1 Starling's equation indicates that reduced oncotic press
2 in whom we induced airflow limitation with
a Starling resistor.
3 egative force-frequency response, an
altered Starling relationship, and blunted contractile responses
4 Bayliss
and Starling first coined the term 'hormone' with reference
5 The landmark discovery by Bayliss
and Starling in 1902 of the first hormone, secretin, emerged
6 dge pressure and LV end-diastolic volume
and Starling curves from pulmonary capillary wedge pressure
7 1 year of training, and pressure-volume
and Starling curves were constructed during decreases (lower
8 d phasic lymphatic smooth muscle that act
as Starling resistors.
9 of the intestine' as postulated by
Bayliss &
Starling (1899).
10 r= 0.59, n= 28, P < 0.001), as predicted
by Starling's law of filtration.
11 A modified
Carnahan-
Starling hard-sphere model was utilized to fit the exper
12 s with right heart catheterization to
define Starling and left ventricular (LV) pressure-volume curve
13 t pulmonary artery catheterization to
define Starling and left ventricular pressure-volume curves.
14 h pulmonary artery catheterization to
define Starling and LV pressure-volume curves; secondary functi
15 These findings suggest that the
dynamic Starling mechanism is impaired with human ageing possibl
16 We hypothesized that the
dynamic Starling mechanism would be impaired with ageing, and th
17 e and SV was used as an index of the
dynamic Starling mechanism.
18 re promulgated by William Bayliss and
Ernest Starling.
19 ition in a species of songbird, the
European Starling (Sturnus vulgaris), using tone sequences that v
20 tes losses and gains in a bird, the
European Starling, to test the implication of SUT that risk prone
21 y venous resistance, are strong evidence
for Starling resistor forces (venocompression) rather than a
22 re located on the flatter portion of a
Frank-
Starling curve because of attenuated decreases in SV per
23 re located on the steeper portion of a
Frank-
Starling curve because of augmented decreases in SV per
24 is operating on a steeper portion of a
Frank-
Starling curve.
25 a altering the operating position on a
Frank-
Starling curve.
26 n 2, or AT1R were unable to generate a
Frank-
Starling force in response to changes in cardiac volume.
27 ese data support the hypothesis that a
Frank-
Starling mechanism contributes to compromised blood pres
28 These data suggest that a
Frank-
Starling mechanism may contribute to improvements in ort
29 neoaortic stroke volume demonstrated a
Frank-
Starling-like curve that shifted upward after HF.
30 e LV pressure-volume relationships and
Frank-
Starling curves.
31 ed over a range of loading conditions (
Frank-
Starling curve).
32 plicates a novel means for controlling
Frank-
Starling relationships.
33 e engineered human myocardium exhibits
Frank-
Starling-type force-length relationships.
34 L) is, in part, the cellular basis for
Frank-
Starling's law of the heart.
35 asurement apparatus exhibited a robust
Frank-
Starling response to external stretch, and a dose-depend
36 ociated with movement along the septal
Frank-
Starling equivalent (septal output versus end-diastolic
37 o a flatter portion of the heat stress
Frank-
Starling curve thereby attenuating the reduction in SV d
38 o a flatter portion of the heat stress
Frank-
Starling curve.
39 cMyBP-C can influence the SL-tension (
Frank-
Starling) relationship in cardiac muscle.
40 We demonstrate that
Frank-
Starling is evident at maximal [Ca(2+) ] activation and
41 The
Frank-
Starling 'law of the heart' is implicated in certain typ
42 ation (LDA), the cellular basis of the
Frank-
Starling cardiac regulatory mechanism.
43 We demonstrate the
Frank-
Starling effect at the single cardiomyocyte level by sho
44 ntain a high ejection fraction via the
Frank-
Starling effect.
45 t contractile forces that followed the
Frank-
Starling law and accepted physiological pacing.
46 The
Frank-
Starling law and the Anrep effect describe exquisite int
47 g will deepen our understanding of the
Frank-
Starling law and the Anrep effect, and also provide a un
48 phosphorylation as a modulator of the
Frank-
Starling law in the heart.
49 The
Frank-
Starling law of the heart is a physiological phenomenon
50 that these effects play a role in the
Frank-
Starling law of the heart.
51 ardiac regulatory mechanisms, like the
Frank-
Starling law of the heart.
