Ventricular arrhythmias following coronary artery occlusion in the streptozotocin diabetic rat

1988 ◽  
Vol 66 (3) ◽  
pp. 312-317 ◽  
Author(s):  
G. N. Beatch ◽  
J. H. McNeill
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Streptozotocin Diabetes ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Diabetic Rat ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Conscious Rat ◽  
Streptozotocin Diabetic Rat

The following investigation was designed to assess whether or not streptozotocin diabetes has an influence on the number and severity of ventricular arrhythmias following coronary artery occlusion in the conscious rat. In addition, electrocardiogram and haemodynamic data were compared between streptozotocin diabetic groups and control. Diabetes was induced in male Sprague–Dawley rats with streptozotocin (55 mg/kg iv) and left anterior descending coronary artery ligation was performed either 6 or 9 weeks later. Rats were allowed to recover from preparative surgery for 1 week prior to ligation. Streptozotocin diabetes (untreated or insulin controlled) appeared to have little influence on the variables tested. When exposed to equivalent degrees of ischaemia (the rat is a microangiopathy-resistant species), the streptozotocin diabetic rat heart was not appreciably more prone to arrhythmias of any type compared with control.

scholarly journals Defining the sham environment for post-myocardial infarction studies in mice

2016 ◽  
Vol 311 (3) ◽  
pp. H822-H836 ◽  
Author(s):  
Rugmani Padmanabhan Iyer ◽  
Lisandra E. de Castro Brás ◽  
Presley L. Cannon ◽  
Yonggang Ma ◽  
Kristine Y. DeLeon-Pennell ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Minimally Invasive ◽  
Invasive Procedure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coronary Artery Ligation ◽  
Surgical Operation ◽  
Artery Ligation ◽  
Sham Surgery

The purpose of this study was to evaluate the effect of sham surgery in a minimally invasive surgical model of permanent coronary artery occlusion used to generate myocardial infarction (MI) in mice. Adult male C57BL/6J mice (3–6 mo old) were divided into five groups: day (D) 0 (no surgical operation), D1 Sham, D1 MI, D7 Sham, and D7 MI. A refined MI surgery technique was used to approach the coronary artery without the ribs being cut. Both sham and MI mice had the left ventricle (LV) exposed through a small incision. To test the effects of surgery alone, the suture was passed around the coronary artery but not ligated. The MI mice were subjected to permanent coronary artery ligation. The mice were killed at D1 or D7 postsurgical procedure. Compared with D0 no surgery controls, the D1 and D7 sham groups exhibited no surgical mortality and similar necropsy and echocardiographic variables. Surgery alone did not induce an inflammatory cell response, as evidenced by the lack of leukocyte infiltration in the sham groups. Analysis of 165 inflammatory cytokines and extracellular matrix factors in sham revealed that a minor gene response was initiated but not translated to protein levels. Collagen deposition did not occur in the absence of MI. In contrast, the D1 and D7 MI groups showed the expected robust inflammatory and scar formation responses. When a minimally invasive procedure to generate MI in mice was used, the D0 (no surgical operation) control was an adequate replacement for the use of sham surgery groups.

Ca2+ sensitivity change and troponin loss in cardiac natural actomyosin after coronary occlusion

1981 ◽  
Vol 240 (5) ◽  
pp. H704-H708 ◽  
Author(s):  
T. Toyo-Oka ◽  
J. Ross
Keyword(s):  
Coronary Artery ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Sensitivity Change ◽  
Binding Subunit

