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R J Boudreau

Publications and source records attributed to R J Boudreau.

62 records · Page 4Linked to original sources

Cardiopulmonary diagnoses by nuclear medicine techniques--where we have been, where we are, where we are going.

In order to not only survive, but to carry out our mission in health care delivery, nuclear medicine procedures will have to be competitive with the many other techniques that are available for assessing cardiopulmonary structure or function. Our tests must also be shown to be cost-effective. According to the American Heart Association, cardiovascular diseases alone had an economic cost of 56.9 billion dollars in 1983. Of this enormous sum only a very small percentage could be attributed to the performance of diagnostic nuclear medicine examinations. In addition to the economic cost, cardiovascular diseases accounted for 51% of all deaths in 1980. Statistics from the U.S. Department of Health show that 8.26 million (26.3%) of the national noninstitutionalized handicapped are the result of heart conditions and hypertension. These statistics are especially tragic since cardiovascular disease tends to strike a large proportion of persons in their most productive working years. We must avoid becoming penny wise and pound foolish when we decide whether or not to perform diagnostic examinations. Information obtained from these tests can be used to evaluate the effectiveness of therapy (or lack thereof), determine those patients who are at greatest risk of subsequent events and, therefore, require the most intensive investigation and therapy, and similarly identify that population at very low risk of having subsequent cardiac events and, therefore, requiring little, if any, therapy and no further investigation. Is such an approach economically feasible? An estimated 1.5 million Americans will have a heart attack this year, and about 550,000 of them will die. Of these persons, 350,000 will die before they reach the hospital. This leaves 1,150,000 persons who will be hospitalized due to myocardial infarction. As an example, if every one of these patients had a GBP study, at an estimated cost of +350.00 per examination, the cost would be about +400,000,000 or 0.7% of the total cost of cardiovascular diseases. This figure would roughly double if either a 201Tl or GBP study was performed with stress. Thus, our examinations constitute only a small percentage of the overall cost of cardiopulmonary disease. If one of these tests results in even a day early CCU to general bed transfer, early discharge, deferment of angiography, or surgery, or long-term medical therapy, then they will be cost-effective. We believe that a strong case can be made for optimism about the continued growth and expansion of nuclear techniques.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiovascular Diseases↗

Observations on serial radionuclide blood-flow studies in Paget's disease: concise communication.

Twenty-four symptomatic patients with symptoms of active Paget's disease of bone were evaluated, during the course of their therapy, a total of 71 times (24 baseline and 47 follow-up examinations) by serial alkaline phosphatase levels (AP), Tc-99m MDP bone scans, and radionuclide blood-flow studies. The flow study correlated with disease activity in all of the baseline studies and in at least 85% of the follow-up studies. In five patients (seven follow-up studies) the changes in local blood flow correctly anticipated the eventual rise or fall of AP. In comparison with the bone scan, the changes in blood flow preceded the bone-scan alterations or were more reliable indicators of disease activity in 12 of the 13 follow-up studies in which the results of the two examinations disagreed. We conclude that the radionuclide flow study provides useful additional clinical information in the management of Paget's disease.

Alkaline Phosphatase↗

Ventilation-perfusion mismatch in tumor embolism.

An unusual case of extensive tumor embolism is reported on which the lung scan was instrumental in demonstrating the underlying pathophysiology. Pulmonary arteriography failed to demonstrate vessel occlusion and the need to perform this study with special care is re-emphasized. A brief review of the literature indicates that tumor embolism occurs much more frequently than is clinically suspected.

Adenocarcinoma↗

Effect of arachidonic acid and indomethacin on renal function of dogs with pericardial tamponade.

Previous studies revealed persistent sodium retention in dogs with chronic pericardial tamponade (induced by injection of Freund adjuvant into pericardial sacs) and pericardiocentesis, revealed in increased sodium excretion. Three groups of dogs were studied. Group 1 was treated with indomethacin (2.5 mg/kg, iv) prior to pericardiocentesis. Compared with experiments without indomethacin, sodium excretion did not increase flowing pericardiocentesis in animals treated with indomethacin despite similar changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity. This effect of indomethacin was presumably mediated through prostaglandin (PG) synthesis inhibition. Group 2 dogs received an infusion of arachidonic acid (AA) (to increase PG synthesis) into the left renal artery (20 micrograms.kg-1. min-1). Sodium excretion increased after AA infusion during tamponade (11.2 to 30.9 mequiv.min-1) with a further increase occurring after pericardiocentesis (84.4 mequiv.min-1). Animals in group 3 were infused with both 20 and 80 micrograms. kg-1. min-1 doses of AA. Although sodium excretion following 80 micrograms.kg-1.min-1 AA(21 mequiv.min-1) was higher than that seen during 20 micrograms.kg-1.min-1 (14.2 mequiv.min-1), a further increase in sodium excretion to 45.6 mequiv.min-1 followed pericardiocentesis. During tamponade, AA did not change any of the measured parameters other than sodium excretion, a result compatible with the proposed distal tubular site of action of PG. Absolute but not fractional cortical blood flow distribution increased during the time sodium excretion increased following pericardiocentesis in all experiments. It is proposed that increased PG synthesis may be one possible mechanism involved in the natriuresis seen following pericardiocentesis. One cannot exclude the possibility that increased absolute blood flow to the superficial cortex also contributes to the observed natriuresis. Changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity appear to contribute to the observed natriuresis but only when PG synthesis is not blocked.