52 sequently the mechanism underlying the
Frank-
Starling law of the heart.
53 cellular mechanism responsible for the
Frank-
Starling law of the heart.
54 but also because it contributes to the
Frank-
Starling law, a mechanism by which the heart increases s
55 The
Frank-
Starling mechanism allows the amount of blood entering t
56 ural unit of the cardiac myocytes, the
Frank-
Starling mechanism consists of the increase in active fo
57 0.005), confirming the presence of the
Frank-
Starling mechanism in the LA.
58 Reconstitution of the
Frank-
Starling mechanism is an important milestone for produci
59 the giant elastic protein titin in the
Frank-
Starling mechanism of the heart by measuring the sarcome
60 titin may be a factor involved in the
Frank-
Starling mechanism of the heart by promoting actomyosin
61 The
Frank-
Starling mechanism of the heart is due, in part, to modu
62 these two proteins are involved in the
Frank-
Starling mechanism of the heart.
63 e-tuning of cardiac performance by the
Frank-
Starling mechanism that relates the pressure exerted by
64 The
Frank-
Starling Mechanism was reduced in a graded fashion in Rb
65 ress, thereby obscuring the use of the
Frank-
Starling mechanism, a fundamental mechanism by which the
66 According to the
Frank-
Starling mechanism, as the heart is stretched, it increa
67 hECTs reconstituted the
Frank-
Starling mechanism, generating an average maximum twitch
68 ng-binding cross-bridges underlies the
Frank-
Starling mechanism, we inhibited force and strong cross-
69 T1R as key regulatory molecules in the
Frank-
Starling mechanism, which potentially can be targeted th
70 rrelation between titin strain and the
Frank-
Starling mechanism.
71 task, revealing a prime aspect of the
Frank-
Starling mechanism.
72 filament activation contributes to the
Frank-
Starling mechanism.
73 neural and hormonal factors and by the
Frank-
Starling mechanism.
74 resulting in better utilization of the
Frank-
Starling mechanism.
75 an exercise-induced modulation of the
Frank-
Starling mechanism.
76 ta-adrenergic stimulation enhances the
Frank-
Starling regulatory mechanism predominantly via cMyBP-C
77 The
Frank-
Starling relation is a fundamental auto-regulatory prope
78 owed us to identify two aspects of the
Frank-
Starling relation.
79 The
Frank-
Starling relationship is based, in part, on the length-t
80 dentified more than a century ago, the
Frank-
Starling relationship is currently known to involve leng
81 According to the
Frank-
Starling relationship, greater end-diastolic volume incr
82 According to the
Frank-
Starling relationship, increased ventricular volume incr
83 beta-arrestin signaling preserved the
Frank-
Starling relationship.
84 The
Frank-
Starling response contributes to the regulation of cardi
85 index as well as reinstitution of the
Frank-
Starling response to the native ventricle.
86 iastolic relaxation and fine-tunes the
Frank-
Starling response.
87 teraction between nitric oxide and the
Frank-
Starling response.
88 zed human cardiac tissue constructs
generate Starling curves, increasing their active force in respon
89 ermine osmotic and hydraulic conductivity
in Starling's equation, and whose expression is driven by a
90 are setting on the basis of perturbations
in Starling's equation, primarily as a result of increased
91 or detection of S. typhimurium in
inoculated Starling bird fecal samples and whole milk with detectio
92 We reaffirm the central role
of Starling's principle, which states that oedema formation
93 ume increased progressively from the
outset;
Starling and pressure-volume curves approached but did n
94 This results in a
steeper Starling relationship, which contributes to orthostatic
95 We tested the hypothesis
that Starling resistor forces render PAOP inaccurate as an in
96 The Starling curve of islet function describes the relations
97 s of the heart as a pump, including: (1)
the Starling mechanism whereby increased diastolic volume (E
98 Moreover, SV was reduced more and
the Starling curve was steeper during orthostatic stress aft
99 pressure characterized the steepness of
the Starling curve.
100 new approach to quantify the dynamics of
the Starling mechanism, namely the beat-to-beat modulation o
101 According to
the Starling fluid equilibrium, the ratio between the reflec
102 t capillary filtration is insensitive to
the Starling force interstitial osmotic pressure in frog mes
103 These results agree
with Starling's hypothesis relating the higher interstitial f