Ca2+ sensitivity of natural actomyosin (NAM) isolated from both the intact left ventricular free wall and an area of myocardial infarction (MI) was analyzed by use of superprecipitation response from 2 to 48 h after left anterior descending coronary artery ligation in the dog. NAM from the intact tissue showed normal superprecipitation and normal Ca2+ sensitivity. Four hours after coronary ligation, Ca2+ sensitivity was lowered only in the endocardial half of MI region; it was markedly decreased both in the epicardial and endocardial halves at 6 h and completely lost at 24 and 48 h. A superprecipitation response was, however, demonstrated in all samples, indicating that both myosin and actin preserved their functions in the course of MI. With polyacrylamide gel electrophoresis in sodium dodecyl sulfate, NAM from the MI region revealed moderate decrease of the tropomyosin-binding subunit of troponin(TN-T) and the Ca2+-binding subunit of troponin(TN-C) and drastic decrease of the inhibitory subunit of troponin(TN-I). This resulted in the formation of extra bands of low molecular weights. These results suggest that degradation of troponin subunits occurs relatively early (4 h after coronary artery occlusion) and from the endocardial half of MI region. This degradation may be caused by one or several proteases that preferentially degrade the regulatory proteins among myofibrillar proteins.

Disparate effects of preconditioning and MLA on 5'-NT and adenosine levels during coronary occlusion

1997 ◽  
Vol 273 (2) ◽  
pp. H945-H951 ◽  
Author(s):  
K. Przyklenk ◽  
K. Hata ◽  
L. Zhao ◽  
R. A. Kloner ◽  
G. T. Elliott
Keyword(s):  
Coronary Artery ◽  
High Performance ◽  
Lipid A ◽  
Coronary Artery Occlusion ◽  
Canine Model ◽  
Artery Occlusion ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Monophosphoryl Lipid A ◽  
Anesthetized Dogs

Ischemic preconditioning has been proposed to protect the heart against infarction by increasing 5'-nucleotidase (5'-NT) activities and augmenting adenosine levels during sustained coronary artery occlusion. To test this theory, anesthetized dogs received four 5-min episodes of preconditioning ischemia, pretreatment with the pharmacological "preconditioning mimetic" monophosphoryl lipid A (MLA, 35 micrograms/kg i.v.) or no intervention before coronary artery ligation. At 20 min into occlusion (the crucial time at which myocyte death begins in this model), myocardial samples were obtained for measurement (by high-performance liquid chromatography) of ectosolic and cytosolic 5'-NT activity and adenosine levels. Preconditioning and MLA pretreatment limit infarct size in the canine model by 75 and 50%, respectively. However, only MLA augmented 5'-NT activity [i.e., cytosolic 5'-NT in the ischemic subendocardium was 26 +/- 1, 39 +/- 7, and 26 +/- 6 nmol. mg protein-1. min-1 in preconditioned, MLA, and control groups (P < 0.05), respectively]. Moreover, adenosine levels (in nmol/mg protein) were increased with MLA treatment (2.30 +/- 0.44) but attenuated in preconditioned dogs (1.11 +/- 0.23; P < 0.05) versus controls (1.87 +/- 0.29). Thus 5'-NT and adenosine levels need not be increased beyond control values during sustained occlusion to elicit cardioprotection.

Suppression of ventricular arrhythmias resulting from acute coronary artery ligation in rat by imipramine

1990 ◽  
Vol 42 (5) ◽  
pp. 360-362
Author(s):  
Samiha A. M. El-Mahdy ◽  
A. A. Alhaider ◽  
Afaf A. Mahgoub ◽  
Abdulwahab M. Bashandy
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Coronary Artery Ligation ◽  
Artery Ligation

scholarly journals Inhibition of N-type calcium channels in cardiac sympathetic neurons attenuates ventricular arrhythmogenesis in heart failure

2020 ◽  
Author(s):  
Dongze Zhang ◽  
Huiyin Tu ◽  
Chaojun Wang ◽  
Liang Cao ◽  
Wenfeng Hu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Sympathetic Neurons ◽  
Coronary Artery Ligation ◽  
Channel Blockers ◽  
Artery Ligation ◽  
Cell Excitability ◽  
Ventricular Arrhythmogenesis

