scholarly journals Corrigendum to “Technetium-99 m-PEGylated dendrimer-G2-(Dabcyle-Lys6,Phe7)-pHBSP: A novel Nano-Radiotracer for molecular and early detecting of cardiac ischemic region” [Bioorg. Chem. 98 (2020) 103731]

2020 ◽  
Vol 100 ◽  
pp. 103926
Author(s):  
Naser Mohtavinejad ◽  
Massoud Amanlou ◽  
Ahmad Bitarafan-Rajabi ◽  
Ali Khalaj ◽  
Ali Pormohammad ◽  
...  
Keyword(s):  
Ischemic Region

scholarly journals Anisotropic Elastography for Local Passive Properties and Active Contractility of Myocardium from Dynamic Heart Imaging Sequence

2006 ◽  
Vol 2006 ◽  
pp. 1-15 ◽  
Author(s):  
Yi Liu ◽  
Ge Wang ◽  
L. Z. Sun
Keyword(s):  
Mechanical Properties ◽  
Adjoint Method ◽  
Heart Diseases ◽  
Imaging Techniques ◽  
Chamber Pressure ◽  
Cardiac Imaging Techniques ◽  
Dynamic Displacement ◽  
Material Parameters ◽  
Ischemic Region ◽  
Imaging Sequence

Major heart diseases such as ischemia and hypertrophic myocardiopathy are accompanied with significant changes in the passive mechanical properties and active contractility of myocardium. Identification of these changes helps diagnose heart diseases, monitor therapy, and design surgery. A dynamic cardiac elastography (DCE) framework is developed to assess the anisotropic viscoelastic passive properties and active contractility of myocardial tissues, based on the chamber pressure and dynamic displacement measured with cardiac imaging techniques. A dynamic adjoint method is derived to enhance the numerical efficiency and stability of DCE. Model-based simulations are conducted using a numerical left ventricle (LV) phantom with an ischemic region. The passive material parameters of normal and ischemic tissues are identified during LV rapid/reduced filling and artery contraction, and those of active contractility are quantified during isovolumetric contraction and rapid/reduced ejection. It is found that quasistatic simplification in the previous cardiac elastography studies may yield inaccurate material parameters.

Ischemic Region Segmentation in Rat Heart Photos Using DRLSE Algorithm

2015 ◽  
pp. 209-218 ◽  
Author(s):  
Regina C. Coelho ◽  
Salety F. Baracho ◽  
Vinícius V. de Melo ◽  
José Gustavo P. Tavares ◽  
Carlos Marcelo G. de Godoy
Keyword(s):  
Rat Heart ◽  
Region Segmentation ◽  
Ischemic Region

scholarly journals Oxidative Stress Induction of DJ-1 Protein in Reactive Astrocytes Scavenges Free Radicals and Reduces Cell Injury

2009 ◽  
Vol 2 (1) ◽  
pp. 36-42 ◽  
Author(s):  
Takashi Yanagida ◽  
Jun Tsushima ◽  
Yoshihisa Kitamura ◽  
Daijiro Yanagisawa ◽  
Kazuyuki Takata ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Primary Cultures ◽  
Artery Occlusion ◽  
Reactive Astrocytes ◽  
Glutathione S Transferase ◽  
Triphenyltetrazolium Chloride ◽  
Ischemic Region

