scholarly journals Nafazatrom-induced salvage of ischemic myocardium in anesthetized dogs is mediated through inhibition of neutrophil function.

1985 ◽  
Vol 57 (1) ◽  
pp. 131-141 ◽  
Author(s):  
M Bednar ◽  
B Smith ◽  
A Pinto ◽  
K M Mullane
Keyword(s):  
Neutrophil Function ◽  
Ischemic Myocardium ◽  
Anesthetized Dogs

Differential cardiac sympathetic activity during acute myocardial ischemia

1990 ◽  
Vol 258 (5) ◽  
pp. H1534-H1541 ◽  
Author(s):  
B. H. Neely ◽  
G. R. Hageman
Keyword(s):  
Sympathetic Activity ◽  
Coronary Occlusion ◽  
Left Ventricular ◽  
Ischemic Myocardium ◽  
Neural Responses ◽  
Ischemic Region ◽  
Innervation Patterns ◽  
Anesthetized Dogs ◽  
Increased Activity ◽  
Cardiac Nerves

Efferent sympathetic activities were simultaneously recorded from two thoracic cardiac nerves in 33 chloralose-anesthetized dogs. Efferent innervation patterns were determined by electrical stimulation prior to recording in each animal. One of the nerves selected for recording was shown to innervate the proposed ischemic region, whereas the other nerve was selected because it was shown to innervate nonischemic regions. Left ventricular ischemia was produced by occlusion of a branch of either the left anterior descending (LAD) or left circumflex (LCX) coronary arteries. Heart rate was paced. Cardiac postganglionic sympathetic efferent activities were recorded during a 30-min coronary occlusion in 22 animals. Thirty minutes after LAD occlusion (n = 10), postganglionic sympathetic activity to ischemic myocardium was decreased (84 +/- 5% of control; P less than 0.05) while activity to nonischemic myocardium was unchanged. Thirty minutes after LCX occlusion (n = 12), postganglionic sympathetic activity to ischemic myocardium was also decreased (87 +/- 3% of control; P less than 0.01); however, sympathetic activity to nonischemic myocardium was increased (159 +/- 10% of control; P less than 0.001). Thus, in the anesthetized canine, regional left ventricular ischemia elicits differential sympathetic neural responses that are dependent on the location of the ischemic myocardium as well as the efferent destinations of the nerves. Changes in cardiac postganglionic sympathetic efferent activities are characterized by decreased activity to ischemic regions, with either no change or increased activity to nonischemic regions.

EFFECT OF THE NEW ALPHA2-ADRENERGIC AGONIST MIVAZEROL ON METABOLISM AND BLOOD FLOW OF ISCHEMIC MYOCARDIUM IN ANESTHETIZED DOGS

1994 ◽  
Vol 81 (SUPPLEMENT) ◽  
pp. A758
Author(s):  
P. M. H.J. Roekaerts ◽  
F. W. Prinzen ◽  
H. W. W. Willigers ◽  
S. De Lange
Keyword(s):  
Blood Flow ◽  
Ischemic Myocardium ◽  
Adrenergic Agonist ◽  
Anesthetized Dogs

Improved performance of ischemic canine myocardium in response to nifedipine and diltiazem

1980 ◽  
Vol 239 (5) ◽  
pp. H658-H663 ◽  
Author(s):  
J. E. Perez ◽  
B. E. Sobel ◽  
P. D. Henry
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Aortic Pressure ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Control Value ◽  
Anesthetized Dogs ◽  
Improved Performance ◽  
Mean Aortic Pressure ◽  
Canine Myocardium

To characterize the effects of Ca2+ antagonists on the performance of the ischemic myocardium, we administered nifedipine and diltiazem to chloralose-anesthetized dogs with coronary artery occlusion and monitored segmental myocardial shortening in ischemic and nonischemic zones with implanted ultrasonic length gauges. Other dogs were treated with nitroglycerin or nitroprusside for comparison. Dosage of all drugs was adjusted to reduce mean aortic pressure by no more than 5 mmHg. Segmental shortening was expressed as percent of control value before occlusion. In control dogs (n = 8), shortening in ischemic zones 20 and 80 min after occlusion averaged -16 +/- 2% and -17 +/- 2%, indicating paradoxical elongation. With nifedipine (1 +/- 0.4 microgram . kg-1 . h-1; n = 8), shortening of ischemic segments before treatment did not differ from controls, but after 60 min of treatment was markedly improved, averaging 31 +/- 4% (P < 0.05). Diltiazem (10 +/- 2 microgram . kg-1 . h-1; n = 8) produced a similar improvement in shortening in ischemic zones. However, nitroglycerin (177 +/- 20 microgram . kg-1 . h-1; n = 8) and nitroprusside (43 +/- 10 microgram . kg-1 . h-1; n = 8) failed to improve shortening in ischemic regions. Thus, Ca2+ antagonists improved performance in ischemic zones, but nitroglycerin and nitroprusside did not.

scholarly journals High Density Intramural Mapping of Post-Infarct Premature Ventricular Contractions.

