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Biomedical subjects

R E Goldstein

Publications and source records attributed to R E Goldstein.

At least 145 records · Page 8Linked to original sources
PubMed1981

Lack of effect of aspirin on myocardial infarct size in the dog.

Pretreatment with platelet-inhibitory doses of aspirin (3 mg/kg body weight) has been shown to augment epicardial collateral flow by more than 50 percent (p less than 0.05) 4 hours after ligation of the left anterior descending coronary artery in dogs. To determine whether this favorable influence of aspirin is sufficient to decrease the amount of infarcted tissue, either intravenous aspirin, 3 mg/kg (n = 17), or saline solution (n = 17) was administered to dogs 10 minutes before occlusion of the left anterior descending coronary artery. Administration of saline solution or aspirin was repeated every 24 hours. By 72 hours, 5 dogs in each treatment group had died. Survivors were killed at 72 hours. The portion of the left ventricle at risk of infarction was delineated by perfusion of the aortic root with Evans blue and simultaneous perfusion of the distal left anterior descending coronary artery with saline solution under equal physiologic pressures. Slices of the stained heart were incubated with triphenyltetrazolium to identify gross infarct (with histologic confirmation). Total mass of left ventricle, myocardium at risk, and infarct size were measured in each dog. A direct relation was found between the mass at risk and the mass infarcted (r = 0.84, p less than 0.001). Aspirin-treated dogs did not differ from control dogs in percent ventricle at risk (mean +/- standard error 37 +/- 2 versus 40 +/- 2), percent infarct weight/left ventricle (29 +/- 3 versus 31 +/- 2) or percent infarct weight/weight of ventricle at risk (78 +/- 4 versus 77 +/- 3). Thus, despite aspirin's ability to inhibit platelet aggregation and to increase epicardial collateral flow by more than 50 percent, aspirin treatment failed to reduce infarct size in this dog model.

Animals↗
PubMed1980

Relative effects of aspirin on platelet aggregation and prostaglandin-mediated coronary vasodilatation in the dog.

Aspirin, as an inhibitor of platelet aggregation, may be of benefit in ischemic heart disease. However, aspirin blocks not only platelet aggregation but also synthesis of prostacyclin, a vasodilator and platelet deaggregator. The relative sensitivity of prostaglandin-mediated coronary vasodilatation and platelet aggregation to inhibition by aspirin remains uncertain. We therefore investigated the relative dose-response relationship of aspirin on arachidonic acid-induced increments in coronary blood flow and on ADP-induced aggregation of platelets. In 11 open-chest dogs, intracoronary arachidonic acid, 0.1-3.0 mg, produced dose-related increases in coronary blood flow that were inhibited progressively by i.v. aspirin over the dose range 0.3-3.0 mg/kg. Aspirin at 3 mg/kg almost completely obliterated the response to 3 mg of arachidonic acid. Similarly, aspirin doses of 0.3-3.0 mg/kg progressively raised the minimal concentration of ADP necessary for platelet aggregation. The threshold concentration of ADP that produced aggregation of platelets from 10 control dogs ranged from 2.3 x 10(-6) M to 1.2 x 10(-5) M. Aspirin at 3 mg/kg completely inhibited aggregation of platelets from 11 of 12 dogs, even with ADP at 2.3 x 10(-4) M concentration, the maximum tested. Aspirin at 0.1 mg/kg failed to inhibit either ADP-induced platelet aggregation or arachidonic acid-induced increments in coronary blood flow. Thus, the two test systems showed similar sensitivity to inhibition by aspirin with respect to threshold dose and maximal effect. These results show that very low doses of aspirin inhibit arachidonic acid-induced coronary vasodilatation and that aspirin at low doses does not appear to selectively inhibit platelet activity relative to coronary vasodilatation.

Adenosine Diphosphate↗
PubMed1979

Exercise performance after septal myotomy and myectomy in patients with obstructive hypertrophic cardiomyopathy.

The effect of left ventriculomyotomy and myectomy on exercise capacity and cardiac function in patients with obstructive hypertrophic cardiomyopathy has not previously been determined. In this study, 29 patients were evaluated during graded treadmill exercise before and after operation. Postoperatively, 27 of 29 patients reported symptomatic improvement and had greatly reduced left ventricular outflow gradient. Twenty-five of 28 patients (89 percent) attained higher exercise levels after operation, and this was accompanied by an increase in total body oxygen consumption from 16 to 21 ml/min per kg (P less than 0.005). A significant increase in cardiac index during maximal exercise also accompanied this improved exercise performance (5.0 to 5.7 liters/min per m2, P less than 0.05). The increase in maximal cardiac index was associated with greater desaturation of mixed venous blood (34 to 24 percent, P less than 0.02) in patients with preoperative angina. At a given level of mixed venous oxygen saturation (30 percent), overall mean cardiac index was higher postoperatively (4.6 to 5.2 liters/min per m2, P less than 0.05). These results suggest that, although several mechanisms probably contribute to symptomatic improvement after myotomy and myectomy, enhanced cardiac performance plays an important role in the majority of patients.

Adolescent↗
PubMed1979

Effect of glyceryl trinitrate on echocardiographic left ventricular dimensions during exercise in the upright position.

