The thyroid hormone analog DITPA restoresI to in rats after myocardial infarction

2000 ◽  
Vol 278 (4) ◽  
pp. H1105-H1116 ◽  
Author(s):  
Alan D. Wickenden ◽  
Roger Kaprielian ◽  
Xiao-Mang You ◽  
Peter H. Backx
Keyword(s):  
Myocardial Infarction ◽  
Thyroid Hormone ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Monophasic Action Potential ◽  
Mrna Levels ◽  
Hormone Analog ◽  
Life Threatening ◽  
The Right

Previous studies have established that reductions in repolarizing currents occur in heart disease and can contribute to life-threatening arrhythmias in myocardium. In this study, we investigated whether the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) could restore repolarizing transient outward K+ current ( I to) density and gene expression in rat myocardium after myocardial infarction (MI). Our findings show that I to density was reduced after MI (14.0 ± 1.0 vs. 10.2 ± 0.9 pA/pF, sham vs. post-MI at +40 mV). mRNA levels of Kv4.2 and Kv4.3genes were decreased but Kv1.4 mRNA levels were increased post-MI. Corresponding changes in Kv4.2 and Kv1.4 protein were also observed. Chronic treatment of post-MI rats with 10 mg/kg DITPA restored I to density (to 15.2 ± 1.1 pA/pF at +40 mV) as well as Kv4.2 and Kv1.4 expression to levels observed in sham-operated controls. Other membrane currents (Na+, L-type Ca2+, sustained, and inward rectifier K+ currents) were unaffected by DITPA treatment. Associated with the changes in I toexpression, action potential durations (current-clamp recordings in isolated single right ventricular myocytes and monophasic action potential recordings from the right free wall in situ) were prolonged after MI and restored with DITPA treatment. Our results demonstrate that DITPA restores I to density in the setting of MI, which may be useful in preventing complications associated with I to downregulation.

Effects of extracellular ATP on ICa, [Ca2+]i, and contraction in isolated ferret ventricular myocytes

1993 ◽  
Vol 264 (3) ◽  
pp. C702-C708 ◽  
Author(s):  
Y. Qu ◽  
H. M. Himmel ◽  
D. L. Campbell ◽  
H. C. Strauss
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Ventricular Myocardium ◽  
Inhibitory Effect ◽  
Extracellular Atp ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Patch Clamp Technique ◽  
Concentration Dependent Manner ◽  
The Right

The effects of extracellular ATP on the voltage-activated "L-type" Ca current (ICa), action potential, resting and transient intracellular Ca2+ levels, and cell contraction were examined in enzymatically isolated myocytes from the right ventricles of ferrets. With the use of the whole cell patch-clamp technique, extracellular ATP (10(-7) to 10(-3) M) inhibited ICa in a time- and concentration-dependent manner. ATP decreased the peak amplitude of ICa without altering the residual current at the end of 500-ms clamp steps. The concentration-response relationship for ATP inhibition of ICa was well described by a conventional Michaelis-Menten relationship with a half-maximal inhibitory concentration of 1 microM and a maximal effect of 50%. Consistent with its inhibitory effect on ICa, ATP hyperpolarized the plateau phase and shortened the action potential duration. In fura-2-loaded myocytes, extracellular ATP did not change the resting myoplasmic Ca2+ levels; however, when current was elicited under voltage-clamp conditions, ATP both decreased the myoplasmic intracellular Ca2+ transient and inhibited the degree of cell shortening. Our results suggest that ATP could be a genuine and potent extracellular modulator of cardiac function in ferret ventricular myocardium.

