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Biomedical subjects

S A Rubin

Publications and source records attributed to S A Rubin.

15 recordsLinked to original sources

Differential regulation of insulin-like growth factor I by growth hormone and thyroid hormone in the heart of juvenile hypophysectomized rats.

Recent data suggest that the heart can act as both a source and target for the actions of polypeptide growth factors. Insulin-like growth factor I (IGF-I) is a polypeptide that has both mitogenic and differentiation properties that function at the autocrine/paracrine level, and has recently been demonstrated to be expressed in the heart. This knowledge, coupled with the observation that thyroid hormone (T3) promotes relative cardiac growth compared to the proportional increases in body and heart growth evoked by growth hormone (GH), lead us to speculate whether differential induction of cardiac IGF-I may account for the specialized trophic effects of T3 on the heart. Cardiac IGF-I gene expression was studied in an in vivo model in which cardiac growth in the hypophysectomized juvenile rat was stimulated with either GH, T3 or GH + T3. Two week infusions of T3 that resulted in cardiac growth, but no gain in body weight, resulted in a 4.6-fold increase in cardiac IGF-I mRNA levels compared to hypophysectomized controls. GH infusions that resulted in similar cardiac growth, but were accompanied by proportional body growth, had no effect on cardiac IGF-I mRNA levels. These data are the first to demonstrate stimulation of cardiac IGF-I mRNA levels by T3 and further support cardiac autocrine/paracrine actions for this polypeptide growth factor.

Animals

Pulmonary blastomycosis.

Pulmonary blastomycosis has a number of chest radiographic manifestations that may closely resemble those of tuberculosis, histoplasmosis, and other fungal diseases. Radiographic presentations of disease include airspace consolidation, nodular opacities, air bronchograms, masslike lesions, and military disease. Because the geographic distribution of blastomycosis overlaps that of histoplasmosis, distinguishing one from the other on the basis of the radiographic features may be difficult. In blastomycosis, the paucity of calcifications, lymphadenopathy, and cavitation is striking. The article reviews the clinical and radiologic features of blastomycosis and provides illustrative cases to enhance understanding of this disease.

Blastomycosis

Thoracic histoplasmosis.

Histoplasmosis is a fungal disease that is seen throughout the world. It is the most common systemic fungal infection in North America, and it is endemic in the Mississippi, Ohio, and St Lawrence River valleys. Its radiographic and clinical spectrum ranges from a totally self-limited disease with minimal or no radiographic findings to a rapidly progressive, disseminated, and sometimes fatal disease. The article discusses the various aspects of thoracic histoplasmosis with emphasis on the radiographic findings.

Histoplasmosis

Pulmonary zygomycosis: a radiographic and clinical spectrum.

Eight documented cases of pulmonary zygomycosis were analyzed retrospectively with regard to radiographic and clinical features. Predisposing factors were diabetes mellitus in six cases, lymphoblastic lymphoma in one case, and surgery to correct a tracheoesophageal fistula in one case. Two of the patients with diabetes had also undergone renal transplantation for diabetic nephropathy and were immunosuppressed. The more usual radiographic findings of pulmonary zygomycosis represent a spectrum that comprises a normal chest radiograph, a lung abscess, subacute or chronic pneumonia that often evolves into a lung abscess, and rapidly progressive fatal pneumonia. Awareness of the various presentations of pulmonary zygomycosis is important because early diagnosis and appropriate therapy clearly have been shown to improve the survival rate of these patients. Zygomycosis should be included in the differential diagnosis when patients with diabetes mellitus, patients with leukemia or lymphoma, or immunocompromised patients present with or develop perplexing pulmonary abnormalities.

Adolescent

Paradox of improved exercise but not resting hemodynamics with short-term prazosin in chronic heart failure.

In patients with chronic heart failure exercise allows the simultaneous observation of the cardiovascular pathophysiology and the symptoms of these patients. We administered short-term, oral prazosin to 10 patients with severe chronic heart failure. Prazosin increased cardiac output and stroke volume significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). Prazosin decreased the arteriovenous oxygen difference and left ventricular filling pressure significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). There was no significant correlation between prazosin-induced changes at rest and during exercise in cardiac output (r = 0.12), stroke volume (r = 0.02), arteriovenous oxygen difference (r = 0.33) or left ventricular filling pressure (r = 0.43). Prazosin predominantly affects hemodynamics during exercise because its pharmacologic activity as an alpha-adrenergic blocking agent is most prominent during exercise. The full evaluation of prazosin-induced changes in the hemodynamics of patients of patients with chronic heart failure requires evaluation during exercise.

Aged

Detection of left ventricular functional reserve by supine exercise hemodynamics in patients with severe, chronic heart failure.