Astrocytes, one of the predominant types of glial cells, function as both supportive and metabolic cells for the brain. Under cerebral ischemia/reperfusion-induced oxidative conditions, astrocytes accumulate and activate in the ischemic region. DJ-1 has recently been shown to be a sensor of oxidative stress in living cells. However, the function of astrocytic DJ-1 is still unknown. In the present study, to clarify the effect of astrocytic DJ-1 protein under massive oxidative insult, we used a focal ischemic rat model that had been subjected to middle cerebral artery occlusion (MCAO) and reperfusion. We then investigated changes in the distribution of DJ-1 in astrocytes, DJ-1 release from cultured astrocytes, and the effects of recombinant DJ-1 protein on hydrogen peroxide (H2O2)-induced death in normal and DJ-1-knockdown SH-SY5Y cells and on in vitro scavenging of hydroxyl radicals (•OH) by electron spin resonance spectrometry. At 24 h after 2-h MCAO and reperfusion, an infarct lesion was markedly observed using magnetic resonance imaging and 2,3,5-triphenyltetrazolium chloride staining. In addition, reactive astrocytes enhanced DJ-1 expression in the penumbral zone of the ischemic core and that DJ-1 protein was extracellularly released from astrocytes by H2O2 in in vitro primary cultures. Although DJ-1-knockdown SH-SY5Y cells were markedly vulnerable to oxidative stress, treatment with glutathione S-transferase-tagged recombinant human DJ-1 protein (GST-DJ-1) significantly inhibited H2O2-induced cell death. In addition, GST-DJ-1 protein directly scavenged•OH. These results suggest that oxidative stress induces the release of astrocytic DJ-1 protein, which may contribute to astrocyte-mediated neuroprotection.

Effects of beta-blockade on regional myocardial flow and function during exercise

1984 ◽  
Vol 247 (1) ◽  
pp. H52-H60 ◽  
Author(s):  
M. Matsuzaki ◽  
J. Patritti ◽  
T. Tajimi ◽  
M. Miller ◽  
W. S. Kemper ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Wall Thickening ◽  
Ischemic Area ◽  
Ischemic Region ◽  
Exercise Induced ◽  
Control Exercise

We examined the effects of a cardioselective beta-blocking drug on exercise-induced regional myocardial ischemia in 10 conscious dogs with chronic coronary artery stenosis. An ameroid constrictor, Doppler flowprobe, and hydraulic cuff were placed around the left circumflex coronary artery, and left ventricular pressure (LVP), systolic wall thickening (% delta WT; by sonomicrometry), and myocardial blood flow (MBF; microspheres) were measured during control standing, control treadmill exercise, and identical exercise after atenolol (1 mg/kg po). Prior to study, in every dog % delta WT and MBF in the ischemic area were normal at rest, indicating collateral development. During control exercise, % delta WT in the ischemic region markedly decreased from 27 to 4%, and transmural ischemia was evident in that region. Heart rate, systolic LVP, and LV (+)dP/dt were significantly lower during exercise after atenolol than during control exercise. % delta WT in the normal area was only 81% of that during control exercise, but dysfunction in the ischemic area was improved (77% increase compared with control exercise). Accompanying the improved function was a significant increase of MBF/beat and relative MBF in the ischemic zone; the endocardial-to-epicardial ratio increased from 0.27 to 0.47. Thus atenolol improved regional MBF distribution, thereby diminishing exercise-induced regional myocardial dysfunction and accelerating its recovery.

Inhibitory effect of cardiac contraction on coronary collateral blood flow

1977 ◽  
Vol 233 (5) ◽  
pp. H541-H546 ◽  
Author(s):  
R. E. Russell ◽  
R. W. Chagrasulis ◽  
J. M. Downey
Keyword(s):  
Blood Flow ◽  
Left Coronary Artery ◽  
Constant Pressure ◽  
Inhibitory Effect ◽  
Cardiac Contraction ◽  
Collateral Blood Flow ◽  
Ischemic Region ◽  
Perfusion Apparatus ◽  
Collateral Vessels ◽  
Coronary Collateral Blood Flow

The present study was undertaken to determine the effect of contraction on overall flow in an area supplied by collateral vessels. Changes in the distribution of blood flow across the wall of ischemic and normally perfused regions of the left ventricle were observed during normal beating and during vagal arrest. The main left coronary artery was cannulated and perfused at constant pressure (125 mmHg) using a servo pump apparatus. An ischemic area supplied by collaterals was created by ligating the left anterior descending artery. Radiomicrospheres (15 micrometer) were injected into the perfusion apparatus during beating. Then spheres with a different label were administered to the same heart during arrest. The results revealed that beating caused a gradient of blood flow inhibition from near zero at the epicardium to about 50% at the endocardium in both zones. Inhibition to flow at the mid wall of the ischemic zone, 71%, was significantly greater than that seen at the corresponding depth in the normally perfused region, 33%. These results indicate that contraction not only inhibits collateral blood flow to an ischemic region, but also that the inhibition is actually magnified at the mid wall.

