戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 n index of sympathetically mediated positive inotropy).
2 ve nitrosylation, thiol reactivity, positive inotropy).
3 uate the potential of this method to predict inotropy.
4 ory system mediating cardiac contraction and inotropy.
5 gnaling and normalize beta1AR expression and inotropy.
6  parasympathetic control of left ventricular inotropy.
7 ce of tonic inhibitory vagal influence on LV inotropy.
8 c inhibitory muscarinic influence on cardiac inotropy.
9 doses did not induce myocyte death or affect inotropy.
10 nase A (PKA) is critical for skeletal muscle inotropy.
11  serine phosphorylation of Akt, and negative inotropy.
12 ibution to caveolae, with diminished cardiac inotropy.
13 rom heavier endosomes while retaining normal inotropy.
14 nomena of rest decay and frequency-dependent inotropy.
15 CE, SKF96365, was also effective in blunting inotropy.
16 allows NO to inhibit beta-adrenergic-induced inotropy.
17 l of chronotropy, lusitropy, dromotropy, and inotropy.
18 ptors (ARs) in the heart results in positive inotropy.
19 d mechanism of beta-AR modulation of cardiac inotropy.
20 ucagon receptors) play a key role in cardiac inotropy.
21 a cascade leading to cardiac chronotropy and inotropy.
22 t-bound receptors, have increased myocardial inotropy.
23  alternative mechanisms of glycoside-induced inotropy: (1) direct activation of sarcoplasmic reticulu
24 pranolol, B-CTX attenuated the cardiomyocyte inotropy and calcium transient alterations as induced by
25 rtrophy and depressed stimulation of cardiac inotropy and chronotropy by beta-adrenergic receptor (be
26 rgic receptors (ARs) are GPCRs that regulate inotropy and chronotropy in the heart and mediate vasodi
27 in the mouse, beta-AR stimulation of cardiac inotropy and chronotropy is mediated almost exclusively
28 tally exerts the same directional effects on inotropy and chronotropy, albeit through different mecha
29 (beta2AR), an important modulator of cardiac inotropy and chronotropy, has significant genetic hetero
30 th the attenuated beta-adrenoceptor-mediated inotropy and chronotropy.
31 red responses to BAY y 5959, which increases inotropy and decreases chronotropy, with those to norepi
32 ng that under conditions of positive cardiac inotropy and enhanced efficiency of EC coupling alternan
33 nol stimulation but had minimal effect on AS inotropy and enhanced lusitropy.
34  genes exacerbate cardiac fibrosis, negative inotropy and heart rate changes, reduce nitric oxide-med
35 s of this agent include a modest increase in inotropy and improvement in diastolic function, both of
36 S3(-/-)+AdVbeta(gal) mice displayed enhanced inotropy and lusitropy over WT at slower heart rates but
37 L-NIL dramatically increased the ISO-induced inotropy and lusitropy, such that the ISO+AG response in
38                                     Positive inotropy and relaxation was evident in comparison to bet
39 d marked augmentation of frequency-dependent inotropy and relaxation, with a peak frequency response
40  nitric oxide (NO), induces positive cardiac inotropy and selective venodilation in the normal in viv
41 fects of T(3) can contribute to the positive inotropy and sinus (atrial) tachycardia traditionally at
42  of atrial 5-HT4 receptors produces positive inotropy and tachycardia that can precipitate arrhythmia
43                                 Both cardiac inotropy and the progression of heart disease are affect
44                     We hypothesize that this inotropy and the resulting increase in tissue blood flow
45 nderlying this chronic IL-6-induced negative inotropy and the role of iNOS.
46  in the short term, controls chronotropy and inotropy and, in the long term, regulates cardiomyocyte
47 cluding a 2.6x increase in systolic calcium (inotropy) and a 28% decrease in calcium half-relaxation
48 py), the strength of myocardial contraction (inotropy), and the rate of myocardial relaxation (lusitr
49 factors were derived: 1) parasympathetic, 2) inotropy, and 3) systemic vascular resistance.
50 is finely tuned by MARK4 to regulate cardiac inotropy, and identify MARK4 as a promising therapeutic
51 AD thus had negative effects on chronotropy, inotropy, and lusitropy, thereby indicating a key role f
52 ator of at least a component of the positive inotropy associated with agents that stimulate phospholi
53         These studies demonstrate a negative inotropy associated with jet ventilation that, during he
54  mechanism for chronic IL-6-induced negative inotropy at 2 h, both sGC/cGMP/PKG and ONOO-, at least i
55 nearly fully inhibited isoproterenol-induced inotropy) but not partial beta-blockade.
56                          AS-induced positive inotropy, but not systemic vasodilatation, was highly re
57 ence of a new molecular pathway for positive inotropy by a cardiac-restricted microRNA (miR).
