Hours Of Coronary Occlusion Research Articles

Reduction in severity and extent of myocardial infarction when nitroglycerin and methoxamine are administered during coronary occlusion.

The effects of treatment with nitroglycerin (TNG) and methoxamine on the degree of ischemic injury occurring during 5 hours of coronary occlusion were studied in 31 closed-chest sedated dogs. Acute coronary occlusion was produced by inflating a cuff previously implanted around the left anterior descending coronary artery. After 10 min of ischemia (assessed by intramyocardial electrodes), dogs were randomized into control and treated groups. Treated dogs received i.v. TNG during the remainder of the 5 hour occlusion. Arterial pressure was maintained at preinfusion levels with i.v. methoxamine. Six of 16 control dogs died; three of 15 treated dogs died. After 24 hours severity of infarct was assessed in survivors by gross inspection, and more quantitatively, by measurement of creatine phosphokinase (CPK) content of myocardium adjacent to each electrode. Transmural infarction was observed in all of the ten surviving control animals but in only two of the 12 treated animals. In control dogs, CPK was inversely related to ST segment elevation observed after 10 min of occlusion: the greater the ST elevation, the lower the myocardial CPK level. This relation was modified in the treated group: at comparable initial levels of ischemia (as judged by ST segment elevation prior to treatment), treated dogs had significantly less CPK depression than control dogs ( P < 0.025). Moreover, in controls, a significant reduction in CPK occurred at 48 of 57 electrode sites where ST elevation was observed after 10 min of occlusion. Only 19 of 69 such sites showed significant CPK reduction in the treated dogs ( P < 0.001). Thus, administration of TNG, with support of arterial pressure by methoxamine, markedly reduces the severity and extent of infarction occurring after 5 hours of coronary occlusion in the dog.

Consequences of reperfusion after coronary occlusion: Effects on hemodynamic and regional myocardial metabolic function

Hemodynamic and regional metabolic measurements were obtained in seven closed chest dogs during a control period, 3 hours of coronary occlusion and 5 hours of reperfusion. Reperfusion resulted in intermittent ectopic arrhythmias in five dogs and severe shock in two. It usually caused increases in heart rate, coronary sinus flow and maximal isovolumetric rate of rise in left ventricular pressure (dP/dt), which were associated with a decrease in systemic pressure, left ventricular end-diastolic pressure, systemic vascular resistance and stroke work. A transitory increase in cardiac output occurred. Global myocardial oxygen consumption, which was reduced during occlusion, increased with reperfusion. Reperfusion induced abnormal lactate metabolism and myocardial potassium loss in the previously occluded area and often in the nonoccluded segment as well. Histopathologic changes of accelerated necrosis, reactive hyperemia and hemorrhage were often noted after reperfusion. These studies indicate that reperfusion after 3 hours of occlusion caused serious abnormalities in hemodynamic states, metabolic function and morphologic features of the heart.

The value of warning arrhythmias in the prediction of ventricular fibrillation within one hour of coronary occlusion. Experimental studies in the baboom

Factors associated with the development of ventricular fibrillation after coronary artery ligation were studied in a subhuman primate (Cape Chacma baboon). In 25 or 66 per cent of 38 baboons, primary ventricular fibrillation occurred within the first hour after the onset of acute myocardial infarction. Increasing age, total heart weight, and the size of the infarct were directly related to the incidence of primary ventricular fibrillation. Anterolateral infarcts had the highest risk of ventricular fibrillation. Anteroseptal and posterior infarcts had the best survival rate for the first hour. Male baboons were more prone to develop ventricular fibrillation than were females. There was no definite progression from ventricular ectopic beats to ventricular fibrillation. In the presence of ventricular tachycardia (even when brief in duration), ventricular bigeminy, or R-on-T beats, ventricular fibrillation has to be expected from the time of onset of the arrhythmia till 30, 20, or 10 minutes have elapsed, respectively. Beyond these times, ventricular fibrillation did not develop during the experimental period. Conversely, the absence of these signs could predict survival for 1 hour. The over-all efficiency of the warning signs in predicting ventricular fibrillation or survival was 85 per cent. Ventricular fibrillation occurred without any of these 3 warning signs in only 1 baboon (5 per cent of all cases). It is suggested that these warning arrhythmias could have a practical value in the management of patients with acute myocardial infarction of recent onset by anticipating the time of impending ventricular fibrillation.

The reflex stimulation of catecholamine secretion during the acute stage of myocardial infarction in the dog.