Detection of delayed ventricular activation on the body surface in dogs

1981 ◽  
Vol 241 (3) ◽  
pp. H363-H369 ◽  
Author(s):  
M. B. Simson ◽  
D. Euler ◽  
E. L. Michelson ◽  
R. A. Falcone ◽  
J. F. Spear ◽  
...  
Keyword(s):  
Body Surface ◽  
The Body ◽  
Acute Ischemia ◽  
Coronary Artery Ligation ◽  
Qrs Complex ◽  
Signal Averaging ◽  
Artery Ligation ◽  
Bipolar Electrodes ◽  
Ischemic Region ◽  
Ventricular Activation

This study describes a noninvasive method for detecting delayed ventricular activation, caused by ischemia, on the body surface. Signal averaging and a newly developed high-pass digital filter were used. The filter has the property that it does not create an artifact or ring after the QRS complex ends, thereby allowing the detection of microvolt-level potentials that occur immediately after the QRS complex. Eleven dogs were studied before and during acute ischemia induced by coronary artery ligation and latex embolization. The ischemic region was mapped with bipolar electrodes and, after the chest was rapidly closed, signal-averaged recordings were made from the body surface. Repeated cycles of ventricular mapping and signal averaging were performed. In each dog, delayed and fractionated electrograms were recorded directly from the ischemic epicardium that lasted a maximum of 118 +/- 18 ms after QRS onset. The duration of the ventricular electrograms varied with time. Whenever delayed epicardial electrograms were recorded, filtered signal-averaged leads showed microvolt-level potentials early in the S-T segment that were continuous with the QRS complex. The duration of ventricular activation, as measured from the bipolar electrograms and from the filtered signal-averaged leads, correlated well (r = 0.93, P less than 0.001). Because of the absence of filter ringing, low-level potentials could be detected less than 40 ms after the QRS complex ended. This study demonstrates that microvolt-level potentials arising from delayed ventricular activation can be reliably detected on the body surface, even when they occur just after the QRS complex.

Coronary sinus occlusion enhances coronary collateral flow and reduces subendocardial ischemia

2001 ◽  
Vol 280 (3) ◽  
pp. H1361-H1367 ◽  
Author(s):  
Akira Ido ◽  
Naoyuki Hasebe ◽  
Hironobu Matsuhashi ◽  
Kenjiro Kikuchi
Keyword(s):  
Blood Flow ◽  
Coronary Sinus ◽  
Regional Myocardial Blood Flow ◽  
Collateral Flow ◽  
Vasomotor Tone ◽  
Coronary Collateral ◽  
Intramyocardial Pressure ◽  
Ischemic Region ◽  
Coronary Collateral Flow ◽  
Anesthetized Dogs

On the hypothesis that coronary sinus occlusion (CSO) may reduce myocardial ischemia, we examined the effects of CSO on coronary collateral blood flow and on the distribution of regional myocardial blood flow (RMBF) in dogs. Thirty-eight anesthetized dogs underwent occlusion of the left anterior descending coronary artery with or without CSO and intact vasomotor tone. We measured RMBF and intramyocardial pressure (IMP) in the subendocardium (Endo) and subepicardium (Epi) separately. With intact vasomotor tone, CSO during ischemia significantly increased RMBF in the ischemic region (IR), particularly in Endo from 0.17 ± 0.03 to 0.33 ± 0.05 ml · min−1· g−1( P < 0.05), and increased the Endo/Epi from 0.59 ± 0.10 to 1.15 ± 0.15 ( P < 0.01). These effects of CSO were partially abolished by adenosine. However, the Endo/Epi was still increased from 0.90 ± 0.13 to 2.09 ± 0.30 ( P < 0.01). The changes in RMBF in IR were significantly correlated with the peak CS pressure during CSO. The Endo/Epi of IMP in IR was significantly decreased during CSO. In conclusion, CSO potentially enhances coronary collateral flow, and preserves the ischemic myocardium, especially in Endo.

