Correlation among Clinicopathological Parameters of Myocardial Damage in Rats Treated with Isoproterenol

Chen

et al. 2011

Circ J

Background: Cardiac angina is the hallmark of myocardial ischemia, but the role of the cardiac sensory nerve has received relatively little attention. Recently, both acid-sensing ion channel 3 (ASIC3) and capsaicin receptor (TRPV1) have been suggested as important mediators in sensing myocardial ischemia. However, studies comparing the physiological roles of ASIC3 and TRPV1 in the neuronal - cardiac sensing circuits in vivo are lacking. Methods and Results:Isoproterenol (1.5 mg/kg, intraperitoneally) was used to induce transient myocardial ischemia in Asic3 +/+ and Asic3 -/-mice and a radio-telemetry system was used for electrocardiography with mice in a conscious state. Isoproterenol-induced myocardial ischemia was first demonstrated with ST-segment depression and further confirmed by hypoxia-mediated chemical reactions in cardiac tissue. Mice lacking Asic3 showed prolonged duration of ST-segment depression compared with Asic3 +/+ mice (44.3±3.1 vs. 31.7±2.9 min; P<0.05). Although ischemia was transient, severe cardiac fibrosis was found in Asic3 -/-but not in Asic3 +/+ mice littermates. In contrast, isoproterenol-injected Trpv1 +/+ and Trpv1 -/-mice showed no difference in duration of ST-segment depression and, surprisingly, deletion of Trpv1 did not aggravate cardiac fibrosis.Conclusions: An isoproterenol-induced myocardial ischemia model mimicking clinical conditions of early cardiac angina was used to demonstrate that ASIC3 but not TRPV1 plays a protective role in sensing myocardial ischemia. (Circ J 2011; 75: 174 - 178)

Section: Cheng Cf Et Almentioning

confidence: 75%

Acid-Sensing Ion Channel 3, But Not Capsaicin Receptor TRPV1, Plays a Protective Role in Isoproterenol-Induced Myocardial Ischemia in Mice

Chen

et al. 2011

Circ J

“…Cardiac troponin I (cTnI) is a sensitive and specific blood borne indicator of myocardial damage, released into the circulation in proportion to myocyte injury in both man (Antman, 2002, Sarko and Pollack, 2002) and experimental animals (Kurata et al, 2007, O'Brien et al, 2006). In these studies, the concentration of cTnI was evaluated in plasma (100 ul) obtained from the arterial catheter 60 min following the onset of SE, and at an identical time in Cont animals.…”

Section: Methodsmentioning

confidence: 99%

Autonomic and cellular mechanisms mediating detrimental cardiac effects of status epilepticus

Bealer¹,

Little²,

Metcalf³

et al. 2010

Epilepsy Research

Prolonged seizure activity (status epilepticus; SE) can result in increased susceptibility to lethal ventricular arrhythmias for an extended period of time following seizure termination. SE is accompanied by acute, intense activation of the sympathetic nervous system (SymNS) and results in myocyte myofilament damage, arrhythmogenic alterations in cardiac electrical activity, and increased susceptibility to ventricular arrhythmias. However, the mechanisms mediating the changes in cardiac function, and the specific arrhythmogenic substrate produced during SE are unknown. To determine if detrimental cardiac effects of SE are mediated by SymNS stimulation of the heart, we examined the effects of B-adrenergic blockade (atenolol) during seizure activity on blood pressure, heart rate, myocyte myofilament injury (cardiac troponin I, cTnI), electrocardiographic activity, and susceptibility to arrhythmias. Furthermore, we determined if SE was associated with altered expression of the Kv4.x potassium channels, which are critical for action potential repolarization and thereby contribute significantly to normal cardiac electrical activity. Lithium-pilocarpine induced SE was associated with acute tachycardia, hypertension, and cardiomyocyte damage. Arrhythmogenic alterations in cardiac electrical activity accompanied by increased susceptibility to experimentally induced arrhythmias were evident during the first 2 wks following SE. Both were prevented by atenolol treatment during seizures. Furthermore, one and two weeks after SE, myocyte ion channel remodeling, characterized by a decreased expression of cardiac Kv4.2 potassium channels, was evident. These data suggest that the cardiac effects of prolonged and intense SymNS activation during SE induce myofilament damage and downregulation of Kv4.2 channels, which alter cardiac electrical activity and increase susceptibility to lethal arrhythmias.

“…There are cardiac and skeletal muscle-specific forms of TnI and TnT, although not for TnC [7]. There is growing evidence to suggest that increases in the serum concentration of cTn may be more sensitive than histologic analysis and other objective measures of cardiac myocyte injury [8].…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective Efficacy of Taurine on Lipid-Metabolism of Isoproterenol-Induced Myocardial Infarction

Abdel-Reheim

2016

Int J Pharm Pharm Sci

Objective: The present study aimed to evaluate the effect of pre-treatment with taurine on rats in which MI had been induced using isoproterenol (ISO).Methods: Rats were randomly allocated into three groups; the 1st group is the normal control (C) one, the 2nd is the isoproterenol cardiotoxic (ISO) one and the 3rd group is the taurine pretreated (T-ISO) one. Results:The activities of the cardiac biomarker enzymes, AST, LDH, CK and CK-MB were elevated in the ISO-treated group. The membrane-bound Na + -K + and Ca 2+ ATPase enzyme activities were decreased in the ISO-treated group. The lipid profile either in sera or cardiac tissues was increased in ISO-treated rats except for HDL-cholesterol and phospholipids. The cholesterol ester synthetase (CES) activity was elevated, while lecithin: Cholesterol acyltransferase (LCAT) and lipoprotein lipase (LPL) activities were decreased in the myocardial infarcted rats. In addition, the high level of the troponins I and T was an indication of cardiac necrosis. Pre-treatment with Taurine, however, ameliorated all of these changes, in addition to its effect in improving the oxidation process, as measured by lipid peroxidation and the antioxidant enzymes, superoxide dismutase and peroxidase enzymes. Conclusion:Taurine showed amelioration effects on the changes in lipid profile, oxidative stress and myocardial infarction biomarkers and therefore, can be protected against cardiotoxicity.