Biomedical subjects
Publications and source records attributed to J C Ehrhardt.
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Calcifications in the breast parenchyma and pigments used in tattooing the skin are indistinguishable on xeroradiographs.
When an abrupt, fixed increase in afterload induces hypertrophy, the myocardium exhibits normal pump function in vivo, depressed muscle function in vitro, and paradoxically increased oxygen consumption. Such abnormalities may be either a transient response to a reversible myocardial injury or instead may be a persistent characteristic of hypertrophy contributing to eventual heart failure. To distinguish between these alternatives, we developed a model of chronic progressive pressure overload. Kittens had either a sham operation or pulmonary banding for 25 (group I) or 60 (group II) weeks. Banding produced a gradually increasing pressure overload with growth, maximum at 16 weeks after operation. The ratio of right ventricular to body weight increase from 0.54 +/- 0.03 to 0.82 +/0.04 g/kg (P less than 0.01) in group I and from 0.50 +/- 0.03 to 0.72 +/- 0.03 (P less than 0.01) in group II. In vivo right ventricular pump function (cardiac output and ejection fraction) was normal in both groups. In vitro contractile function and metabolism were measured in papillary muscles from the same right ventricles. Both experimental groups showed marked contractile abnormalities: preloaded shortening velocity was reduced from 0.80 +/- 0.05 to 0.53 +/- 0.05 muscle length/sec (P less than 0.01) in group I and from 0.84 +/- 0.04 to 0.60 +/- 0.06 (P less than ).01) in group II. Maximum isometric active tension was reduced from 60 +/- 7 to 35 +/- 5 mN/mm2 (P less than 0.01) in group I and from 56 +/- 5 to 27 +/- 4 (P less than 0.01) in group II. Metabolism was normal in both experimental groups. Thus, under conditions relevant to the study of clinical cardiac hypertrophy that are unlikely to cause acute injury, hypertrophy produces persistently abnormal intrinsic contractile function
Cystine calculi are said to be either radiolucent or radiopaque. In the past, contamination of the calculi with calcium has been given as the reason for a radiopaque appearance. However, most cystine stones are pure cystine and contain essentially no calcium. When compared to adjacent fluids and tissues, they are radiopaque because of their higher physical density and their higher effective atomic number.
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This brief report describes an artifact that is seen as a thin, white rim outlining an air collection on the EMI 80 X 80 and 160 X 160 matrix CT scanners. This artifact is not associated with fat density and, therefore, its recognition allows presumptive differentiation between air and fat densities. The attenuation numbers of the lesion should then be obtained for confirmation.
Morphologic observations suggest that the inner layers of the thoracic aorta in man and dog are avascular and the outer layers have vasa vasorum. It appears that vasa vasorum are essential in the thoracic aorta because their interruption produces medial necrosis. These experiments provide the first measurements of blood flow through aortic vasa vasorum and examine physiologic regulation of that flow. During control conditions the outer two-thirds of the media of the thoracic aorta received 10 ml/min per 100 g blood flow through vasa vasorum. Flow to the inner third of the aorta was 1 ml/min per 100 g. Flow to both the inner and outer media of the abdominal aorta was less than 1 ml/min per 100 g. Adenosine increased blood flow to vasa vasorum in the outer media of the thoracic aorta from 7 to 18 ml/min per 100 g, but did not increase flow to the inner layers of the aorta. Hemorrhagic hypotension decreased flow in the outer media of the thoracic aorta from 14 to 2 ml/min per 100 g. Acute hypertension failed to increase blood flow through vasa vasorum, as conductance decreased significantly. These studies indicate that vasa vasorum provide a considerable amount of blood flow to the outer layers of the thoracic aorta. The vessels are responsive to physiologic stimuli because they dilate during infusion of adenosine and constrict during both hemorrhagic hypotension and acute hypertension. We speculate that the failure of blood flow to the aortic wall to increase during acute hypertension might, if it were sustained, contribute to aortic medial necrosis.
The effect of aorto-coronary bypass graft surgery (CBG) upon regional myocardial perfusion (RMP) was studied in 23 patients using thallium-201 myocardial perfusing imaging after exercise. We compared the changes in RMP with the clinical status and ECG's during graded treadmill exercise (GTX) before and after CBG. After CBG, the New York Heart Association's "functional class" improved from 3.2 +/- 0.1 (mean +/- SE) to 1.2 +/- 0.2, p less than 0.005. The GTX performance of the patients was also significantly improved postoperatively as judged by the total exercise time (11.7 +/- 0.6 min postop, compared with 7.2 +/- 0.5 min preop; p less than 0.005). Postoperative improved Tl-201 scintigrams were observed in 19 patients, but in only nine patients did the perfusion distribution return to normal. Thus, Tl-201 exercise scintigrams following CBG demonstrate improved RMP in most patients. Failure of regional myocardial perfusion to improve postoperatively, however, does not preclude marked alleviation of angina and improved exercise tolerance.
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An adult with anomalous origin of the left coronary artery (originating from the pulmonary artery) had implantation of the anomalous vessel into the aorta. Exercise myocardial perfusion imaging with thallium-201, performed before and after the operation, disclosed a marked improvement in anterior-wall Tl-201 uptake. Postoperative isotope ventriculogram showed improved regional contraction in the revascularized anterolateral wall of the left ventricle. Thus, it has been demonstrated that implantation of an anomalous left coronary into the aorta improves regional myocardial perfusion and regional left-ventricular motion.
