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.

Protection of Ischemic Myocardium: Comparison of Effects of Propranolol, Bevantolol and N-Dimethyl Propranolol on Infarct Size Following Coronary Artery Occlusion in Anesthetized Dogs

Cardiology ◽  
1980 ◽  
Vol 66 (3) ◽  
pp. 133-146 ◽  
Author(s):  
David C. Warltier ◽  
Garrett J. Gross ◽  
Gary J. Jesmok ◽  
Harold L. Brooks ◽  
Harold F. Hardman
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Anesthetized Dogs

Antifibrillatory effects of α1-adrenoceptor blocking drugs in experimental coronary artery occlusion and reperfusion

1993 ◽  
Vol 71 (2) ◽  
pp. 103-111 ◽  
Author(s):  
B. G. Benfey
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Guinea Pig ◽  
Ventricular Arrhythmias ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coronary Reperfusion ◽  
Isolated Hearts ◽  
Anesthetized Dogs

The myocardium of animals and man possesses α1-adrenoceptors in addition to β-adrenoceptors. Ischemia increases sympathetic tone, and ventricular arrhythmias can occur by β- and α1-adrenoceptor stimulation. I believe that α1-adrenoceptor blocking drugs have antifibrillatory effects and will review the data that support this condition. The effect of α1,-adrenoceptor blocking drugs on the incidence of ventricular fibrillation in acute coronary artery occlusion and (or) reperfusion has been determined in 24 studies in conscious and anesthetized dogs and rats, anesthetized cats and pigs, and rat and guinea-pig isolated hearts. The drugs reduced the incidence of fibrillation from 35 to 24% in coronary occlusion and from 61 to 29% in reperfusion.Key words: heart, coronary occlusion, coronary reperfusion, ventricular fibrillation, α1-adrenoceptor blocking drugs.

Effects of yohimbine and desipramine on cardiac noradrenaline release and ventricular arrhythmias during acute coronary artery occlusion and reperfusion in anesthetized dogs

1987 ◽  
Vol 65 (11) ◽  
pp. 2244-2253 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Daniel Lamontagne ◽  
Ghislain Boudreau ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Coronary Artery ◽  
Nerve Stimulation ◽  
Left Ventricular Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Neuronal Uptake ◽  
Ischemic Region ◽  
Anesthetized Dogs ◽  
Na Release

Effects of yohimbine (YHMB, an α2-antagonist) and desipramine (DMI, a neuronal uptake inhibitor) were compared on cardiac noradrenaline (NA) release either upon left ansa subclavia nerve stimulation during acute occlusion of the left anterior descending coronary artery (LAD) or upon subsequent LAD reperfusion without stimulation in anesthetized dogs. In control dogs, before LAD occlusion, coronary sinus (CS) NA output increased from 5.4 ± 1.0 to 26.8 ± 4.0 ng/min (p < 0.05) upon stimulation (2 Hz, 30 s). The response to stimulation remained unchanged 25 min after LAD occlusion. During reperfusion 60 min after occlusion, the output of CS-NA and lactate increased from 6.1 ± 0.8 to 51.3 ± 19.4 ng/min (p < 0.05) and from 2.7 ± 0.5 to 6.7 ± 1.3 mg/min (p < 0.05), respectively. In dogs treated with YHMB, the stimulation-induced increase in NA output was potentiated at least fourfold (p < 0.05) either before or during LAD occlusion, but not during reperfusion. In dogs receiving DMI, stimulation-induced CS-NA output was enhanced to a similar extent (approximately twofold, p < 0.05) either before or during occlusion, while reperfusion-induced NA output was markedly potentiated by approximately ninefold (p < 0.05). Maximum dP/dt of left ventricular pressure remained unchanged upon reperfusion in all groups. The total arrhythmic ratio in the drug-treated groups did not significantly differ from the ratio in control dogs upon either stimulation or reperfusion. The data suggest that an abrupt increase in NA output upon reperfusion may result from a washout of NA locally accumulated in the ischemic and (or) peri-ischemic region during the preceding occlusion period, and that N A thus released does not have substantial hemodynamic effects. The results indicate that in the presence of YHMB or DMI, the potentiated increase in NA release in response to either nerve stimulation during LAD occlusion or to reperfusion without stimulation did not aggravate ventricular arrhythmia, most probably owing to the antiarrhythmic properties of these substances.

scholarly journals Effects of Coenzyme Q10 on Ischemic Myocardium during Coronary Artery Occlusion

1986 ◽  
Vol 8 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Yoshiya ISHIKURA ◽  
Shigetoh ODAGIRI ◽  
Masato NAGATA ◽  
Tadashi NAGANO ◽  
Hiroshi YOSHIMATU
Keyword(s):  
Coronary Artery ◽  
Coenzyme Q ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium

scholarly journals Protection of ischemic myocardium by whole-body hypothermia after coronary artery occlusion in dogs

1978 ◽  
Vol 96 (6) ◽  
pp. 772-780 ◽  
Author(s):  
Dana R. Abendschein ◽  
Willis A. Tacker ◽  
Charles F. Babbs
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Whole Body
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