58  myofilament-based molecular manipulation of inotropy by histidine-modified troponin I maintains card
59 a-adrenergic receptor stimulation of cardiac inotropy, cAMP, PKA, L-type Ca(2+) current, Ca(2+) trans
60 igher sensitivity to isoprenaline-stimulated inotropy compared with control subjects.
61                                       Thus, "inotropy" does not sufficiently describe the range of po
62                             The time to peak inotropy for both phases depended on the light intensity
63                    Glycoside-induced cardiac inotropy has traditionally been attributed to direct Na(
64 es lymphatic contractions stronger (enhanced inotropy - higher contraction amplitude) and propels mor
65 aptan], and adenosine) and non-cAMP-mediated inotropy (ie, levosimendan), are currently under investi
66 ite (ONOO-) in chronic IL-6-induced negative inotropy in ARVM.
67 ions of ouabain resulted in positive cardiac inotropy in both isolated hearts and intact animals expr
68 ng EMD-57033 dose further augmented positive inotropy in CON and HF, accompanied by vasodilation, inc
69         Acetylcholine reversed isoproterenol inotropy in controls (108+/-21% reduction of +dP/dt resp
70  thereby partially normalize beta-adrenergic inotropy in DM phospholamban mice.
71 a novel form of calcium-independent positive inotropy in failing cardiac myocytes by fast alpha-myosi
72 trolled trials examining the use of positive inotropy in HF with reduced ejection fraction was conduc
73 pe mice, cTnI(PKC-P) mice exhibited negative inotropy in isolated hearts (14% decrease in peak develo
74 t induces arterial vasodilation and positive inotropy in larger mammals.
75  the regulation of basal and beta-adrenergic inotropy in normal and chronically infarcted hearts.
76 sfer can confer calcium-independent positive inotropy in slow beta-myosin-dominant rabbit and human f
77 c regulation of CaV1.2 channels and positive inotropy in the heart, but are dispensable for CaV1.2 tr
78 on in skeletal muscle and may play a role in inotropy in the heart.
79 or physiological mechanisms of modulation of inotropy in the heart.
80 nhibition augmented isoproterenol-stimulated inotropy in wild-type (WT), but not in beta(3)(-/-) mice
81  for enhanced Ca(2+) handling (i.e. enhanced inotropy) in each species, suggesting that electrophysio
82 (lusitropy), and increased force production (inotropy) in response to epinephrine.
83 ed, and to prevent excessive ssTnI-dependent inotropy (increased Ca(2+) sensitivity) in the embryonic
84                 Peak aortic acceleration (LV inotropy) increased by 0.8 g in EA but only by 0.2 g in
85 ere left-ventricular dP/dt(max,) an index of inotropy, increased with HR in mavacamten-treated animal
86     The underlying mechanism of the positive inotropy incurred with L-755,507 in the TGbeta(3) mice w
87             These treatments did not inhibit inotropy induced by activation of adenylate cyclase thro
88                 Thus, CGRP-mediated positive inotropy is load-independent but indirect and attributab
89 of nitric oxide (NO), exert positive cardiac inotropy/lusitropy in vivo and in vitro, due in part to
90 ique cardiovascular features (i.e., positive inotropy/lusitropy) that may have relevance for pharmaco
91      However, their negative chronotropy and inotropy may potentially lead to an inappropriately low
92                            Myofilament-based inotropy may represent a therapeutic avenue to improve m
93 ls demonstrated that ouabain-induced cardiac inotropy occurred in hearts from wild type but not from
94            Enhancement of contractile force (inotropy) occurs in skeletal muscle following neuroendoc
95 sion of human beta(3)ARs results in positive inotropy only on stimulation with a beta(3)AR agonist.
96                                    Molecular inotropy refers to cardiac contractility that can be mod
97 lecular mechanism underlying skeletal muscle inotropy requires enhanced SR Ca(2+) release due to PKA
98 e (NO) production, which attenuates positive inotropy, suggesting a possible negative feedback mechan
99 on and were studied under varying degrees of inotropy (using increasing extracellular calcium [Ca2+]o
100 y alter cardiac muscle contraction: negative inotropy via decreased cross-bridge formation and negati
101 ne hydrochloride (L-NMMA) on beta-adrenergic inotropy was assessed in conscious dogs before and after
102 ion were similar, beta-adrenergic-stimulated inotropy was increased in beta(3)(-/-) mice, and similar
103                                CGRP-positive inotropy was not attributable to reflex activation becau
104 on by hyperglycemia of phenylephrine-induced inotropy was reversed with azaserine and mimicked by glu
105 se isozyme, mediates ouabain-induced cardiac inotropy, we developed animals expressing a ouabain-inse
106 he heart results in positive chronotropy and inotropy, which together rapidly increase cardiac output
107 eficiency results in a sustained increase of inotropy without structural or functional remodeling of

 
Page Top