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Oxygen radical-induced myocardial lipid peroxidation may cause injury during regional ischemia and reperfusion. However, in vivo detection of lipid peroxidation is difficult. Since conjugated dienes are lipid peroxidation products of unsaturated fatty acids, we evaluated the potential value of detection of these double-bonded fatty acids as a marker of oxygen radical injury. In seven untreated and five superoxide dismutase-treated anesthetized dogs exposed to 90 min of coronary occlusion and subsequent reperfusion, coronary sinus plasma draining the ischemic and reperfused region was assayed for dienes. Lipids were extracted and diene optical density measured at 233 nm wavelength. Superoxide dismutase (5 mg/kg, total dose) was infused into the left atrium during ischemia and the first 30 min of reperfusion. Coronary sinus diene optical density increased in untreated animals at 5 and 10 min of reperfusion (reperfusion optical density (x +/- SEM): 5 min = 1.49 +/- 0.20 absorbance units, 10 min = 1.36 +/- 0.06; both p less than 0.05 vs preocclusion optical density = 1.10 +/- 0.05 and 25 min reperfusion = 1.20 +/- 0.07). No increase in diene optical density occurred in superoxide dismutase-treated dogs. Myocardial lipid peroxidation products, as conjugated dienes, increased in coronary sinus plasma during early reperfusion and this increase was prevented by superoxide dismutase infusion.
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PMID:Superoxide dismutase decreases early reperfusion release of conjugated dienes following regional canine ischemia. 273 May 25

To better define the usefulness of blood myoglobin measurements in evaluating the effectiveness of attempted thrombolysis, we studied the kinetics of myoglobin entry into and removal from the circulation after coronary artery reperfusion and the relation between directly measured depletion of myocardial myoglobin after coronary occlusion and reperfusion and the amount of depletion predicted from plasma myoglobin concentration-time curves. Initially, canine myoglobin was administered to 11 dogs by both bolus injection and 40-minute infusion, and the subsequent disappearance patterns of myoglobin from plasma monitored by radioimmunoassay. A monoexponential regression line (corresponding to a one-compartment model) and a biexponential regression line (corresponding to a two-compartment model) were determined for each set of washout data, the kinetic parameters were calculated, and the goodness of fit of each model was assessed. Results were similar after both methods of myoglobin administration. In five of 11 animals, the one-compartment model described the myoglobin kinetics better; in the other six animals, the two-compartment model was statistically superior, but values for the volume of distribution and elimination rate constant differed by only 10% from the one-compartment estimates. After bolus administration of myoglobin and with a one-compartment model, the volume of distribution of myoglobin was determined to be 1,601 +/- 77 (SEM) ml, representing 6.8 +/- 0.2% of total body weight; the elimination rate constant averaged 0.132 +/- 0.006/min and corresponded to a mean half-time of disappearance of 5.5 +/- 0.2 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of myoglobin release and prediction of myocardial myoglobin depletion after coronary artery reperfusion. 276 16

This study examined whether N-acetylcysteine, a low molecular weight compound used clinically to replenish glutathione, could limit tissue necrosis during acute myocardial infarction in hearts with minimal coronary collateral flow. Fifty rabbits underwent 45 mins ischemia with and without coronary reperfusion for 3h. Four groups were studied. Saline or N-acetylcysteine (140 mg/kg) was administered intravenously 10 mins before occlusion and continued for 35 mins after occlusion. The area at risk of necrosis was assessed with fluorescent particles and the area of tissue necrosis was defined using triphenyltetrazolium chloride staining. No differences were observed for tissue necrosis expressed as a percentage of the risk zone size (mean +/- SEM, 46.7 +/- 8.2% versus 46.3 +/- 8.2%) for saline and N-acetylcysteine treated rabbits subjected to 45 mins coronary occlusion. Tissue necrosis in rabbits with 45 mins ischemia followed by 3 h reperfusion was not significantly reduced with N-acetylcysteine treatment (36.4 +/- 5.1%) compared to untreated controls (36.5 +/- 6.4%). Risk zone size and hemodynamic parameters were similar between the treatment groups. Thus, treatment before and during short term coronary occlusion did not limit tissue necrosis during acute myocardial infarction.
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PMID:Effect of N-acetylcysteine on tissue necrosis during acute myocardial infarction in rabbits. 279 May 79

