Morphofunctional Feature in Experimental Myocardial Damage Heart on the Background of Diabetes and Cytoprotector

10.12737/2735 ◽  
2013 ◽  
Vol 20 (4) ◽  
pp. 78-82
Author(s):  
Блинов ◽  
Dmitry Blinov ◽  
Елизарова ◽  
Yu. Elizarova ◽  
Сингх ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Myocardial Hypertrophy ◽  
Water Solution ◽  
Venous Blood ◽  
Myocardial Damage ◽  
Acute Ischemia ◽  
Insulin Dependent ◽  
Prolonged Immobilization ◽  
Destructive Processes ◽  
Ischemic Stress

The article highlights the experiments on white mice and purebred cats, which simulated insulin-dependent diabetes by intra-abdominal injection of water solution streptozotocin in the dose of 15 mg/kg, which destroys (3-cells of the pancreas within 14 days and leads to increased blood glucose animals by 70-80% compared with intact animals. In the experiment, the authors studied the derivative of L-glutamic acid deanol aceglumate at the preventive intragastric introduction, which showed the presence of cardioprotec-tive effect in the animals with ischemic, stress and metabolic damage to the heart. This was expressed in the reduction of deaths mice with diabetes subjected to 25% immobilization stress in the period of 28 days, and in improving the adaptation of animals to prolonged immobilization. The data obtained are confirmed by the absence of reducing the weight of the animals during the experiment, an obstacle to development of relative and absolute myocardial hypertrophy, lack of pronouced destructive processes in the contractile car-diomyocytes left stomach animals, increased life expectancy, animals when modeling adrenaline micronecrosis in mice with diabetes, improving gas and acid-base composition of venous blood outflow from ischemia heart cats with acute ischemia and diabetes.

scholarly journals Influence of dibornol-HES on electrophysiological parameters in the period of restoration of blood flow in rabbit myocardium

2018 ◽  
Vol 17 (4) ◽  
pp. 6-15
Author(s):  
M. A. Vaykshnorayte ◽  
V. A. Vityazev ◽  
N. A. Vahnina ◽  
V. D. Shadrina ◽  
M. A. Torlopov ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Occlusion ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Water Soluble ◽  
Control Group ◽  
Acute Ischemia ◽  
30Th Minute ◽  
Dispersion Of Repolarization ◽  
Experimental Group

Objective. Dibornol-HES, a water-soluble drug based on the derivative of 2,6-diisobornyl-4-methylphenol Dibornol conjugated with hydroxyethyl starch, can reduce the occurrence and severity of arrhythmias by preventive intravenous administration, but it is unknown whether the drug could reduce the myocardial arrhythmogenicity once ischemia has developed at the developed ischemia.Materials and methods. In the model of acute ischemia / reperfusion of the rabbit heart, the effect of Dibornol-HEC (80 mg/kg body weight of the animal) on the electrophysiological indices characterizing myocardial arrhythmogenicity (global and border dispersion of repolarization) was studied during the restoration of blood flow. In the model of acute ischemia / reperfusion with 64 unipolar epicardial leads, the activation-recovery intervals were measured and global and border dispersion of repolarization in the native rabbits (control group, n = 9) and in the rabbits treated by Dibornol-HES (on the 25th minute of occlusion, the experimental group, n = 6).Results. The introduction of Dibornol-HES did not lead to a change in the electrocardiographic parameters of rabbits. By the 30th minute of the coronary occlusion on the ECG in the animals of the control and the experimental groups, the intervals RR, QT, QTc were shortened (p < 0.05). In the animals of both groups by the 30th minute of coronary occlusion, the global dispersion of repolarization increased (p < 0.05), the boundary dispersion of repolarization also increased (p < 0.05), due to the decrease in the duration of the activation-recovery intervals in the ischemic zone (p < 0.05). During the 30-minute reperfusion the magnitude of the global dispersion of repolarization did not change in animals of the both groups, and the magnitude of the border dispersion of repolarization in the control rabbits decreased (p < 0.05), while in the rabbits treated by Dibornol-HES the border dispersion of repolarization did not changed.Conclusion. In rabbits of the experimental group, the values of the global and border dispersions of repolarization did not differ from those of the animals in the control group. Therefore, the administration to Dibornol-HES just prior to reperfusion does not lead to the decrease in the dispersion of repolarization increased as a result of acute ischemic myocardial damage.

IKKβ inhibition attenuates myocardial injury and dysfunction following acute ischemia-reperfusion injury

2007 ◽  
Vol 293 (4) ◽  
pp. H2248-H2253 ◽  
Author(s):  
Nancy C. Moss ◽  
William E. Stansfield ◽  
Monte S. Willis ◽  
Ru-Hang Tang ◽  
Craig H. Selzman
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Nuclear Factor Κb ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Artery Ligation ◽  
Cardiac Morbidity

Despite years of experimental and clinical research, myocardial ischemia-reperfusion (IR) remains an important cause of cardiac morbidity and mortality. The transcription factor nuclear factor-κB (NF-κB) has been implicated as a key mediator of reperfusion injury. Activation of NF-κB is dependent upon the phosphorylation of its inhibitor, IκBα, by the specific inhibitory κB kinase (IKK) subunit, IKKβ. We hypothesized that specific antagonism of the NF-κB inflammatory pathway through IKKβ inhibition reduces acute myocardial damage following IR injury. C57BL/6 mice underwent left anterior descending (LAD) artery ligation and release in an experimental model of acute IR. Bay 65-1942, an ATP-competitive inhibitor that selectively targets IKKβ kinase activity, was administered intraperitoneally either prior to ischemia, at reperfusion, or 2 h after reperfusion. Compared with untreated animals, mice treated with IKKβ inhibition had significant reduction in left ventricular infarct size. Cardiac function was also preserved following pretreatment with IKKβ inhibition. These findings were further associated with decreased expression of phosphorylated IκBα and phosphorylated p65 in myocardial tissue. In addition, IKKβ inhibition decreased serum levels of TNF-α and IL-6, two prototypical downstream effectors of NF-κB activity. These results demonstrate that specific IKKβ inhibition can provide both acute and delayed cardioprotection and offers a clinically accessible target for preventing cardiac injury following IR.