Hemodynamic changes during exercise were evaluated in 20 patients with severe, chronic congestive heart failure. Two groups were identified by their stroke work response to maximal exercise. Group I (eight patients) showed an increase in stroke work index. This occurred because the stroke volume increased and the difference between mean systolic pressure and left ventricular filling pressure increased. Group II (12 patients) showed a decrease in stroke work index. This occurred because stroke volume decreased while the difference between mean systolic pressure and left ventricular filling pressure did not change. Despite hemodynamic differences, the groups could not be distinguished by the usual clinical criteria for heart failure including etiology, New York Heart Association functional class, heart size on chest X-ray film or duration of heart failure. Clinical criteria are relatively insensitive in predicting the exercise hemodynamics of any given patient with chronic severe heart failure. Determining the exercise hemodynamics may be helpful as a means of assessing left ventricular functional reserve in heart failure. Prognostic implications, drug therapy and prescription of activities may require adjustment based on this spectrum of hemodynamic response to exercise in patients with chronic heart failure.

Adult

Influence of short-term oral hydralazine therapy on exercise hemodynamics in patients with severe chronic heart failure.

Changes in left ventricular performance were evaluated in 14 patients with functional New York Heart Association class III or IV chronic heart failure before and after the addition of oral hydralazine to conventional therapy. With conventional therapy, cardiac output increased from 3.4 +/- 0.8 (mean +/- 1 standard deviation) at rest to 4.7 +/- 1.4 liters/min during exercise. This increase in cardiac output on exercise during conventional therapy was mainly due to an increase in heart rate. After the addition of hydralazine, cardiac output at rest increased to 5.0 +/- 1.4 liters/min. The increase in cardiac output was essentially due to an increase in stroke volume. This enhanced stroke volume after hydralazine therapy was maintained during exercise. Hydralazine therapy did not change either the left ventricular filling pressure at rest or the magnitude of increase in left ventricular filling pressure during exercise. Nevertheless, increased cardiac output and stroke volume with similar changes in left ventricular filling pressure during exercise indicated improved left ventricular performance after hydralazine therapy. After short-term hydralazine therapy, symptom-limited peak exercise work load, duration of exercise and maximal oxygen consumption during exercise did not increase. Clinical follow-up at 2 months after long-term therapy revealed subjective improvement in exercise tolerance in 13 of the 14 patients.

Administration, Oral

Resistance and volume changes caused by nitroprusside in the dog.

Changes in vascular volume caused by a pharmacologic agent are frequently inferred rather than directly measured. We investigated the effects of nitroprusside in 8 dogs divided into 2 groups: control and splenectomized. We anesthetized the dogs using pentobarbital, and surgically prepared a veno-right atrial bypass preparation whose controlled cardiac output and external reservoir allowed measurement of both changes in vascular resistance and changes in vascular volume. In both groups, blood pressure (mean +/- SD) decreased at each successive level of nitroprusside: 114 +/- 24 mmHg (base line), 101 +/- 19 mmHg (45 microgram/min), 90 +/- 16 mmHg (90 microgram/min), 81 +/- 17 mmHg (180 microgram/min), 68 +/- 18 mmHg (360 microgram/min). Nitroprusside caused a large and similar decrease in vascular resistance in both groups. In the control group, vascular volume increased above base line 5.5 +/- 2.7, 8.3 +/- 3.2, 11.6 +/- 2.9, and 14.7 +/- 3.5 ml/kg at each successive level of nitroprusside infusion, whereas in the splenectomized group vascular volume increased above base line 0.9 +/- 0.3, 2.5 +/- 1.0, 3.3 +/- 1.1, and 4.0 +/- 1.3 ml/kg at each successive level of nitroprusside infusion, but increased significantly less than the control group. We concluded that nitroprusside decreases vascular resistance and increases vascular volume and that the spleen is the major site of changes in vascular volume caused by nitroprusside.

Animals

Pulmonary artery--bronchial fistula: a new complication of Swan-Ganz catheterization.

A patient with a Swan-Ganz catheter developed massive hemoptysis. Injection of radiographic contrast media through the catheter revealed rapid filling of the tracheo-bronchial tree, consistent with direct pulmonary artery-bronchial communication. Development of hemoptysis in a patient with a Swan-Ganz catheter should alert the clinician to this possibility.

Aged

Radiographic spectrum of pleuropulmonary tularemia.

Pleuropulmonary disease was seen in 50 of 62 patients (81%) with proven tularemia. Radiographic findings included patchy subsegmental air space opacities (74%), hilar lymphadenopathy (32%), and pleural effusion (30%). Less common manifestations were air space opacification of an entire lobe or segment, cavitation, oval opacities, pericardial effusion, linear opacities and septal lines, apical and miliary disease resembling tuberculosis, a mediastinal mass, empyema with bronchopleural fistula, and residual cystic changes, calcification, and fibrosis. Pleuropulmonary tularemia may be easily misdiagnosed as other infectious diseases, neoplastic diseases, and occasionally cardiac or other pericardial disease. It should be considered whenever patients from endemic areas present a perplexing radiographic and clinical picture. Such patients should have the benefit of a serologic examination for tularemia, since this disease may be effectively controlled with appropriate antibiotics.

Adolescent