To examine the effects of ischemic preconditioning on efferent autonomic responses following acute transmural myocardial ischemia/infarction (MI), the time course and extent of efferent sympathetic and vagal denervation were compared between control dogs that received a one-stage sustained coronary occlusion and preconditioned dogs that received four 5-minute coronary occlusions separated by 5 minutes of reperfusion before sustained occlusion. Effective refractory periods (ERP) basal and apical to MI were determined in the baseline state and during neural stimulation before and after preconditioning occlusions and 20, 60, 120, and 180 minutes after sustained occlusion by ligature ligation of diagonal branches of the left anterior descending coronary artery. In 10 control dogs with transmural MI, ERP shortening induced by bilateral ansae subclaviae stimulation (4-msec pulses, 2-4 Hz and 2-4 mA) was unchanged at basal sites but was attenuated at apical sites. Four of 40 apical test sites exhibited efferent sympathetic denervation (less than or equal to 2 msec shortening) 20 minutes after sustained occlusion. Thirteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, ERP shortening at apical sites was unchanged after preconditioning occlusions and during the first 60 minutes of sustained ischemia but was attenuated at 120 minutes. Three of 40 apical test sites became denervated during a 3-hour period. The cumulative percentage of denervated apical test sites was significantly less in the preconditioned group compared with the control group (p = 0.006) despite a comparable degree of subepicardial involvement in the MI (8.2 +/- 1.0% vs. 8.4 +/- 1.4%, the ratio to the left ventricular circumference, mean +/- SEM). In 11 control dogs tested for efferent vagal response after MI, ERP prolongation induced by bilateral vagal stimulation (4-msec pulses, 20 Hz with current strength 0.05 mA greater than that required to produce asystole) was unchanged at basal sites, but was attenuated at apical sites, and five of 44 test sites exhibited denervation (less than or equal to 1 msec prolongation) 20 minutes after sustained coronary occlusion. Fourteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, vagally induced ERP prolongation was unchanged both at basal and apical sites, and none of 36 apical test sites exhibited denervation after preconditioning and during a 3-hour period of sustained coronary occlusion (p less than 0.001 vs. control group) despite a comparable degree of subendocardial involvement in the MI (11.8 +/- 0.8% vs. 11.9 +/- 1.3%).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Protection against autonomic denervation following acute myocardial infarction by preconditioning ischemia. 291 77

The effect of a brief period of coronary occlusion on a regional myocardial cross-sectional area was studied in 6 conscious dogs. Subendocardial segment length and wall thickness were continuously measured with a sonomicrometer in the central ischemic area perfused by the left circumflex coronary artery during a 2-min circumflex occlusion and subsequent reperfusion. Measurements were repeated before and after collateral development induced by 180 +/- 30 (SEM) 2-min circumflex occlusions (20 +/- 3 days). In order to evaluate the changes in regional myocardial volume, end-diastolic regional cross-sectional area was calculated as a product of end-diastolic segment length and wall thickness. Before collateral development, end-diastolic regional cross-sectional area transiently decreased 1.4 +/- 0.6% (NS) at 10 sec following sudden coronary occlusion, thereafter gradually increased to 3.7 +/- 1.0% (P less than 0.05) at the end of a 2-min occlusion. At 10 sec of reperfusion, end-diastolic regional cross-sectional area further increased to 7.0 +/- 1.1% (P less than 0.05) probably due to increased intravascular volume. Increase in end-diastolic regional cross-sectional area was still 2.5 +/- 0.6% (NS) at 3 min after the release of occlusion. After collateral development, the changes in end-diastolic regional cross-sectional area were 0.1 +/- 0.1% (NS), 0.4 +/- 0.3% (NS), 1.0 +/- 0.6% (NS) and 0.2 +/- 0.4% (NS), respectively. Thus, a significant increase in the regional myocardial cross-sectional area occurs during a brief period of coronary occlusion and reperfusion.
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PMID:Changes in regional myocardial cross-sectional area during brief coronary occlusion and reperfusion in conscious dogs. 292 85