Animals↗

Cardiac edema in dogs: distribution of renal blood flow and glomerular filtrate.

The injection of Freund's adjuvant into the pericardial sac of 29 dogs resulted in chronic pericardial tamponade with persistent sodium retention. Micropuncture, clearance, and radioactive microsphere experiments were initiated 6--13 days after pericardial injection and 60 min after pericardiocentesis. Pericardiocentesis increased sodium excretion (from 12.2 to 41.3 microequiv./min) and mean arterial pressure (+ 20 mmHg (1 mmHg = 133.322 Pa)). Central venous pressure decreased 6.5 mmHg, as did hematocrit (from 45.7 to 39.8%) and plasma protein concentration (from 5.88 to 5.15 g%). Pericardiocentesis had no significant effect on renal blood flow (RBF), nor plasma flow. Redistribution of glomerular filtrate was suggested by the observation that superficial nephron glomerular filtration rate increased (from 91 to 108 nL/min) while glomerular filtration rate remained unaltered. Determination of intrarenal distribution of RBF revealed that cortical blood flow also distributed superficially. A significant increase in the fraction of RBF perfusing zone 1 (outer cortex) and a decrease in fractional perfusion of zones 2, 3 and 4 (juxtamedullary cortex) were observed in each experiment following pericardiocentesis. RBF distribution examined in a series of six animals prior to and during the development of pericardial tamponade showed the opposite effect. These results indicate that pericardiocentesis causes redistribution of both glomerular filtrate and RBF to superficial nephrons. The development of pericardial tamponade was associated with increased fractional juxtamedullary blood flow. These changes may have been the result of altered blood pressure, hematocrit, plasma protein concentration, or altered renal resistance.

Animals↗

Activation of 3',5'-cyclic adenosine monophosphate phosphodiesterase by calcium ion and a protein activator.

3',5'-CAMP phosphodiesterase was partially purified from bovine cerebral cortex. A heat-stable activating factor was separated from the enzyme by chromatography on DEAE-cellulose. The enzyme in crude ammonium sulfate fractions was stimulated by 5 mM CaCl2. This stimulation was reversed by the calcium chelator EGTA. The main phosphodiesterase peak obtained by DEAE-cellulose chromatography was not stimulated by Ca2+. Upon addition of column effluent containing a heat stable factor, Ca2+ activation was restored. Protein activator was inactive when endogenous contaminating Ca2+ was complexed with EGTA. It was concluded that activation of phosphodiesterase requires the presence of both activator and Ca1+. From an analysis of activation of cGMP hydrolysis a kinetic model for the interaction of Ca2+ and protein activator with the phosphodiesterase was developed. Heterotropic cooperativity between the binding of Ca2+ and protein activator to the phosphodiesterase was observed, i.e., Ca1+ decreased the apparent dissociation constant for protein activator and protein activator decreased the apparent dissociation constant for Ca2+.

Animals↗

The effect of Ca++ on cyclic nucleotide phosphodiesterases of superior cervical ganglion.

Cyclic nucleotide phosphodiesterase was examined in canine and bovine superior cervical ganglia. Activity in crude supernatant fractions was only slightly stimulated by Ca++ despite the presence of protein activating factor. Three forms of phosphodiesterase were resolved from bovine ganglia supernatant extracts by chromatography on DEAE-cellulose. The first enzyme eluted, (DI), was almost completely specific for cyclic GMP, while the other two (DII and DIII), hydrolyzed both cyclic AMP and cyclic GMP; all were free of heat-stable protein activator. Each enzyme was inhibited by low concentrations of Ca++ in the assay medium. Inhibition by Ca++ was reversed by addition of protein activator, but activity did not increase above the control level. Cyclic AMP hydrolysis by enzyme DII was stimulated by micromolar concentrations of cyclic GMP. This stimulation was reduced by Ca++ unless protein activator was present.

3',5'-Cyclic-AMP Phosphodiesterases↗