Abstract Aims Cardiac sympathetic overactivation is an important trigger of ventricular arrhythmias in patients with chronic heart failure (CHF). Our previous study demonstrated that N-type calcium (Cav2.2) currents in cardiac sympathetic post-ganglionic (CSP) neurons were increased in CHF. This study investigated the contribution of Cav2.2 channels in cardiac sympathetic overactivation and ventricular arrhythmogenesis in CHF. Methods and results Rat CHF was induced by surgical ligation of the left coronary artery. Lentiviral Cav2.2-α shRNA or scrambled shRNA was transfected in vivo into stellate ganglia (SG) in CHF rats. Final experiments were performed at 14 weeks after coronary artery ligation. Real-time polymerase chain reaction and western blot data showed that in vivo transfection of Cav2.2-α shRNA reduced the expression of Cav2.2-α mRNA and protein in the SG in CHF rats. Cav2.2-α shRNA also reduced Cav2.2 currents and cell excitability of CSP neurons and attenuated cardiac sympathetic nerve activities (CSNA) in CHF rats. The power spectral analysis of heart rate variability (HRV) further revealed that transfection of Cav2.2-α shRNA in the SG normalized CHF-caused cardiac sympathetic overactivation in conscious rats. Twenty-four-hour continuous telemetry electrocardiogram recording revealed that this Cav2.2-α shRNA not only decreased incidence and duration of ventricular tachycardia/ventricular fibrillation but also improved CHF-induced heterogeneity of ventricular electrical activity in conscious CHF rats. Cav2.2-α shRNA also decreased susceptibility to ventricular arrhythmias in anaesthetized CHF rats. However, Cav2.2-α shRNA failed to improve CHF-induced cardiac contractile dysfunction. Scrambled shRNA did not affect Cav2.2 currents and cell excitability of CSP neurons, CSNA, HRV, and ventricular arrhythmogenesis in CHF rats. Conclusions Overactivation of Cav2.2 channels in CSP neurons contributes to cardiac sympathetic hyperactivation and ventricular arrhythmogenesis in CHF. This suggests that discovering purely selective and potent small-molecule Cav2.2 channel blockers could be a potential therapeutic strategy to decrease fatal ventricular arrhythmias in CHF.

Stretch-induced ventricular arrhythmias during acute ischemia and reperfusion

2004 ◽  
Vol 97 (1) ◽  
pp. 377-383 ◽  
Author(s):  
Kevin Kit Parker ◽  
James A. Lavelle ◽  
L. Katherine Taylor ◽  
Zifa Wang ◽  
David E. Hansen
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Mechanical Stretch ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Acute Ischemia ◽  
Ischemia And Reperfusion ◽  
A Value ◽  
Action Potential Waveform ◽  
Electrophysiological Effects

Mechanical stretch has been demonstrated to have electrophysiological effects on cardiac muscle, including alteration of the probability of excitation, alteration of the action potential waveform, and stretch-induced arrhythmia (SIA). We demonstrate that regional ventricular ischemia due to coronary artery occlusion increases arrhythmogenic effects of transient diastolic stretch, whereas globally ischemic hearts showed no such increase. We tested our hypothesis that, during phase Ia ischemia, regionally ischemic hearts may be more susceptible to triggered arrhythmogenesis due to transient diastolic stretch. During the first 20 min of regional ischemia, the probability of eliciting a ventricular SIA ( PSIA) by transient diastolic stretch increased significantly. However, after 30 min, PSIA decreased to a value comparable with baseline measurements, as expected during phase Ib, where most ventricular arrhythmias are of reentrant mechanisms. We also suggest that mechanoelectrical coupling may contribute to the nonreentrant mechanisms underlying reperfusion-induced arrhythmia. When coronary artery occlusion was relieved after 30 min of ischemia, we observed an increase in PSIA and the maintenance of this elevated level throughout 20 min of reperfusion. We conclude that mechanoelectrical coupling may underlie triggered arrhythmogenesis during phase 1a ischemia and reperfusion.

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