Reflex vagal control of atrial repolarization

1996 ◽  
Vol 271 (3) ◽  
pp. H870-H875
Author(s):  
D. E. Euler ◽  
B. Olshansky ◽  
S. Y. Kim
Keyword(s):  
Action Potential ◽  
Sinus Bradycardia ◽  
Aortic Pressure ◽  
Aortic Occlusion ◽  
Monophasic Action Potential ◽  
Atrial Pacing ◽  
Sinus Arrhythmia ◽  
Vagal Control ◽  
The Right ◽  
Atrial Repolarization

The reflex vagal control of atrial repolarization was investigated in eight open-chest, anesthetized dogs. A monophasic action potential was recorded from the right atrium, and the action potential duration to 90% repolarization (APD90) was determined every cardiac cycle. beta-Adrenergic receptors were blocked with timolol (0.1 mg/kg). Under baseline conditions, sinus slowing during sinus arrhythmia was accompanied by a significant shortening of APD90 (24 +/- 4.0 ms). Transient occlusion (30 s) of the descending thoracic aorta increased systolic aortic pressure from 138 +/- 2.8 to 181 +/- 3.3 mmHg (P < 0.01). Heart rate decreased from 99 +/- 3.6 to 42.5 +/- 3.4 beats/min (P < 0.01), and APD90 shortened from 168 +/- 5.1 to 94 +/- 3.3 ms (P < 0.01). Release of the occlusion caused arterial hypotension (95 +/- 2.8 mmHg) and an overshoot in both rate (126 +/- 5.2 beats/min) and APD90 (189 +/- 2.3 ms). Aortic occlusion during atrial pacing (130-160 beats/min) decreased APD90 from 147 +/- 7.0 to 78 +/- 3.4 ms (P < 0.01). Cervical vagotomy or atropine eliminated changes in rate and APD90 evoked by aortic occlusion. The results indicate that there is parallel central vagal control of both sinus rate and atrial repolarization. Sinus bradycardia during reflex vagal activation does not prevent the acceleration of atrial repolarization.

Acetylcholine release by a stimulus train lowers atrial fibrillation threshold

1987 ◽  
Vol 253 (4) ◽  
pp. H863-H868 ◽  
Author(s):  
D. E. Euler ◽  
P. J. Scanlon
Keyword(s):  
Atrial Fibrillation ◽  
Action Potential ◽  
Right Atrium ◽  
Single Pulse ◽  
Monophasic Action Potential ◽  
Adrenergic Blockade ◽  
The Right ◽  
Alpha Chloralose ◽  
Electrical Stimuli ◽  
Local Release

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.

Quinidine elicits proarrhythmic changes in ventricular repolarization and refractoriness in guinea-pig

2013 ◽  
Vol 91 (4) ◽  
pp. 306-315 ◽  
Author(s):  
Oleg E. Osadchii
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Left Ventricular ◽  
Ventricular Repolarization ◽  
Monophasic Action Potential ◽  
Delayed Rectifier ◽  
Rate Dependent ◽  
Delayed Rectifier Current ◽  
Left Ventricular Chamber ◽  
The Right

Quinidine is a class Ia Na+ channel blocker that prolongs cardiac repolarization owing to the inhibition of IKr, the rapid component of the delayed rectifier current. Although quinidine may induce proarrhythmia, the contributing mechanisms remain incompletely understood. This study examined whether quinidine may set proarrhythmic substrate by inducing spatiotemporal abnormalities in repolarization and refractoriness. The monophasic action potential duration (APD), effective refractory periods (ERPs), and volume-conducted electrocardiograms (ECGs) were assessed in perfused guinea-pig hearts. Quinidine was found to produce the reverse rate-dependent prolongation of ventricular repolarization, which contributed to increased steepness of APD restitution. Throughout the epicardium, quinidine elicited a greater APD increase in the left ventricular chamber compared with the right ventricle, thereby enhancing spatial repolarization heterogeneities. Quinidine prolonged APD to a greater extent than ERP, thus extending the vulnerable window for ventricular re-excitation. This change was attributed to increased triangulation of epicardial action potential because of greater APD lengthening at 90% repolarization than at 30% repolarization. Over the transmural plane, quinidine evoked a greater ERP prolongation at endocardium than epicardium and increased dispersion of refractoriness. Premature ectopic beats and monomorphic ventricular tachycardia were observed in 50% of quinidine-treated heart preparations. In summary, abnormal changes in repolarization and refractoriness contribute greatly to proarrhythmic substrate upon quinidine infusion.

