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 results of PCI and non-obstructive causes of myocardial ischaemia.
2 tamine stress in the presence and absence of myocardial ischaemia.
3 stress echocardiography to detect or exclude myocardial ischaemia.
4 terization of atherosclerosis in relation to myocardial ischaemia.
5 n of Hand1 is protective in a mouse model of myocardial ischaemia.
6 ors released from activated platelets during myocardial ischaemia.
7 ardiac spinal afferents are activated during myocardial ischaemia.
8 n progress in some disease states, including myocardial ischaemia.
9 n and T wave changes characteristic of acute myocardial ischaemia.
10 cardiogenic sympathoexcitatory reflex during myocardial ischaemia.
11 e therapy using angiogenic growth factors in myocardial ischaemia.
12 l cultures, and protects mice from prolonged myocardial ischaemia.
13 g gross distension, possibly associated with myocardial ischaemia.
14 c acid production is associated closely with myocardial ischaemia.
15 cardiac sympathetic C-fibre afferents during myocardial ischaemia.
16 fied according to their response to 5 min of myocardial ischaemia.
17 ts (i.e. prostaglandins (PGs)) occurs during myocardial ischaemia.
18 ception to the central nervous system during myocardial ischaemia.
19  procedural complications or evidence of new myocardial ischaemia.
20 cise testing (CPET) has been associated with myocardial ischaemia.
21 on may decrease the work of the heart during myocardial ischaemia.
22 tile dysfunction that follows brief bouts of myocardial ischaemia.
23 cardial coronary artery obstruction, causing myocardial ischaemia (a mismatch between myocardial bloo
24                We conclude that during early myocardial ischaemia, a major component of [K+]o accumul
25                                              Myocardial ischaemia activates blood platelets and cardi
26                                              Myocardial ischaemia activates blood platelets, which in
27                                              Myocardial ischaemia activates cardiac sympathetic affer
28 n of p38-MAPK by dual phosphorylation during myocardial ischaemia aggravates lethal injury.
29 ne the relationship between CPET parameters, myocardial ischaemia and anginal symptoms in patients wi
30 gical process relies on clinical evidence of myocardial ischaemia and biomarker evidence of myocardia
31 d limitations for each test in investigating myocardial ischaemia and discusses a comprehensive algor
32 ated tool for the non-invasive evaluation of myocardial ischaemia and enables the recording of heart
33 ddition to stress test findings on inducible myocardial ischaemia and exercise capacity.
34 rfusion are the most effective ways to limit myocardial ischaemia and infarct size and thereby reduce
35 e patients aged 18-85 years with evidence of myocardial ischaemia and one or two de-novo native lesio
36 e patients aged 18-85 years with evidence of myocardial ischaemia and one or two de-novo native lesio
37 oxygen-pulse plateau detects the severity of myocardial ischaemia and predicts the placebo-controlled
38                                        Acute myocardial ischaemia and reperfusion (I-R) are major cau
39                                       During myocardial ischaemia and reperfusion, tirofiban, a speci
40 monizes different pathophysiologic causes of myocardial ischaemia and should result in more refined d
41                    These findings show acute myocardial ischaemia and subacute myocardial microinfarc
42                                    Events of myocardial ischaemia and venous thromboembolism can be p
43 detected in cardiomyopathies, heart failure, myocardial ischaemia, and hypertrophy.
44 de in obtunding cardiovascular responses and myocardial ischaemia, and the provision of effective per
45                     We have focused on acute myocardial ischaemia as it is the most strikingly proarr
46  depletion of cellular energy reserves (e.g. myocardial ischaemia), ATP generated from glycolysis may
47 undergone coronary angiography for suspected myocardial ischaemia between 1st January 2011 and 31st D
48  most widely used test for the assessment of myocardial ischaemia, but its diagnostic accuracy is rep
49 fication of pathophysiological parameters of myocardial ischaemia can be achieved.
50  from clinical studies on oxygen therapy for myocardial ischaemia, cardiac arrest, heart failure and
51 tion of cardiac sympathetic afferents during myocardial ischaemia causes angina and induces important
52                                              Myocardial ischaemia causes the release of metabolites s
53                            In the absence of myocardial ischaemia, dobutamine stress is associated wi
54           The dose-limiting toxic effect was myocardial ischaemia due to excessive prolongation of sy
55  stable CAD patients with moderate or severe myocardial ischaemia enrolled in ISCHEMIA, an initial IN
56           Using a non-human primate model of myocardial ischaemia followed by reperfusion, we show th
57 sed the activity of cardiac afferents during myocardial ischaemia from 1.5 +/- 0.4 to 0.8 +/- 0.4 imp
58 etermined whether individuals with transient myocardial ischaemia had different autonomic responses t
59 h usually causes cell volume changes, during myocardial ischaemia, hypertrophy and heart failure.
60 Incremental atrial pacing was used to induce myocardial ischaemia in 18 patients with coronary artery
61 ) activity and LV remodelling in response to myocardial ischaemia in vivo.