We have previously reported that regional wall motion abnormalities in a canine model of acute myocardial infarction may show substantial improvement in the first 6 weeks after infarction. To determine whether the mechanism of this improvement in function is the result of scar contraction within the infarct, we studied the relationship between changes in regional wall motion defined by cross-sectional echocardiography and the regional concentration of radioactive microspheres injected immediately before coronary occlusion and sampled 6 weeks after occlusion. Eight dogs underwent serial echocardiographic and microsphere blood flow measurements immediately before and 30 minutes, 48 hours, 1 week, 3 weeks, and 6 weeks after ligation of the left anterior descending or the left circumflex coronary artery. Wall motion and blood flow were measured in the short-axis section of the left ventricle at the level of the midpapillary muscle in each 10-degree radial segment around the circumference of the ventricle. Infarct histology was assessed at 6 weeks by means of the same radial coordinate system. Control data were collected in a similar manner from four dogs that underwent sham operations and had no histologic evidence of infarction. In all of the animals with infarcts, but not in the sham animals, the calculated preocclusion endocardial and epicardial blood flow values in the histologic infarct zone (252 +/- 44 and 168 +/- 17 ml/min/100 gm, respectively, mean +/- SEM) were significantly higher than those in the normal opposite wall (endocardial: 106 +/- 3 ml/min/100 gm, p less than 0.01); epicardial: 108 +/- 3 ml/min/100 gm, p less than 0.01. The location and circumferential extent of myocardium showing this elevation of preocclusion blood flow correlated well (r = 0.93, p less than 0.001) with the location and circumferential extent of the histologic infarct. The amount of wall motion abnormality, measured from the "correlation plot area," decreased significantly from its maximum value of 39 +/- 3 degrees at 48 hours after coronary occlusion to 3 +/- 1 degrees (p less than 0.001) at 6 weeks after occlusion. The ratio of the preocclusion transmural blood flow in the infarct zone to that in the noninfarct zone, a measure of the condensation of the microspheres injected before coronary occlusion, and therefore of the degree of scar contraction at 6 weeks, correlated well (r = 0.83, p less than 0.01) with the recovery of wall motion 6 weeks after infarction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Relationship of functional recovery to scar contraction after myocardial infarction in the canine left ventricle. 292 98

The effects of isosorbide dinitrate on acute myocardial ischaemia were studied in 19 patients during coronary angioplasty. The duration of balloon inflation to the onset of ST segment depression was increased by the administration of intracoronary isosorbide dinitrate from (mean +/- SEM) 13 +/- 2 to 20 +/- 2 s (48%) (P less than 0.01) and the duration to 1 mm ST segment depression increased form 23 +/- 2 to 29 +/- 3 s (28%) (P less than 0.01). Systolic blood pressure fell from 118 +/- 3 to 111 +/- 4 mmHg but there was no change in intracoronary distal occlusion pressure. Thus during coronary occlusion isosorbide dinitrate prolongs the time to the onset of myocardial ischaemia.
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PMID:Effects of intracoronary isosorbide dinitrate during acute myocardial ischaemia: a study during angioplasty. 297 Mar 88

An increase in plasma renin activity (PRA) following experimental coronary occlusion has previously been demonstrated in anaesthetized and conscious dogs. The purpose of the present study was to analyse the mechanism of this renin release. In two distinct models of myocardial ischaemia in anaesthetized dogs--i.e. occlusion of the left-anterior descending coronary artery (model A, n = 21) and atrial pacing in the presence of stenosis of the left-anterior descending coronary artery (model B, n = 23), an increase in arterial PRA was found from 1.68 +/- 0.43 to 3.06 +/- 0.63 ng ml-1 h-1 (model A, mean +/- SEM, P less than 0.025) and from 9.87 +/- 3.59 to 14.96 +/- 4.06 ng ml-1 h-1 (model B, P less than 0.05), respectively. The increase in PRA following coronary occlusion was not blunted by adrenergic beta-receptor blockade with propranolol (3 mg kg-1 i.v.; n = 4). Coronary sinus PRA was lower than arterial PRA and the increase in PRA did not occur in nephrectomized dogs (n = 5). The data suggest that myocardial ischaemia induces a release of renin from the kidney which is not mediated by adrenergic beta receptors.
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PMID:On the mechanism of renin release during experimental myocardial ischaemia. 300 60