The Monophasic Action Potential of the Right Atrium

Cardiology ◽  
1972 ◽  
Vol 57 (4) ◽  
pp. 200-207 ◽  
Author(s):  
S. Gavrilescu ◽  
S. Cotoi ◽  
T. Pop
Keyword(s):  
Action Potential ◽  
Right Atrium ◽  
Monophasic Action Potential ◽  
The Right

scholarly journals Expression of Vesicular Glutamate Transporter-2 in Gonadotrope and Thyrotrope Cells of the Rat Pituitary. Regulation by Estrogen and Thyroid Hormone Status

Endocrinology ◽  
2006 ◽  
Vol 147 (8) ◽  
pp. 3818-3825 ◽  
Author(s):  
Erik Hrabovszky ◽  
Imre Kalló ◽  
Gergely F. Turi ◽  
Katalin May ◽  
Gábor Wittmann ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Thyroid Hormone ◽  
Glutamate Transporter ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
Vesicular Glutamate Transporter ◽  
Local Synthesis ◽  
Enhanced Secretion

Immunocytochemical studies of the rat adenohypophysis identified a cell population that exhibits immunoreactivity for type-2 vesicular glutamate transporter (VGLUT2), a marker for glutamatergic neuronal phenotype. The in situ hybridization detection of VGLUT2 mRNA expression in adenohypophysial cells verified that VGLUT2 immunoreactivity is due to local synthesis of authentic VGLUT2. Dual-immunofluorescent studies of the hypophyses from male rats showed the presence of VGLUT2 in high percentages of LH (93.3 ± 1.3%)-, FSH (44.7 ± 3.9%)-, and TSH (70.0 ± 5.6%)-immunoreactive cells and its much lower incidence in cells of the prolactin, GH, and ACTH phenotypes. Quantitative in situ hybridization studies have established that the administration of a single dose of 17-β-estradiol (20 μg/kg; sc) to ovariectomized rats significantly elevated VGLUT2 mRNA in the adenohypophysis 16 h postinjection. Thyroid hormone dependence of VGLUT2 expression was addressed by the comparison of hybridization signals in animal models of hypo- and hyperthyroidism to those in euthyroid controls. Although hyperthyroidism had no effect on VGLUT2 mRNA, hypothyroidism increased adenohypophysial VGLUT2 mRNA levels. This coincided with a decreased ratio of VGLUT2-immunoreactive TSH cells, regarded as a sign of enhanced secretion. The presence of the glutamate marker VGLUT2 in gonadotrope and thyrotrope cells, and its up-regulation by estrogen or hypothyroidism, address the possibility that endocrine cells of the adenohypophysis may cosecrete glutamate with peptide hormones in an estrogen- and thyroid status-regulated manner. The exact roles of endogenous glutamate observed primarily in gonadotropes and thyrotropes, including its putative involvement in autocrine/paracrine regulatory mechanisms, will require clarification.

scholarly journals Hypertrophic cardiomyopathy mimicking inferior wall myocardial infarction

2021 ◽  
Vol 8 (5) ◽  
pp. 708
Author(s):  
Prachi Sharma ◽  
Akshyaya Pradhan ◽  
Pravesh Vishwakarma
Keyword(s):  
Myocardial Infarction ◽  
Hypertrophic Cardiomyopathy ◽  
Troponin T ◽  
Chronic Obstructive ◽  
Inferior Wall ◽  
Troponin Elevation ◽  
Obstructive Lesion ◽  
Life Threatening ◽  
The Right ◽  
High Sensitive Troponin

Electrocardiogram is most often the first-hand diagnostic tool with a cardiologist. Promptly identifying life threatening arrhythmias and myocardial infarction with ECG saves many lives. Quite often the electrocardiogram may have dubious findings and further testing helps arriving at the right diagnosis. Herein, we present a case of hypertrophic cardiomyopathy where the ECG mimicked inferior wall myocardial infarction along with a raised high sensitive Troponin T (hsTnT). A coronary angiogram failed to reveal any acute or chronic obstructive lesion in the coronary arteries. We discussed the varied ECG patterns in hypertrophic cardiomyopathy and causes of troponin elevation apart from myocardial infarction. We also discussed other causes of ‘pseudo-infarct’ pattern on ECG. This provides insight into a more comprehensive approach in management of each patient.

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