INT38255

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Context Info
Confidence 0.80
First Reported 1986
Last Reported 2011
Negated 0
Speculated 0
Reported most in Abstract
Documents 32
Total Number 32
Disease Relevance 10.98
Pain Relevance 11.07

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytoplasm (Chkb)
Anatomy Link Frequency
hearts 7
plasma 2
paw 2
tubes 1
myocardium 1
Chkb (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Enkephalin 8 100.00 Very High Very High Very High
narcan 2 99.70 Very High Very High Very High
Calcitonin gene-related peptide 79 99.58 Very High Very High Very High
lidocaine 24 99.54 Very High Very High Very High
ischemia 118 99.24 Very High Very High Very High
antagonist 11 98.72 Very High Very High Very High
qutenza 21 97.20 Very High Very High Very High
Central nervous system 3 97.00 Very High Very High Very High
Opioid 36 92.72 High High
opioid receptor 5 92.68 High High
Disease Link Frequency Relevance Heat
Heat Stress Disorders 28 99.84 Very High Very High Very High
Contracture 2 99.82 Very High Very High Very High
Coronary Artery Disease 24 99.24 Very High Very High Very High
Fever 12 99.20 Very High Very High Very High
Cv Unclassified Under Development 101 99.02 Very High Very High Very High
Injury 47 98.96 Very High Very High Very High
Apoptosis 37 98.96 Very High Very High Very High
Arrhythmias 2 Under Development 25 98.34 Very High Very High Very High
Hypoxia 64 98.12 Very High Very High Very High
Myocardial Infarction 26 90.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Complete interruption of the coronary perfusion led to the release of only small CK activities during subsequent coronary reperfusion, whereas the metabolic alterations were more distinct than in fibrillating hearts.
Localization (release) of CK in hearts
1) Confidence 0.80 Published 1986 Journal Basic Res. Cardiol. Section Abstract Doc Link 3741357 Disease Relevance 0.41 Pain Relevance 0.12
When a relative ischemia was induced by perfusion at a low pressure, the CK release from fibrillating hearts was not greater, but less than at a higher perfusion pressure.
Localization (release) of CK in hearts associated with ischemia
2) Confidence 0.80 Published 1986 Journal Basic Res. Cardiol. Section Abstract Doc Link 3741357 Disease Relevance 0.50 Pain Relevance 0.12
In isolated perfused rat hearts ventricular fibrillation (VF), elicited electrically and persisting further spontaneously, led to an extensive release of creatine kinase (CK).
Localization (release) of CK in hearts associated with arrhythmias 2 under development
3) Confidence 0.80 Published 1986 Journal Basic Res. Cardiol. Section Abstract Doc Link 3741357 Disease Relevance 0.40 Pain Relevance 0.04
It appeared unlikely, therefore, that the CK release from fibrillating hearts was simply due to an oxygen deficiency, although a decrease of ATP and glycogen, and an increase of glucose-6-phosphate and lactate in the myocardium were found.
Localization (release) of CK in myocardium associated with hypoxia
4) Confidence 0.80 Published 1986 Journal Basic Res. Cardiol. Section Abstract Doc Link 3741357 Disease Relevance 0.50 Pain Relevance 0.13
In contrast, the CK release was only very small in hearts which were stimulated permanently with rhythmic impulses of 10 Hz, whereas the increase in coronary flow and oxygen consumption was significantly greater.
Localization (release) of CK in hearts
5) Confidence 0.80 Published 1986 Journal Basic Res. Cardiol. Section Abstract Doc Link 3741357 Disease Relevance 0.46 Pain Relevance 0.04
Lidocaine also protects against CK release in the Ca(2+)-paradox when present only during Ca(2+)-reperfusion.
Localization (release) of CK associated with lidocaine
6) Confidence 0.78 Published 1996 Journal Pathobiology Section Abstract Doc Link 9031331 Disease Relevance 0 Pain Relevance 0.53
Lidocaine protected against creatine kinase (CK) release when perfused throughout or only during the priming stage in all three protocols.
Localization (release) of CK associated with lidocaine
7) Confidence 0.78 Published 1996 Journal Pathobiology Section Abstract Doc Link 9031331 Disease Relevance 0 Pain Relevance 0.51
But the contracture and the release of CK were suppressed with the omission of Ca ion.
Localization (release) of CK associated with contracture
8) Confidence 0.77 Published 1986 Journal Nippon Seikeigeka Gakkai Zasshi Section Abstract Doc Link 3722966 Disease Relevance 0.27 Pain Relevance 0.07
In the vehicle group, myocardial ischemia-reperfusion induced creatine kinase (CK) release and caused cardiomyocyte apoptosis, as evidenced by DNA ladder formation and terminal dUTP deoxynucleotidyltransferase nick end-labeling (TUNEL) staining.