2021 ◽  
Author(s):  
Eugene Downar ◽  
Michiel Janse ◽  
Abhishek Bhaskaran ◽  
Ahmed Niri ◽  
Arulalan Velluppillai ◽  
...  
Keyword(s):  
Canine Model ◽  
High Density ◽  
Ischemic Myocardium ◽  
Acute Ischemia ◽  
Ectopic Activity ◽  
Premature Ventricular Contractions ◽  
Diagonal Branch ◽  
Graded Responses ◽  
Anesthetized Dogs ◽  
Unipolar Electrograms

Background: Spontaneous ventricular premature contractions (PVCs) in the post infarct milieu is assumed to be due to automaticity. However, the mechanism has not been studied with appropriate mapping tools. Objective: To study the mechanism of spontaneous PVCs with high density intramural mapping in a canine model, to test the hypothesis that post-infarct PVCs are due to re-entry rather than automaticity. Methods: In 15 anesthetized dogs, using 768 intramural unipolar electrograms, simultaneous recordings were made. After 30 mins of stabilization, recordings were made during the first 10 minutes of ischemia, and activation maps were constructed of individual beats. Acute ischemia was produced by clamping the left anterior descending coronary artery proximal to the first diagonal branch. The analysis was limited to the activation pattern of spontaneous ventricular beats. Results: In all experiments ST-T alternans occurred. In 8 of 15 dogs spontaneous ventricular beats occurred. In all 8 of these experiment earliest, ectopic activity occurred in the endocardium, well within the ischemic zone. From there, activity spread rapidly along the subendocardium, with endo-to epicardial spread along the non ischemic myocardium. Epicardial breakthrough always occurred at the border of the ischemic myocardium. In 3 dogs, delayed potentials were observed, which were earliest at the ischemic epicardium and extended transmurally with increasing delay towards the endocardium, where they culminated in a premature beat. Conclusion: Graded responses that occur with each sinus beat intramurally, when able to propagate from epicardium to endocardium is the mechanism by which PVCs are generated in post-infarct myocardium.

Effect of sympathetic tone on ventricular arrhythmias during circumflex coronary occlusion

1985 ◽  
Vol 249 (5) ◽  
pp. H1045-H1050 ◽  
Author(s):  
D. E. Euler ◽  
S. Nattel ◽  
J. F. Spear ◽  
E. N. Moore ◽  
P. J. Scanlon
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Ventricular Fibrillation ◽  
Sympathetic Nervous System ◽  
Ischemic Myocardium ◽  
Total Incidence ◽  
Arrhythmogenic Effect ◽  
Anesthetized Dogs ◽  
Sympathetic Nervous ◽  
Arrhythmogenic Effects

To determine if the sympathetic nervous system exerts an arrhythmogenic effect on the ischemic myocardium independent of heart rate, the proximal circumflex coronary artery was occluded for 1 h in 62 open-chest, anesthetized dogs. The atrial rate was maintained at 200/min, and the vagosympathetic trunks were transected in all dogs. The total incidence of ventricular fibrillation was 35% in 20 dogs with intact stellates and not significantly different from the incidence of ventricular fibrillation (15%) in another 20 dogs in which both stellate ganglia had been decentralized. Electrical stimulation of the left ansae subclavia (3 Hz, 2 ms, 6-8 V) in the remaining 22 dogs significantly increased the incidence of ventricular fibrillation to 73% (P less than 0.05). The magnitude of S-T segment elevation in the lead II electrocardiogram 90 s after occlusion was 0.69 +/- 0.08 mV in the group with left ansae stimulation and significantly elevated (P less than 0.01) compared with dogs with intact stellates (0.35 +/- 0.06 mV) and with the denervated dogs (0.19 +/- 0.05 mV). The data indicate that the sympathetic nervous system is capable of a direct arrhythmogenic influence on the ischemic myocardium independent of heart rate. The rate-independent arrhythmogenic effects of the sympathetic nervous system may be mediated by an increase in severity of the ischemic insult.

Left stellate stimulation: regional myocardial flows and ischemic injury in dogs

1980 ◽  
Vol 239 (3) ◽  
pp. H359-H364 ◽  
Author(s):  
J. F. Giudicelli ◽  
A. Berdeaux ◽  
F. Tato ◽  
M. Garnier
Keyword(s):  
Stellate Ganglion ◽  
Ischemic Myocardium ◽  
Regional Myocardial Blood Flow ◽  
Adrenergic Blockade ◽  
Flow Ratio ◽  
Adrenergic Stimulation ◽  
Anesthetized Dogs ◽  
Coronary Steal ◽  
Oxygen Requirements ◽  
Regional Myocardial Blood

The effects of left stellate ganglion stimulation (LSGS) on regional myocardial blood flow (RMBF) and epicardial S-T segment were investigated in the normal and ischemic myocardium of anesthetized dogs. In nonischemic myocardium LSGS decreased calculated coronary resistance, increased RMBF, and reduced the endocardial-to-epicardial (endo-to-epi) ratio. These effects were reversed after atenolol (1 mg/kg) and abolished after combined atenolol and phenoxybenzamine (3 mg/kg) treatments. In ischemic myocardium LSGS did not change RMBF but increased S-T segment. However, after atenolol, LSGS increased ischemic RMBF and the ischemic-to-nonischemic areas flow ratio (reverse coronary steal phenomenon), these effects being abolished by phenoxybenzamine. We conclude that 1) LSGS increases RMBF and decreases endo-to-epi ratio in nonischemic areas by beta 1-adrenergic stimulation through metabolic autoregulation, 2)beta 1-adrenergic blockade in nonischemic areas unmasks alpha-adrenergic vasoconstriction inducing a redistribution of flow towards ischemic areas, and 3) further elevation of S-T segment by LSGS is due to oxygen requirements enhancement by beta 1-adrenoceptors stimulation.

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