Acute Coronary Occlusion In Dogs Research Articles

Coronary steal: Its role in detrimental effect of isoproterenol after acute coronary occlusion in dogs

Using epicardial electrograms others have established that infusion of isoproterenol increases myocardial injury after acute coronary occlusion. To define the contribution of alterations in collateral blood flow to this increased ischemia, isoproterenol was administered to 10 dogs. After pretreatment with practolol in doses that successfully block inotropic but not vascular effects of beta adrenergic stimulants, intracoronary isoproterenol continued to enhance the magnitude of S-T segment elevation in ischemic areas. Thus, vasodilation induced by isoproterenol appears to divert flow from the ischemic area. To test this hypothesis, intracoronary adenosine was given to cause coronary vasodilation without enhancing inotropy. S-T segment elevation at ischemic and adjacent sites was significantly increased. Neither agent had systemic effects, but each increased coronary blood flow while concomitantly decreasing collateral flow as evidenced by a reduction in retrograde coronary flow and peripheral coronary pressure. In addition, adenosine significantly diminished the rate of xenon-133 clearance from the ischemic myocardium. Thus, isoproterenol, in addition to its positive inotropic effect, increases myocardial injury by its vascular action. Collateral blood flow to acutely ischemic myocardium is diminished by the production of a coronary steal. Intravenously administered isoproterenol additionally diminishes collateral flow by decreasing coronary perfusion pressure. It is postulated that any agent that causes either a primary or secondary coronary vasodilation may cause a coronary steal and subsequently enhance myocardial injury.

Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease.

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.

Pulmonary function following acute coronary occlusion in dogs.

SummaryThe immediate cardiopulmonary effects following acute induced coronary occlusion are hyperpnea, systemic hypotension, and hyperventilation. The onset of hyperpnea and systemic hypotension is quite rapid. Arterial blood gas tensions reveal arterial hyperoxemia and hypocapnia, which may be partly due to hyperventilation. Arterial hypoxemia, following myocardial infarction, is a later event and possibly related to the pulmonary complications following myocardial infarction.

The influence of adrenaline secretion on the enzymes in heart muscle after acute coronary occlusion in dogs.

The influence of catecholamine secretion in the early stages of myocardial infarction upon the degree of myocardial lesions was investigated in dogs. It has been found that adrenaline release into the blood after the ligation of the coronary artery aggravates histoenzymatic changes in ventricular myocardium, manifested by the decrease in lactic and succinic dehydrogenases activity.

Cardiac rhythm disturbances and the release of catecholamines after acute coronary occlusion in dogs.

Acute occlusion of the anterior descending branch of the left coronary artery in dogs led to a development of ventricular arrhythmias in 39 of 68 animals examined. In 35 of these 39 dogs ventricular arrhythmias were associated with an increased release of catecholamines into the bloodstream. In dogs which failed to secrete catecholamines and showed no ectopic activity after coronary ligation, intravenous infusions of adrenaline provoked ventricular arrhythmias after coronary ligation, but not before. The specific β-receptor blocking agents, propranolol and I.C.I. 50 172, suppressed arrhythmias after coronary occlusion.

Role of magnesium ion in the initiation of ventricular fibrillation produced by acute coronary occlusion.

The incidence of ventricular fibrillation following acute coronary occlusion in dogs was reduced by perfusing the ischemic area of the myocardium with Locke-Ringer's solution and solutions of magnesium ion in physiological saline. In contrast, normal serum concentrations of magnesium in 5 per cent dextrose appeared to induce ventricular fibrillation in these circumstances. The results suggest that changes in the concentration of magnesium and sodium ion in extracellular fluid may initiate ventricular fibrillation in the ischemic heart.