Localization (release) of CK in cardiomyocyte associated with coronary artery disease, ischemia and apoptosis
9) Confidence 0.75 Published 2006 Journal Life Sci. Section Abstract Doc Link 16647091 Disease Relevance 0.78 Pain Relevance 0.21
Antidromic stimulation of sectioned sciatic and saphenous nerves did not have any significant effect on the release of Met-enkephalin (Met-EK), while immersion of the hind paw in hot water (47 degrees C) for 30 min caused an increase in Met-EK release into the perfusate.
Localization (release) of Met-EK in paw associated with enkephalin
10) Confidence 0.74 Published 1993 Journal Regul. Pept. Section Abstract Doc Link 8278628 Disease Relevance 0.15 Pain Relevance 0.81
Antidromic stimulation of sectioned sciatic and saphenous nerves did not have any significant effect on the release of Met-enkephalin (Met-EK), while immersion of the hind paw in hot water (47 degrees C) for 30 min caused an increase in Met-EK release into the perfusate.
Localization (release) of Met-EK in paw associated with enkephalin
11) Confidence 0.74 Published 1993 Journal Regul. Pept. Section Abstract Doc Link 8278628 Disease Relevance 0.17 Pain Relevance 0.80
High-pressure liquid chromatography of the perfusate revealed that noxious heat stimulation induced increase in release of Leu-enkephalin (Leu-EK) as well as Met-EK, although the maximal concentration of Leu-EK was less than 16% of that of Met-EK.
Localization (release) of Leu-EK associated with enkephalin
12) Confidence 0.74 Published 1993 Journal Regul. Pept. Section Abstract Doc Link 8278628 Disease Relevance 0.14 Pain Relevance 0.80
Lidocaine protects against myofilament damage in the Ca(2+)-paradox but not in the O2-paradox and caffeine protocols, even though CK release is inhibited.
Localization (release) of CK associated with lidocaine
13) Confidence 0.68 Published 1996 Journal Pathobiology Section Abstract Doc Link 9031331 Disease Relevance 0 Pain Relevance 0.52
Sixty minutes of left coronary artery occlusion and followed by 60 min of reperfusion caused a significant decrease in cardiac function and a significant increase in creatine kinase (CK) release and infarct size.
Localization (release) of CK in left coronary artery
14) Confidence 0.61 Published 2008 Journal Regul. Pept. Section Abstract Doc Link 18166234 Disease Relevance 0.09 Pain Relevance 0.48
Postconditioning with three cycles of 1-min ischemia and 1-min reperfusion produced a marked improvement of cardiac function and decreased CK release and infarct size, concomitantly with an increase in the release of CGRP release in coronary effluent.
Localization (release) of CK associated with ischemia and calcitonin gene-related peptide
15) Confidence 0.61 Published 2008 Journal Regul. Pept. Section Abstract Doc Link 18166234 Disease Relevance 0.10 Pain Relevance 0.62
Heart rate, coronary flow, left ventricular pressure, and its first derivative (+/- dp/dtmax) were recorded, and the calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) and the release of creatine kinase (CK) were measured.
Localization (release) of CK in Heart
16) Confidence 0.57 Published 1999 Journal Zhongguo Yao Li Xue Bao Section Body Doc Link 11270991 Disease Relevance 0 Pain Relevance 0
Hyperthermia treatment significantly reduced infarct size and CK release concomitantly with a dramatic increase in plasma concentrations of CGRP and the expression of alpha-CGRP mRNA, but not beta-CGRP mRNA, which was completely abolished by pretreatment with capsazepine (38 mg/kg, s.c.), a competitive vanilloid receptor 1 antagonist.
Localization (release) of CK in plasma associated with antagonist, fever and calcitonin gene-related peptide
17) Confidence 0.55 Published 2003 Journal Neuropeptides Section Abstract Doc Link 12906841 Disease Relevance 0.48 Pain Relevance 0.44
Lactate was lowest in the HTK group, CK and LDH releases in the effusate remained lowest after HTK and NIH preservation.
Localization (releases) of CK
18) Confidence 0.53 Published 1998 Journal Eur Surg Res Section Abstract Doc Link 9704750 Disease Relevance 0.12 Pain Relevance 0.08
Pretreatment with hyperthermia significantly reduced infarct size and CK release.
Localization (release) of CK associated with fever
19) Confidence 0.53 Published 2002 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 12060099 Disease Relevance 0.75 Pain Relevance 0.69
The inactive isomer L-naloxone decreased the CK release by half.
Localization (release) of CK associated with narcan
20) Confidence 0.52 Published 2000 Journal Ross Fiziol Zh Im I M Sechenova Section Abstract Doc Link 10808507 Disease Relevance 0.07 Pain Relevance 0.58

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