Artery Occlusion In Conscious Dogs Research Articles

Differences in myocardial stunning following coronary artery occlusion in conscious dogs, pigs, and baboons.

To determine whether myocardial stunning differs among dogs, pigs, and baboons and is reproducible within species, we examined the effects of 10-min coronary artery (CA) occlusion (CAO) on 9 conscious dogs, 12 minipigs, and 6 baboons. During 10-min CAO, systolic wall thickening in the ischemic zone fell similarly in dogs (-108 +/- 5.6%), pigs (-102 +/- 1.8%), and baboons (-107 +/- 5.7%), but blood flow fell more (P < 0.05) in the subepicardium in pigs (0.07 +/- 0.01 ml.min-1.g-1) and baboons (0.07 +/- 0.02 ml.min-1.g-1) than in dogs (0.18 +/- 0.03 ml.min-1.g-1). At 1 h after CA reperfusion (CAR), wall thickening was reduced more (P < 0.05) in dogs (-40 +/- 4.2%) than in pigs (-22 +/- 2.1%) and baboons (-4 +/- 2.4%). In five dogs and five pigs, three separate 10-min CAO, each 2 days apart, were also examined. In dogs, reductions in wall thickening after CAR were significantly less following the second (-26 +/- 4.2%) or third (-30 +/- 3.2%) CAO, compared with the first CAO (-47 +/- 4.9%). In contrast, repetitive CAO did not induce differences in recovery of wall thickening in pigs. These results indicate that myocardial stunning is less severe in conscious pigs and baboons, compared with conscious dogs, despite more intense transmural ischemia. The dogs demonstrated a "preconditioning-like effect" with serial brief CAO, which was not exhibited in pigs.

Responses to coronary artery occlusion in conscious dogs with selective cardiac denervation.

The extent to which cardiac denervation alters responses to myocardial ischemia remains controversial. This study compared responses to 24-h coronary artery occlusion (CAO) on measurements of wall thickness (ultrasonic crystals), regional myocardial blood flow (microspheres), and infarct size (triphenyltetrazolium chloride technique) in three groups of conscious dogs with 1) selective posterior left ventricular (LV) wall denervation, 2) selective ventricular denervation, or in 3) intact dogs. After CAO, hemodynamic changes were not different among the three groups. Wall thickening in the ischemic zone became akinetic or paradoxical early after CAO and did not recover in any group over the 24-h monitoring period. Blood flow in the area at risk fell similarly in all groups. Infarct size, as a percentage of the area at risk, was 45 +/- 7% in intact, 48 +/- 6% in posterior LV wall-denervated, and 48 +/- 8% in ventricular-denervated group. There was, however, a lower (P less than 0.05) frequency of arrhythmic beats per minute after 3 h of CAO in the ventricular-denervated group (3.2 +/- 1.4) compared with the intact (11.3 +/- 4.1) or posterior wall-denervated (12.6 +/- 3.2) group. An additional group of ventricular-denervated dogs was studied to determine the effects of sequential, brief 2-min CAO at 2, 4, and 8 wk after denervation. Responses of regional wall thickening to CAO were not affected significantly even after 8 wk following ventricular denervation. Thus, in conscious dogs, neither selective ventricular denervation nor selective denervation of the posterior LV wall improved collateral blood flow, affected regional function favorably, or reduced infarct size after CAO.

The effects of RO-22-4679, a thromboxane synthetase inhibitor, on ventricular fibrillation induced by coronary artery occlusion in conscious dogs.

The effects of RO-22-4679, a thromboxane synthetase inhibitor, on ventricular fibrillation induced by coronary artery occlusion in conscious dogs.

Myocardial function in areas of heterogeneous perfusion after coronary artery occlusion in conscious dogs.

Regional myocardial function and blood flow in endocardial layers were correlated in myocardial segments subtending severely ischemic and adjacent, normally perfused myocardium in conscious dogs 1--3 weeks after recovery from coronary artery occlusion. With coronary artery occlusion induced by a hydraulic occluder, endocardial blood flow (measured with radioactive microspheres) and function (determined with an ultrasonic dimension gauge) in homogeneously nonischemic segments increased slightly but not significantly. In homogeneously ischemic segments, blood flow and function decreased (p less than 0.01) by 96 +/- 1% and 98 +/- 4%, respectively. In segments subtending zones of unequal perfusion, endocardial blood flow increased nonsignificantly in the myocardium surrounding the nonischemic crystal, while decreasing by 93 +/- 2% (p less than 0.01) in myocardium surrounding the ischemic crystal. Surprisingly, these segments behaved like homogeneously ischemic segments, i.e., endocardial shortening decreased by 92 +/- 6% (p less than 0.01). Thus, the failure to detect shortening despite normal perfusion of the myocardium surrounding one of the transducers suggest a potential problem with interpretation of regional function measurements or an inability of the apparently nonischemic myocardium to contract.

Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs.

When acute myocardial infarction occurs in patients with hypertension and left ventricular hypertrophy (LVH), the incidence of sudden cardiac death increases markedly. Possible explanations include increased size of the occluded vascular bed secondary to more extensive atherosclerotic coronary vascular disease in the presence of hypertension, decreased coronary reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in hypertrophied cardiac muscle. To explore these possibilities, we produced acute circumflex coronary occlusion during the resting, conscious state in 32 control dogs and in 28 dogs with hypertensive LVH. Before coronary occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and 125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and 32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less than 0.01 vs control). The perfusion fields of the occluded vessel defined by postmortem coronary angiography were similar in the two groups (31 +/- 2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH). Thus, the increased incidence of sudden cardiac death after coronary artery occlusion in hypertensive LVH dogs cannot be explained by increased size of the occluded vascular bed and is probably related to the decreased coronary reserve or intrinsic electrophysiologic abnormalities that characterize pressure-induced hypertrophied cardiac muscle.

Regional left ventricular wall thickness early and late after coronary occlusion in the conscious dog.

Regional wall thickness and endocardial segment lengths in normal and ischemic zones of the left ventricle were measured simultaneously with ultrasonic-dimension gauges before and after chronic circumflex artery occlusion in conscious dogs. After 3 wk, end-diastolic segment lengths (EDL) in normal zones increase 10% (P less than 0.01), shortening increased 22% (P less than 0.05), and end-diastolic wall thickness (EDWT) was reduced by 12.8% (P less than 0.01). In ischemic zones at 3 wk, EDL was reduced by 15.4% (P less than 0.01), and subendocardial shortening recovered slightly to 15% of control; EDWT increased 11% at 3 days postocclusion and thereafter remained near control values (change not significant), but systolic wall thickening improved substantially, reaching 38% of control at 3 wk. Thus, tissue loss and slight return of function occurred in the ischemic subendocardium, whereas overall wall function (as reflected by regional wall thickening) improved considerably over time. These findings suggest that recovery of function in the outer layers of the wall after myocardial infarction modifies the close correlation between regional subendocardial segment and wall thickening dynamics observed acutely.

The circulatory influences of vagal afferents at rest and during coronary occlusion in conscious dogs.

We studied the role of cardiopulmonary vagal afferents in the cardiovascular responses to coronary artery occlusion in conscious dogs with intact carotid sinuses and following functional denervation of the arterial baroreceptors. The contributions of vagal afferents were determined by cold blocking the vagi. In dogs with intact carotid sinuses, coronary artery occlusion produced small decreases in mean cardiac output and arterial pressure, whereas heart rate increased by 35 beats/min. In dogs with intact carotid sinuses, vagal cold block increased mean arterial pressure by 22 +/- 2 (mean +/- SE) mm Hg and heart rate by 90 +/- 6 beats/min. Mean cardiac output increased by 505 +/- 90 ml/min. With the exception of heart rate, responses to coronary occlusion during vagal cold block were similar to the occlusion response prior to vagal cold block. Furthermore, prior occlusion of the coronary artery did not significantly influence the responses to vagal cold block. After arterial baroreceptor denervation, coronary artery occlusion resulted in a substantially greater fall in systemic arterial pressure (-52 mm Hg as compared to -8 mm Hg, with intact carotid sinuses) and peripheral resistance decreased by -0.49 peripheral resistance units (PRU). Vagal cold block following denervation increased the arterial pressure by 49 +/- 10 mm Hg and peripheral resistance by 0.59 +/- 0.13 PRU. Both values were significantly greater than those observed during vagal cold block prior to denervation. In arterial baroreceptor-denervated dogs, vagal blockade significantly attenuated the response to coronary occlusion. Therefore, in conscious dogs, vagal afferents from cardiopulmonary receptors exert a significant inhibitory influence on the peripheral vascular tone. When the carotid sinuses are intact, this inhibitory influence appears to be marked during myocardial ischemia. In the absence of functional arterial baroreflexes, vagal afferent activity contributes to the depressor responses observed during ischemia.

Prostaglandin inhibition increases infarct size after coronary artery occlusion in conscious dogs

Prostaglandin inhibition increases infarct size after coronary artery occlusion in conscious dogs

Treatment of ventricular arrhythmias occurring during acute coronary artery occlusion in conscious dogs

Treatment of ventricular arrhythmias occurring during acute coronary artery occlusion in conscious dogs

Ineffectiveness of prophylactic atropine in decreasing arrhythmias and enhancing survival following acute coronary artery occlusion in conscious dogs

Ineffectiveness of prophylactic atropine in decreasing arrhythmias and enhancing survival following acute coronary artery occlusion in conscious dogs