1. The mechanism of catecholamine secretion after coronary occlusion was investigated in open-chest, anaesthetized dogs; the blood-bathed organ technique was used for continuous measurement of the changes in concentration of circulating catecholamines. 2. In dogs with increased output of adrenaline during the first hour after acute coronary occlusion, topical application of lignocaine to the infarcted area of the heart, spinal block at C1, bilateral section of thoracic splanchnic nerves, or ganglionic blockade virtually abolished adrenaline secretion. 3. Adrenaline secretion was abolished by bilateral vagotomy in 50% of the dogs, decreased in 28% and unchanged in the remaining 22%. Bretylium or guanethidine had no effect on adrenaline secretion in the early stages of myocardial infarction. 4. Seventeen of nineteen reserpinized dogs failed to secrete catecholamines during the first hour of coronary occlusion, even though the adrenal medulla responded to bradykinin, acetylcholine or nicotine. Noradrenaline infused either into the unoccluded carotid artery or intravenously restored adrenal medullary secretion. 5. When a sustained noradrenaline release occurred after coronary ligation, it was abolished by topical application of lignocaine to the ischaemic area of the heart or by ganglionic blockade. Neither bilateral vagotomy nor section of both thoracic splanchnic nerves suppressed noradrenaline liberation. 6. It is concluded that the adrenal medullary secretion of adrenaline which occurs in the early stages of myocardial infarction in the dog is induced reflexly from stimulation of cardiac receptors at the site and the boundary of the infarct. The reflex involves vagal as well as extra-vagal pathways and supraspinal structures. Enhanced liberation of noradrenaline in the early stage of infarction may reflect release from postganglionic sympathetic nerve endings in the heart.

News of a new blue

To characterize the functional and biochemical recovery of myocardium salvaged by reperfusion, 19 anesthetized mongrel dogs underwent 2 hour occlusion of the proximal left anterior descending coronary artery, followed by reperfusion for up to 2 weeks. Thirteen dogs had a permanent occlusion and served as the control group. All dogs had serial two-dimensional echocardiograms and in vivo biopsies for adenosine triphosophate (ATP) and creatine phosphate after occlusion and at the time of sacrifice (6 hours, n = 15; 7 days, n = 6; or 14 days after occlusion, n = 11). The area of necrosis and area at risk of necrosis were identified in dogs sacrificed at 6 hours.After 4 hours of reperfusion, the area of necrosis determined by the triphenyltetrazolium chloride technique, expressed as a function of the area at risk by in vivo monastral blue injection, was 23.9 ± 5.8% (mean ± standard error of the mean) and largely subendocardial, compared with 89.1 ± 5.3% in dogs with permanent (6 hour) occlusion (probability [p] < 0.001), in which it was transmural. Myocardial contractility was assessed by measuring systolic wall thickening by computer-assisted two-dimensional echocardiography. Before occlusion, this variable averaged 47.9 ± 6.3% in the region to become ischemic. An early salutary effect of reperfusion in the central ischemic zone was seen as a decrease in wall thinning from -11.9 ± 2.9%, 90 minutes after occlusion, to -7.4 ± 2.0%, 4 hours after reperfusion, contrasted with a change from -6.2 ± 3.3%, 90 minutes after occlusion, to -11.7 ± 3.3%, 6 hours after occlusion in the permanently occluded group (p < 0.05). Active thickening was not observed until 72 hours of reperfusion (13.1 ± 4.6%); this increased to 19.5 ± 2.8% at 14 days, compared with 1.5 ± 5.9% in the permanently occluded group at this time (p < 0.05). However, preocclusion values were not achieved in the reperfused group. Some recovery of ATP in the salvaged subepicardium was also noted, with return of levels from 8.0 ±1.9 nmol/mg protein, 90 minutes after occlusion, to 13.2 ± 1.8 nmol/mg protein, after 4 hours of reperfusion (p < 0.05); however, 7 days were required for recovery approaching preocclusion values of 34.9 ± 1.9 nmol/mg protein.Thus, reperfusion after 2 hours of coronary occlusion resulted in recovery of jeopardized myocardium, in which the deterioration of function observed in nonreperfused tissue was reversed and biochemical improvement occurred over the course of 2 weeks. Computer-assisted two-dimensional echocardiography, a noninvasive but quantitative technique, appears well suited to monitor the rate of functional recovery of myocardium salvaged by reperfusion.