Changes in left ventricular size may be of importance in the development of angina and in its amelioration by glyceryl trinitrate, but left ventricular dimensions have not been measured during exercise in the upright position, the circumstance in which angina most often occurs. To assess changes in left ventricular end-systolic and end-diastolic dimensions, echocardiograms were obtained from 5 normal subjects and 6 patients with angina during rest and exercise upright, both before and after glyceryl trinitrate. The end-systolic dimension was considered an index of regional performance rather than an estimate of overall left ventricular behaviour. During exercise the end-diastolic dimension rose both in the normal subjects and in the patients. The end-systolic dimension fell progressively with exercise in the normal subjects but changed inconsistently in the patients. Glyceryl trinitrate lowered the end-diastolic dimension during exercise below comparable pretreatment values in both groups; the glyceryl trinitrate-induced decrease in end-diastolic dimension in the patients diminished at higher exercise levels. In all normal subjects and in 4 of the 6 patients with normal systolic shortening (= end-diastolic--end-systolic dimension) glyceryl trinitrate caused relatively small changes in the end-systolic dimension and systolic shortening on exercise. In contrast, in the 2 patients with hypokinetic ventricles glyceryl trinitrate conspicuously decreased the end-systolic dimension and increased systolic shortening. Thus, during exercise, in the normal subjects and in the patients with normally functioning left ventricles on echocardiography, glyceryl trinitrate caused a modest fall in the end-diastolic dimension and little change in the end-systolic dimension, but in patients with ventricular hypokinesia it greatly improved regional contractile performance. Alleviation of ischaemic hypokinesia during exercise may be an important part of the benefit of glyceryl trinitrate.

Adult↗
PubMed1979

Aspirin-induced increase in collateral flow after acute coronary occlusion in dogs.

Aspirin (acetylsalicylic acid) has inhibitory effects on platelet function and prostaglandin synthesis. Since alterations in either platelet function or prostaglandin-mediated vascular responses could influence blood flow to ischemic myocardium, we tested the effects of aspirin on coronary collateral flow after acute occlusion of the left anterior descending coronary artery in dogs. Aspirin dose (600 mg i.v.) consistently inhibited in vitro ADP-induced platelet aggregation. In 13 open-chest dogs, regional myocardial blood flows (radioactive microsphere technique) were determined at 5 minutes and 4 hours after occlusion). In seven of these dogs, aspirin (600 mg i.v.) was administered 1 hour before occlusion. In the aspirin-treated dogs, collateral flow increased significantly (p less than 0.05), from 0.09 +/- 0.02 ml/min/g at 5 minutes to 0.15 and 0.02 ml/min/g 4 hours after occlusion. Collateral flow was not significantly altered over 4 hours in control dogs. The aspirin-induced increase in collateral flow was confined to epicardium (12 +/- 4% of normal zone flow at 5 minutes to 23 +/- 4% at 4 hours after occlusion).

Acute Disease↗
PubMed1978

Nitroglycerin-induced improvement in exercise tolerance and hemodynamics in patients with chronic rheumatic heart valve disease.

Nitroglycerin reduces elevated left ventricular filling and pulmonary arterial pressures in resting patients with rheumatic valve disease and reduces symptoms when given over long periods to patients with primary myocardial disease. To determine whether nitroglycerin may prove effective therapeutically in ambulatory patients with heart valve disease, its effects on hemodynamics and exercise capacity were studied in 11 severely symptomatic adults who were already receiving optimal treatment with digitalis and diuretic agents. Seven had predominant mitral valve disease, one had predominant aortic insufficiency and three had equally severe mitral and aortic valve disease. Maximal exercise capacity was assessed with graded treadmill exercise after placebo and after nitroglycerin (0.5 mg sublingually) administered in random sequence to each patient. Exercise capacity (exercise time to limiting fatigue or dyspnea) increased from a mean of 8.3 minutes after placebo to 9.8 minutes after nitroglycerin (P less than 0.005). Eight patients were studied hemodynamically during further intense treadmill exercise. Pulmonary arterial pressure was significantly lower (P less than 0.05) after nitroglycerin than after placebo (mean 44 versus 56 mm Hg), but cardiac output was greater after nitroglycerin (5.0 versus 4.6 liters/min, P less than 0.005). Thus, nitroglycerin appears to increase exericse tolerance and improve the hemodynamic response to exercise in patients with heart valve disease and may be valuable in the long-term pharmacologic therapy of such patients.

Administration, Oral↗
PubMed1978

Beneficial effect of physical training on blood flow to myocardium perfused by chronic collaterals in the exercising dog.

To determine the effect of physical training on collateral blood flow, we measured regional myocardial blood flow (MBF) by injecting 15 mu radioactive microspheres at rest and during exercise in 14 dogs with chronic coronary occlusive lesions. Seven dogs subsequently trained for 6 weeks while the other seven remained in kennels. Training effect was documented by decrease in heart rate during exercise that averaged 35 beats/min. MBF studies were repeated after 6 weeks. Myocardial samples were obtained from normally perfused zones (NZ) and from regions supplied via collaterals (collateral dependent zones or CZ). Initially, endocardial blood flow in CZ averaged 1.110 ml/min/g (83% of NZ, P less than 0.05) at rest and 1.36 ml/min/g (69% of NZ, P less than 0.05) during exercise, indicating relative underperfusion. Epicardial blood flow was equal in NZ and CZ. After 6 weeks MBF was not significantly changed in control animals. After training, however, MBF to underperfused endocardium of CZ during exercise was 39% greater than it had been prior to training. The epicardial portion of CZ (not exhibiting underperfusion) showed no change in MBF during exercise after training. Our data suggest that beneficial effects of training in coronary disease may include improvement in MBF to underperfused collateral-dependent portions of myocardium.

Animals↗