Defining the mechanical border zone: a study in the pig heart

1985 ◽  
Vol 249 (1) ◽  
pp. H88-H94 ◽  
Author(s):  
K. Sakai ◽  
K. Watanabe ◽  
R. W. Millard
Keyword(s):  
Blood Flow ◽  
Wall Motion ◽  
Left Ventricular ◽  
Border Zone ◽  
Free Wall ◽  
Left Ventricular Free Wall ◽  
Ischemic Region ◽  
Wall Motion Abnormalities ◽  
Distal Border ◽  
Proximal Border

Wall motion abnormalities can occur in nonischemic areas contiguous with ischemic myocardium. The extent of the mechanical border zone contiguous with an acute myocardial ischemic region was mapped in eight open-chest anesthetized pigs using sonomicrometer crystals implanted parallel with the visible ischemic border in the subepicardium of ischemic (IZ), proximal border (BZ1), distal border (BZ2), and remote normal (NZ) zones. Regional systolic shortening fraction was near 15%, and epicardial blood flow was approximately 1.5 ml X min-1 X g-1 in all locations before ischemia was induced. Blood flow fell to less than 0.05 ml X min-1 X g-1 and the left ventricular free wall supplied by the distal one-third of the left anterior descending artery exhibited holosystolic lengthening when the vessel was occluded. After occlusion, systolic shortening fraction was depressed by 45% in the BZ1 located 3.1 +/- 1.1 mm from the ischemic margin and by 25% in the BZ2, which was measured at 9.3 +/- 1.5 mm from the ischemic margin without significant flow reduction. The NZ, 22.3 +/- 4.6 mm from ischemic margin, was unaffected by occlusion. Computer analysis of the data shows that wall motion is depressed as far as 12 mm from the ischemic margin. This abnormal wall motion surrounding focal transmural myocardial ischemia is presumed to result from mechanical tethering.

Effect of acute regional ischemia on pressure in the subepicardium and subendocardium

1982 ◽  
Vol 242 (2) ◽  
pp. H240-H244 ◽  
Author(s):  
H. N. Sabbah ◽  
P. D. Stein
Keyword(s):  
Diastolic Pressure ◽  
Control Period ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Ventricular Systolic Pressure ◽  
Intramyocardial Pressure ◽  
Ischemic Region ◽  
Catheter Tip ◽  
Extravascular Resistance

The effects of acute ischemia on regional intramyocardial pressure were studied in eight open-chest dogs. Aortic, left ventricular, subepicardial, and subendocardial pressures were measured with catheter-tip micromanometers. During the control period subendocardial pressure during systole (180 +/- 13 mmHg; mean +/- SE) was higher than left ventricular intracavitary pressure (137 +/- 9 mmHg; P less than 0.001). Subepicardial pressure during systole was lower (95 +/- 6 mmHg; P less than 0.001). Acute ischemia caused a reduction of subendocardial pressure during systole to levels below left ventricular systolic pressure (92 +/- 7 mmHg vs. 116 +/- 6 mmHg; P less than 0.01). Ischemia also caused a reduction of systolic subepicardial pressure to 67 +/- 2 mmHg (P less than 0.001). After reperfusion all pressures returned nearly to control values. During diastole subendocardial pressure during the control period (13 +/- 1 mmHg) was high than left ventricular end-diastolic pressure (6 +/- 1 mmHg; P less than 0.001). Subepicardial pressure during diastole (29 +/- 2 mmHg) was higher than subendocardial pressure and left ventricular end-diastolic pressure (P less than 0.001). Acute ischemia had little or no effect on subendocardial pressure during diastole, whereas it caused a reduction of subepicardial diastolic pressure to 16 +/- 1 mmHg (P less than 0.001). Reperfusion of the ischemic region caused a return of all diastolic pressures nearly to control values. These observations indicate that coronary extravascular resistance is affected by ischemia and that the most prominent effects are in the subendocardium during systole and in the subepicardium during diastole.

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