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 This review, which arose from the
Bayliss-
Starling Prize Lecture, focuses on the basic development
11 This process is driven
by Starling forces determined by hydrostatic and osmotic pr
12 r= 0.59, n= 28, P < 0.001), as predicted
by Starling's law of filtration.
13 otential using the Boublik-Mansoori-
Carnahan-
Starling-Leland (BMCSL) model, which treats ions as hard
14 A modified
Carnahan-
Starling hard-sphere model was utilized to fit the exper
15 s with right heart catheterization to
define Starling and left ventricular (LV) pressure-volume curve
16 t pulmonary artery catheterization to
define Starling and left ventricular pressure-volume curves.
17 h pulmonary artery catheterization to
define Starling and LV pressure-volume curves; secondary functi
18 vascular regulation by enhancing the
dynamic Starling mechanism and arterial-cardiac baroreflex sensi
19 vascular regulation by enhancing the
dynamic Starling mechanism and arterial-cardiac baroreflex sensi
20 After 2 years, the
dynamic Starling mechanism gain (Group x Time interaction: P = 0
21 The
dynamic Starling mechanism gain and arterial-cardiac baroreflex
22 These findings suggest that the
dynamic Starling mechanism is impaired with human ageing possibl
23 We hypothesized that the
dynamic Starling mechanism would be impaired with ageing, and th
24 lar function, which incorporates the
dynamic Starling mechanism, dynamic arterial elastance and arter
25 The
dynamic Starling mechanism, dynamic arterial elastance and arter
26 Our method incorporated the
dynamic Starling mechanism, dynamic arterial elastance and arter
27 e and SV was used as an index of the
dynamic Starling mechanism.
28 William Bayliss and
Ernest Starling are not only famous as pioneers in cardiovascul
29 re promulgated by William Bayliss and
Ernest Starling.
30 ition in a species of songbird, the
European Starling (Sturnus vulgaris), using tone sequences that v
31 tes losses and gains in a bird, the
European Starling, to test the implication of SUT that risk prone
32 y venous resistance, are strong evidence
for Starling resistor forces (venocompression) rather than a
33 re located on the flatter portion of a
Frank-
Starling curve because of attenuated decreases in SV per
34 re located on the steeper portion of a
Frank-
Starling curve because of augmented decreases in SV per
35 is operating on a steeper portion of a
Frank-
Starling curve.
36 a altering the operating position on a
Frank-
Starling curve.
37 n 2, or AT1R were unable to generate a
Frank-
Starling force in response to changes in cardiac volume.
38 ese data support the hypothesis that a
Frank-
Starling mechanism contributes to compromised blood pres
39 These data suggest that a
Frank-
Starling mechanism may contribute to improvements in ort
40 neoaortic stroke volume demonstrated a
Frank-
Starling-like curve that shifted upward after HF.
41 e LV pressure-volume relationships and
Frank-
Starling curves.
42 ed over a range of loading conditions (
Frank-
Starling curve).
43 plicates a novel means for controlling
Frank-
Starling relationships.
44 e engineered human myocardium exhibits
Frank-
Starling-type force-length relationships.
45 cyte active stiffness and by extension
Frank-
Starling reserve in human heart failure.
46 L) is, in part, the cellular basis for
Frank-
Starling's law of the heart.
47 asurement apparatus exhibited a robust
Frank-
Starling response to external stretch, and a dose-depend
48 ociated with movement along the septal
Frank-
Starling equivalent (septal output versus end-diastolic
49 o a flatter portion of the heat stress
Frank-
Starling curve thereby attenuating the reduction in SV d
50 o a flatter portion of the heat stress
Frank-
Starling curve.
51 cMyBP-C can influence the SL-tension (
Frank-
Starling) relationship in cardiac muscle.
52 We demonstrate that
Frank-
Starling is evident at maximal [Ca(2+) ] activation and
53 The
Frank-
Starling 'law of the heart' is implicated in certain typ
54 ation (LDA), the cellular basis of the
Frank-
Starling cardiac regulatory mechanism.
55 We demonstrate the
Frank-
Starling effect at the single cardiomyocyte level by sho
56 ntain a high ejection fraction via the
Frank-
Starling effect.
57 t contractile forces that followed the
Frank-
Starling law and accepted physiological pacing.
58 The
Frank-
Starling law and Anrep effect describe two intrinsic mec
59 The
Frank-
Starling law and the Anrep effect describe exquisite int
60 g will deepen our understanding of the
Frank-
Starling law and the Anrep effect, and also provide a un
61 phosphorylation as a modulator of the
Frank-
Starling law in the heart.
62 The
Frank-
Starling law of the heart is a physiological phenomenon
63 that these effects play a role in the
Frank-
Starling law of the heart.
64 ardiac regulatory mechanisms, like the
Frank-
Starling law of the heart.
65 sequently the mechanism underlying the
Frank-
Starling law of the heart.