62 us studies have shown that a brief period of myocardial ischaemia increases endothelin in cardiac ven
63  study was to test the hypothesis that acute myocardial ischaemia increases QT dispersion measured fr
64               These results demonstrate that myocardial ischaemia induced by incremental atrial pacin
65  sensitive cardiac visceral afferents during myocardial ischaemia induces both angina and cardiovascu
66 utamine stress is augmented as the burden of myocardial ischaemia is increased.
67                         Chest pain caused by myocardial ischaemia is mediated by cardiac sympathetic
68 g the precise mechanism of activation during myocardial ischaemia is of considerable importance, sinc
69            Responses of cardiac afferents to myocardial ischaemia, lactic acid, sodium lactate, acidi
70 inistration of ET-1 (n = 7) and to recurrent myocardial ischaemia (n = 7).
71 istration of U46619 (n = 6) and to recurrent myocardial ischaemia (n = 7).
72 onymized electronic medical records from the Myocardial Ischaemia National Audit Project and the Gene
73 tistics for National Health Service England, Myocardial Ischaemia National Audit Project and the Offi
74 05 and 31 March 2019 was derived from the UK Myocardial Ischaemia National Audit Project and the UK H
75  in England and Wales were obtained from the Myocardial Ischaemia National Audit Project between Janu
76  propensity score analyses, of data from the Myocardial Ischaemia National Audit Project for patients
77 nal English and Welsh registry data from the Myocardial Ischaemia National Audit Project.
78 NT] 63) and decrease (OR 0.36, 0.26-0.50) in myocardial ischaemia (NNT 16) at the expense of an incre
79 depletion and Ca(2+) overload occur, such as myocardial ischaemia or anoxia.
80 hich frequently occur in patients with acute myocardial ischaemia or heart failure - can have an infl
81 anisms and the relevance of these results to myocardial ischaemia or hypoxia is considered.
82                                        While myocardial ischaemia plays a major role in the pathogene
83 sure its efficacy, compared with placebo, on myocardial ischaemia reduction and symptom improvement.
84                         The PROVE IT and the Myocardial Ischaemia Reduction with Aggressive Cholester
85 cture that can be selectively removed during myocardial ischaemia reperfusion by mu-calpain proteolys
86 arrow transfer chimeric mice underwent MI or myocardial ischaemia-reperfusion (IR).
87  been evaluated for its efficacy in treating myocardial ischaemia-reperfusion injury in an ex vivo ro
88 ascular thrombosis to protect the heart from myocardial ischaemia-reperfusion injury in ApoE-/- mice.
89 ctive effects of short-term exercise against myocardial ischaemia-reperfusion injury in male and fema
90 nning and hibernation result from reversible myocardial ischaemia-reperfusion injury, and contractile
91 g processes in atherosclerosis, vascular and myocardial ischaemia-reperfusion injury, and heart failu
92 ith various CVDs, including atherosclerosis, myocardial ischaemia-reperfusion injury, cardiac hypertr
93  This Review revisits the pathophysiology of myocardial ischaemia-reperfusion injury, including the r
94 atherosclerosis, drug-induced heart failure, myocardial ischaemia-reperfusion injury, sepsis-induced
95 patient that experiences an episode of acute myocardial ischaemia-reperfusion injury.
96 en peroxide at mild concentrations mitigates myocardial ischaemia-reperfusion-induced functional decl
97 ement activation is a recognised mediator of myocardial ischaemia-reperfusion-injury (IRI) and cardio
98    Fasting increases susceptibility to acute myocardial ischaemia/reperfusion injury (IRI) but the me
99  p38-MAPK pathway plays an important role in myocardial ischaemia/reperfusion injury and has been imp
100                                              Myocardial ischaemia resulting from obstructive coronary
101 rction, non-fatal stroke, heart failure, and myocardial ischaemia, safety outcomes of perioperative b
102                              Five minutes of myocardial ischaemia stimulated all 38 cardiac afferents
103                              Five minutes of myocardial ischaemia stimulated all 39 cardiac afferents
104                                Biomarkers of myocardial ischaemia, such as troponins and electrocardi
105 ex sensitivity is a strong indicator of post-myocardial ischaemia survival and is variable among indi
106 ive and non-obstructive causes of angina and myocardial ischaemia that fosters conceptual clarity and
107              These data indicate that during myocardial ischaemia the activated platelets stimulate c
108                 However, under conditions of myocardial ischaemia, there was a directionally opposite
109 es to activation of cardiac afferents during myocardial ischaemia through direct stimulation of ET(A)
110 o the activation of cardiac afferents during myocardial ischaemia through direct stimulation of TP re
111 ersely, for chronic stable manifestations of myocardial ischaemia, various classifications have emerg
112 cardiogram (ECG) and imaging evidence of new myocardial ischaemia, we propose the same post-PCI cTn c

 
Page Top