scholarly journals The mechanism of action of metabolic cytoprotector trimetazidine in acute ischemia-reperfusion injury

2014 ◽  
Vol 5 (2) ◽  
pp. 24-30
Author(s):  
M. G Glezer ◽  
E. I Astashkin ◽  
M. V Novikova
Keyword(s):  
Reperfusion Injury ◽  
Mechanism Of Action ◽  
Stress Reduction ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Acute Ischemia ◽  
Positive Effects ◽  
Coronary Syndrome ◽  
New Concepts

The review presents, as the classical data on the mechanism of action of metabolic cytoprotector trimetazidine in acute ischemia/reperfusion injury associated with a partial inhibition of the oxidation of long chain fatty acids and increased metabolism of pyruvate, as well as new concepts of reducing the level of oxidative stress, reduction of cardiomyocyte apoptosis, elimination areas of myocardial stunning and hibernation state. Described cytoprotective effects associated with inhibition of activation of mitochondrial pore with transient (temporary) permeability. Presented clinical studies showing significant anti-anginal and anti-ischemic effect of the trimetazidine in patients with stable angina, to decrease myocardial damage in acute coronary syndrome, during intervention on the coronary arteries. Particular attention is given to the latest data on the positive effects of prolonged use of trimetazidine on the course and prognosis in patients with heart failure.

scholarly journals Activity of endogenous aldehydes catabolism enzymes in subcellular fractions of liver, heart and brain of rats at pubertal age under stress

2012 ◽  
Vol 58 (6) ◽  
pp. 691-701
Author(s):  
L.L. Sukhova ◽  
A.V. Guryeva ◽  
E.A. Berezhnaya ◽  
V.V. Davydov
Keyword(s):  
Aldehyde Dehydrogenase ◽  
Rat Heart ◽  
Immobilization Stress ◽  
Mitochondrial Fraction ◽  
Subcellular Fractions ◽  
Brain Cells ◽  
Redox Transformation ◽  
Effective Utilization ◽  
Old Rats ◽  
Prolonged Immobilization

Activities of enzymes involved in redox transformation of endogenous aldehydes have been investigated in subcellular fractions of liver, heart, and brain of pubertal rats exposed to prolonged immobilization stress. In the liver aldo-keto reductase (AKR) activity in the postmitochondrial fraction and aldehyde dehydrogenase (ALDH) acivity of the mitochondrial fraction demonstrated a more pronounced decrease in 2-month-old rats. Rat heart postmitochondrial AKR and ALDH demonstrated opposite changes in their enzymatic activities, while activity of mitochondrial ALDH remained unchanged. Brain cells create conditions that favor effective utilization of endogenous aldehydes in metabolic redox pathways.

scholarly journals Selective cyclooxygenase-2 inhibition protects against myocardial damage in experimental acute ischemia

Clinics ◽  
2009 ◽  
Vol 64 (3) ◽  
pp. 245-252 ◽  
Author(s):  
Alberto Carnieto Jr. ◽  
Paulo Magno Martins Dourado ◽  
Protásio Lemos da Luz ◽  
Antonio Carlos Palandri Chagas
Keyword(s):  
Myocardial Damage ◽  
Cyclooxygenase 2 ◽  
Acute Ischemia

scholarly journals Diagnosis of Pulmonary Embolism

2021 ◽  
Author(s):  
Sachin M. Patil
Keyword(s):  
Pulmonary Embolism ◽  
Blood Clot ◽  
Venous Blood ◽  
Pulmonary Arteries ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Imaging Modalities ◽  
Arterial Blood Gas ◽  
Pulmonary Angiogram ◽  
Prolonged Immobilization

Pulmonary embolism is an acute emergency due to the occlusion of the pulmonary arteries by a venous blood clot. The pathophysiology of pulmonary embolism follows Virchow\'s triad, which encompasses stasis in veins, increased coagulation, and vessel wall trauma. Pregnancy, major trauma or surgery, prolonged immobilization, obesity, medication, and inherited risks are important risks. It is an essential rule-out diagnosis in chest pain and dyspnea patients in the emergency room. It is also responsible for significant mortality if not diagnosed and treated promptly. Physicians utilize multiple algorithmic scores and calculators to supplement diagnosis along with a high degree of clinical suspicion at initial presentation. Clinical diagnosis involves utilizing multiple modalities, including D-dimer, troponin, arterial blood gas analysis, electrocardiogram, bedside echocardiogram, and imaging modalities such as venous duplex, chest computed tomography, ventilation-perfusion scans, and pulmonary angiogram. Some imaging modalities carry the risk of radiation and being invasive. The treatment can itself be short-term or lifelong based on the causative factor. Anticoagulants used in the therapy can itself cause devastating complications if not monitored appropriately. Despite adequate treatment, some of these patients progress to chronic disease resulting in secondary pulmonary hypertension.

ACTH, corticosterone, and ?-endorphin in rat blood plasma after prolonged immobilization stress

1985 ◽  
Vol 100 (2) ◽  
pp. 1026-1029 ◽  
Author(s):  
E. A. Kiyatkin ◽  
Yu. V. Polyntsev ◽  
N. E. Kushlinskii ◽  
M. G. Amiragova
Keyword(s):  
Blood Plasma ◽  
Immobilization Stress ◽  
Rat Blood ◽  
Prolonged Immobilization
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