66 cellular mechanism responsible for the
Frank-
Starling law of the heart.
67 but also because it contributes to the
Frank-
Starling law, a mechanism by which the heart increases s
68 on (LDA), the mechanism underlying the
Frank-
Starling Law.
69 The
Frank-
Starling mechanism allows the amount of blood entering t
70 (a) The
Frank-
Starling mechanism and Anrep effect are dynamically link
71 ural unit of the cardiac myocytes, the
Frank-
Starling mechanism consists of the increase in active fo
72 ible therapeutic target to restore the
Frank-
Starling mechanism in patients with heart failure.
73 al stretch serves as the basis for the
Frank-
Starling mechanism in the heart.
74 0.005), confirming the presence of the
Frank-
Starling mechanism in the LA.
75 Reconstitution of the
Frank-
Starling mechanism is an important milestone for produci
76 the giant elastic protein titin in the
Frank-
Starling mechanism of the heart by measuring the sarcome
77 titin may be a factor involved in the
Frank-
Starling mechanism of the heart by promoting actomyosin
78 The
Frank-
Starling mechanism of the heart is due, in part, to modu
79 a2(+) sensitivity, contributing to the
Frank-
Starling Mechanism of the heart.
80 these two proteins are involved in the
Frank-
Starling mechanism of the heart.
81 e-tuning of cardiac performance by the
Frank-
Starling mechanism that relates the pressure exerted by
82 The
Frank-
Starling Mechanism was reduced in a graded fashion in Rb
83 ress, thereby obscuring the use of the
Frank-
Starling mechanism, a fundamental mechanism by which the
84 According to the
Frank-
Starling mechanism, as the heart is stretched, it increa
85 hECTs reconstituted the
Frank-
Starling mechanism, generating an average maximum twitch
86 ng-binding cross-bridges underlies the
Frank-
Starling mechanism, we inhibited force and strong cross-
87 T1R as key regulatory molecules in the
Frank-
Starling mechanism, which potentially can be targeted th
88 task, revealing a prime aspect of the
Frank-
Starling mechanism.
89 s and regulates cardiac output via the
Frank-
Starling mechanism.
90 rrelation between titin strain and the
Frank-
Starling mechanism.
91 filament activation contributes to the
Frank-
Starling mechanism.
92 neural and hormonal factors and by the
Frank-
Starling mechanism.
93 resulting in better utilization of the
Frank-
Starling mechanism.
94 an exercise-induced modulation of the
Frank-
Starling mechanism.
95 ta-adrenergic stimulation enhances the
Frank-
Starling regulatory mechanism predominantly via cMyBP-C
96 The
Frank-
Starling relation is a fundamental auto-regulatory prope
97 owed us to identify two aspects of the
Frank-
Starling relation.
98 nger contraction in the next beat- the
Frank-
Starling relation.
99 The
Frank-
Starling relationship is based, in part, on the length-t
100 dentified more than a century ago, the
Frank-
Starling relationship is currently known to involve leng
101 According to the
Frank-
Starling relationship, greater end-diastolic volume incr
102 According to the
Frank-
Starling relationship, increased ventricular volume incr
103 beta-arrestin signaling preserved the
Frank-
Starling relationship.
104 The
Frank-
Starling response contributes to the regulation of cardi
105 index as well as reinstitution of the
Frank-
Starling response to the native ventricle.
106 teraction between nitric oxide and the
Frank-
Starling response.
107 iastolic relaxation and fine-tunes the
Frank-
Starling response.
108 zed human cardiac tissue constructs
generate Starling curves, increasing their active force in respon
109 ermine osmotic and hydraulic conductivity
in Starling's equation, and whose expression is driven by a
110 are setting on the basis of perturbations
in Starling's equation, primarily as a result of increased
111 or detection of S. typhimurium in
inoculated Starling bird fecal samples and whole milk with detectio
112 We used the Thevenin model
of Starling resistors to represent the intra-extra-cranial
113 We reaffirm the central role
of Starling's principle, which states that oedema formation
114 ume increased progressively from the
outset;
Starling and pressure-volume curves approached but did n
115 This results in a
steeper Starling relationship, which contributes to orthostatic
116 We tested the hypothesis
that Starling resistor forces render PAOP inaccurate as an in
117 The Starling curve of islet function describes the relations
118 s of the heart as a pump, including: (1)
the Starling mechanism whereby increased diastolic volume (E
119 Moreover, SV was reduced more and
the Starling curve was steeper during orthostatic stress aft
120 pressure characterized the steepness of
the Starling curve.
121 new approach to quantify the dynamics of
the Starling mechanism, namely the beat-to-beat modulation o
122 According to
the Starling fluid equilibrium, the ratio between the reflec
123 t capillary filtration is insensitive to
the Starling force interstitial osmotic pressure in frog mes
124 These results agree
with Starling's hypothesis relating the higher interstitial f
125 tic pressures, which were then combined
with Starling's law to predict transmural flow.