.
3 y abdominal palpation until the cessation of cardiac contraction.
4 n heart failure, while hyperglycemia impairs cardiac contraction.
5 rotein kinase A (PKA) activation to regulate cardiac contraction.
6 the cardiac action potential and initiating cardiac contraction.
7 a(2+) efflux across the sarcolemma following cardiac contraction.
8 nd valves, is not dependent on blood flow or cardiac contraction.
9 ficant enhancement of in vitro parameters of cardiac contraction.
10 ortant role in ion homeostasis and regulates cardiac contraction.
11 Troponin is essential for the regulation of cardiac contraction.
12 allosterically involved in calcium-mediated cardiac contraction.
13 gulatory complex that is required for normal cardiac contraction.
14 culation, and dictate the rate and rhythm of cardiac contraction.
15 nin tail region, modulates the regulation of cardiac contraction.
16 acellular Ca2+ concentration and strengthens cardiac contraction.
17 Na,K-ATPase isoform in Ca2+ signaling during cardiac contraction.
18 in heart and regulates the rate and force of cardiac contraction.
19 anges in sarcoplasmic reticulum function and cardiac contraction.
20 activity, Ca(2+) signalling and arterial and cardiac contraction.
21 ovel biomechanical forces upon initiation of cardiac contractions.
22 e, MLC2, is recognized as a key regulator of cardiac contraction, a MLCK that is preferentially expre
23 Gaskell's elucidation of the sequence of cardiac contraction and atrioventricular block and his c
26 ies demonstrate essential roles for Dicer in cardiac contraction and indicate that miRNAs play critic
28 d leads to heart failure by interfering with cardiac contraction and intracellular transport is a den
29 ms involved in the opposing effects of NO on cardiac contraction and investigated whether NO modulate
33 The normal influence of heart rate (HR) on cardiac contraction and relaxation in the mouse remains
34 of Ca(2+) channels, allowing fine control of cardiac contraction and rhythmicity in cardiac tissue wh
35 lating evidence indicates a crucial role for cardiac contraction and the resulting fluid forces in sh
36 erbb2 mutants, tnnt2a morphants, which lack cardiac contractions and flow, and myh6 morphants, which
38 lamine release resulting in the formation of cardiac contraction bands may represent the cause of dea
39 ein C (cMyBP-C) has a key regulatory role in cardiac contraction, but the mechanism by which changes
40 Isoflurane and propofol are known to depress cardiac contraction, but the molecular mechanisms involv
41 crease in heart rate affects the strength of cardiac contraction by altering the Ca(2+) transient as
43 that enables quantitative analysis of normal cardiac contraction, disease phenotypes, and pharmacolog
44 we observed pulses that were coincident with cardiac contraction documented by esophageal echocardiog
45 y regulator of the kinetics and amplitude of cardiac contraction during beta-adrenergic stimulation a
47 Tolerance was defined as the persistence of cardiac contraction for the duration of evaluation (125-
48 el unexpected role of BDNF in regulating the cardiac contraction force independent of the nervous sys
50 art development, we investigated the role of cardiac contraction in chamber maturation, focusing on t
51 reorientation of myofiber aggregates during cardiac contraction in patients with dilated cardiomyopa
52 hip between this faster motility and altered cardiac contraction in patients with HCM is discussed.
53 nC) is the regulatory protein that initiates cardiac contraction in response to Ca(2+) TnC binding Ca
54 ion of the mutant protein and a disabling of cardiac contraction in the submaximal range of myoplasmi
55 ation of cardiac contraction, we showed that cardiac contraction is required for trabeculation throug
57 isoforms play key roles in the regulation of cardiac contraction, ischemic preconditioning, and hyper
59 es cGMP formation, which, in turn, modulates cardiac contraction/relaxation by a) altering cardiomyoc
60 at forced Notch activation in the absence of cardiac contraction rescues efnb2a and nrg1 expression.
61 tent increases in cAMP signals for sustained cardiac contraction response; and arrestin acts as an ag
62 our findings describe an essential role for cardiac contraction-responsive transcriptional changes i
63 , including humans, have a positive FFR, and cardiac contraction strength increases with heart rate.
64 defect in the primary mechanism controlling cardiac contraction, switching between different conform
66 e critical free energy of ATP hydrolysis for cardiac contraction that is consistent with these findin
67 hat seems to contribute to the regulation of cardiac contraction through interactions with either myo
68 myosin in the primed state prior to onset of cardiac contraction, thus increasing the number of heads
70 otential importance of stretch activation in cardiac contraction, we examined the effects of cMyBP-C
71 By genetic and pharmacological ablation of cardiac contraction, we showed that cardiac contraction
72 omyocyte excitation/contraction coupling and cardiac contraction were evaluated in isolated mouse and
73 cytosolic Ca(2+) to physiologically augment cardiac contraction, whereas excessive betaAR activation
74 process lags 2-3 months behind the onset of cardiac contraction, which may be a prerequisite for car
75 There were more pronounced impairments of cardiac contraction with greater eccentric cardiac hyper
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