This study investigated whether nitroglycerin can improve ischemic zone blood flow and function when its infusion is delayed following left anterior descending (LAD) occlusion. Nitroglycerin (200 micrograms/min, 11 dogs) or saline (six dogs) was infused for 2 hours starting 2 hours after occlusion. Regional myocardial blood flow (MBF) was measured (9 +/- 1 micron radioactive microspheres) before and at 2 and 4 hours after occlusion. Segmental contraction was determined by cineroentgenography of implanted tantalum markers. For all ischemic samples (defined as MBF less than or equal to 0.4 ml/min/gm), the average improvement in MBF in the epicardial half (EPI) was 0.05 +/- 0.02 ml/min/gm (mean +/- SEM) with nitroglycerin vs 0.06 +/- 0.06 with saline (p greater than 0.5). Improvement in the endocardial half (ENDO) averaged 0.03 +/- 0.03 ml/min/gm with nitroglycerin vs 0.09 +/- 0.08 with saline (p = 0.5). Contraction in the ischemic zone ceased following occlusion and was unaffected by nitroglycerin or saline. Control blood flows in the ischemic region were 22% less in the ENDO (p less than 0.001) and 19% less in the EPI (p less than 0.005) than in nonischemic myocardium. These results indicate that 2 hours after LAD occlusion in dogs, nitroglycerin was unable to improve ischemic zone collateral flow or contractile function compared to untreated controls. Lower ischemic zone control flows indicate that infarct volume expansion may occur within 4 hours after coronary occlusion.
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PMID:Failure of nitroglycerin introduced after prolonged myocardial ischemia to improve collateral blood flow and function in tranquilized dogs. 309 9

In the anesthetized open-chest dog the ischemic area produced by coronary occlusion is surrounded by an area of nonischemic contractile dysfunction, identified as the functional border zone. To establish whether a similar functional border zone exists in the conscious animal during acute regional ischemia and to determine its spatial dimensions and temporal changes, we performed simultaneous two-dimensional echocardiography and radioactive microsphere studies in nine chronically instrumented dogs. We produced circumferential flow-function maps at 22.5-degree intervals over the full circumference of the left ventricle at the midpapillary muscle level during control conditions, 5 minutes after left circumflex occlusion, and 2.5 hours after left circumflex occlusion. After occlusion there was no change in left ventricular end-diastolic area, an increase in left ventricular end-systolic area (p less than 0.01), and a decrease in left ventricular area ejection fraction (p less than 0.01). The circumferential extent of left ventricular dysfunction was 197 +/- 11 degrees (mean +/- SEM) at 5 minutes of left circumflex occlusion, whereas the extent of subendocardial hypoperfusion was 144 +/- 6 degrees (p less than 0.0005). This produced a functional border zone measuring 54 +/- 8 degrees, or 25% of the nonischemic myocardium, which did not change over the 2.5-hour occlusion period. Despite a modest but significant decrease in wall thickening (70 +/- 6% to 43 +/- 6%; p less than 0.01) in the functional border zone, there was no difference in subendocardial blood flow between the functional border zone and the control nonischemic area. We conclude that a discrete functional border zone exists in the conscious dog during acute regional ischemia produced by circumflex coronary occlusion, which does not change during the early evolution of myocardial infarction. The functional border zone likely contributes to minor overestimation of infarct size in the early hours after myocardial infarction if extent of left ventricular dysfunction is used as an index of infarction in humans.
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PMID:Spatial and temporal characteristics of circumferential flow-function relations during acute myocardial ischemia in the conscious dog. 319 36


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