Sixteen acromegalic patients underwent echocardiography, phonocardiography, stress electrocardiography with Thallium perfusion scanning and gated radioisotope left ventricular angiocardiograms. Abnormalities consisting of increased echo left ventricular mass index, low velocity of circumferential fiber shortening or elevated pre-ejection period to left ventricular ejection time ratio were found in six patients with coexistent hypertension or coronary disease. Concentric left ventricular hypertrophy was also found in three patients with no known etiology other than acromegaly of greater than thirteen years' duration or with fasting growth hormone concentrations greater than 100 ng/ml. One of these three also had left ventricular dysfunction. Neither hypertrophy nor ventricular dysfunction was found in other acromegalics with shorter duration of disease or lower growth hormone concentrations or with normal growth hormone concentrations after therapy. A high prevalence of coronary artery and hypertensive heart disease is associated with acromegaly. A few patients with acromegaly have a specific, potentially reversible cardiomyopathy probably related to prolonged acromegaly or very high growth hormone concentrations.
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Cerebral arteriovenous shunting of 7-10-, 15-, 25-, and 50-mum labeled microspheres was studied in 12 anesthetized dogs. Approximately 8% of the 7-10-mum spheres were shunted to cerebral venous blood, whereas less than 2% of the 15-, 25-, and 50-mum spheres were shunted. Cerebral vascular dilatation induced by hypoxia or hypercapnia did not alter the shunting. The calculated total cerebral flow was 10-15% lower with 7-10-mum microspheres as compared with simultaneous flows measured with the larger microspheres which also suggests that 7-10-mu spheres were shunted through the brain. The calculated distribution of cerebral flow was similar with 7-10- and 15-mum spheres but markedly altered when 50-mum spheres were used. Repeated injections of 15-mum spheres were used. Repeated injections of 15-mum microspheres given under stable conditions yielded total cerebral blood flows which averaged +/- 6% of their respective mean and the regional distribution of flow was highly reproducible. These data suggest that, in dogs, 15-mum spheres are an appropriate size to use to measure cerebral blood flows, since shunting is minimal, the distribution is not artifactually distorted, and the measurements are reproducible.
The reliability of myocardial perfusion scintigrams with thallium-201 (201Tl) for detecting areas of hypoperfusion was assessed in 16 closed-chest dogs. Variable areas of ischemia were produced either by occluding or stenosing the left anterior descending coronary artery. Cardiac scintigrams taken in four projections were compared with regional myocardial perfusion maps. Segmental concentrations and segmental perfusions were quantitated by counting the emissions from 201Tl and the microspheres in each of 96 segments of the left ventricle. In addition, studies with a phantom were performed. The results indicate: 1) The emissions from 201Tl and from microspheres correlated well in ischemic segments (r = 0.93 +/- SE 0.02). 2) Seven of twelve ischemic hearts had definitely abnormal scintigrams and in each of these the hypoperfused zone was greater than 4.9 grams and perfusion was decreased by more than 45%. 3) In the phantom, abnormal scintigrams could be detected in the presence of lesser deficits than in the dogs. The limitation of the thallium perfusion scintigrams will be the inconsistent detection of small perfusion deficits.
The quantitative relationship between abnormalities seen on technetium-99m pyrophosphate (99mTc-PYP) infarct scintigrams and the size of the myocardial infarction is unclear. We evaluated two possible determinants of 99mTc-PYP accumulation: myocardial perfusion measured with 7-10 mu microspheres and the extent of necrosis determined histologically. Hemodynamics and myocardial perfusion to small segments of the left ventricle were measured prior to, 5-10 min, and 44-48 hours following sudden occlusion of the left anterior descending coronary artery in ten awake dogs. 99mTc-PYP was injected i.v. following the third injection of microspheres and the animals were killed 2 hours later. The important findings were as follows: 1) there is a close relationship between the extent of myocardial necrosis observed and the perfusion of segments 5-10 min following coronary occlusion; and 2) that segmental myocardial perfusion is an important determinant of 99mTc-PYP accumulation by myocardial segments which contain areas of necrosis. Although the present data preclude statistical analysis of the relationship between the level of necrosis in a segment and the accumulation of 99mTc-PYP by that segment, the two do not appear to be related, a finding which would discourage use of intensity of 99mTc-PYP images for infarct size. The distribution of an abnormality on the scintigram may provide an estimate of infarct size. However, the geometry of the infarct and the resolving power of the scanning equipment will significantly limit this in many clinical situations.
This study was performed to determine whether stimulation of the carotid chemoreceptors increases total or regional cerebral blood flow and whether activation of arterial chemoreceptors contributes to cerebral vasodilation during systemic hypoxemia. In anesthetized and ventilated dogs, carotid chemoreceptors were stimulated with nicotine or hypoxic and hypercapnic blood. To measure total and regional cerebral blood flow, we used labeled 15-mu microspheres. Stimulation of chemoreceptors did not increase cerebral blood flow or produce significant redistribution of cerebral blood flow, even though the chemoreflex was intact in these animals (as manifested by vasoconstriction in muscle, kidney, and small bowel) and the cerebral vessels dilated in response to systemic hypercapnia. In other studies in anesthetized, ventilated dogs and rhesus monkeys, cerebral vasodilator responses to systemic hypoxemia were observed before and after denervation of carotid and aortic chemoreceptors. Systemic hypoxemia produced large and equivalent increases in cerebral blood flow before and after chemodenervation. We conclude that stimulation of carotid chemoreceptors does not produce cerebral vasodilation and that chemoreceptors do not contribute significantly to cerebral vasodilation during systemic hypoxemia.