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Biomedical subjects

R R Miller

Publications and source records attributed to R R Miller.

At least 199 records · Page 11Linked to original sources
PubMed1984

Pulmonary alveolar proteinosis and aluminum dust exposure.

A 44-yr-old male presented with shortness of breath, diffuse X-ray infiltrates, and physiologic evidence of a restrictive lung disease. Biopsy revealed pulmonary alveolar proteinosis. The patient had worked for the previous 6 yr as an aluminum rail grinder in a very dusty environment. Analysis of his lung tissue revealed greater than 300 X 10(6) particles of aluminum/g dry lung; all of the particles appeared as spheres of less than 1 mu diameter. We believe that this case represents an example of pulmonary alveolar proteinosis induced by inhalation of aluminum particles; this finding confirms animal studies which suggest that proteinosis can be produced by very large doses of many types of finely divided mineral dust.

Adult↗
PubMed1984

Ethylene glycol monomethyl ether and propylene glycol monomethyl ether: metabolism, disposition, and subchronic inhalation toxicity studies.

Short-term and subchronic vapor inhalation studies have shown that there are pronounced differences in the toxicological properties of ethylene glycol monomethyl ether (EGME) and propylene glycol monomethyl ether (PGME). Overexposure to EGME has resulted in adverse effects on testes, bone marrow and lymphoid tissues in laboratory animals. PGME does not affect these tissues, and instead, overexposure to PGME has been associated with increases in liver weight and central nervous system depression. EGME is primarily oxidized to methoxyacetic acid in male rats, while PGME apparently undergoes O-demethylation to form propylene glycol. Since methoxyacetic acid has been shown to have the same spectrum of toxicity as EGME in male rats, the observed differences in the toxicological properties of EGME and PGME are thought to be due to the fact that the two materials are biotransformed via different routes to different types of metabolites.

Air Pollutants↗
PubMed1983

Ethmozine suppression of single and repetitive ventricular premature depolarizations during therapy: documentation of efficacy and long-term safety.

This study reports a total of 1677 patient days' experience with the use of Ethmozine to suppress ventricular premature depolarizations. A total of 39 patients were studied on three placebo-controlled protocols. Ethmozine, given at a mean total daily dose of 830 mg +/- 318 mg on a dosing schedule of every 8 hours, resulted in a mean plasma Ethmozine level of 0.42 micrograms/ml +/- 0.28 micrograms/ml. In addition to reducing ventricular premature depolarizations from 11,049/24 hr during placebo to 2231/24 hr during Ethmozine therapy (80% reduction), the drug also resulted in a 95% reduction in paired forms and a 99% reduction in total runs of ventricular tachycardia. Ethmozine is extraordinarily well tolerated with only mild side effects of dizziness, perioral tingling, and euphoria, with no serious toxicity requiring discontinuation of therapy. Ethmozine demonstrates great potential as an effective drug in suppressing ventricular premature depolarizations with minimal side effects or toxicity.

Adult↗
PubMed1983

Beneficial effects of the alpha-adrenergic antagonist nicergoline during acute myocardial ischemia and reperfusion in the dog.

Recent experimental and clinical data have stimulated interest in the use of alpha-adrenergic antagonists in acute myocardial infarction. We evaluated nicergoline, a new relatively selective alpha 1-antagonist which uniquely lowers heart rate. Open-chest dogs, randomized to control (n = 25) or intravenously treated group (n = 20; 0.5 mg/kg bolus, then 0.10 to 0.15 mg/kg/min), underwent coronary artery occlusion (CAO) followed after 25 minutes by coronary artery reperfusion (CAR). Nicergoline decreased heart rate by 47 +/- 5 bpm and mean aortic pressure by 39 +/- 4 mm Hg. Following CAO, nicergoline reduced total coronary collateral resistance (radiolabeled microspheres; 698 +/- 75 vs 2167 +/- 530 mm Hg/ml/min/gm, p less than 0.05), increased the ischemic zone/nonischemic zone flow ratio (0.14 +/- 0.04 vs 0.06 +/- 0.02, p less than 0.05), and reduced the rise in intramyocardial CO2 tension in the ischemic zone (mass spectrometry, p less than 0.001). Furthermore, the drug decreased the rate of ventricular tachycardia (VT; 191 +/- 13 vs 243 +/- 3 bpm, p less than 0.001) and the incidence of ventricular fibrillation (VF; 1 of 20 [5%] vs 7 of 25 [28%], p less than 0.05). Following CAR, nicergoline did not significantly reduce the incidence of VF but did lower rate (154 +/- 8 vs 212 +/- 10 bpm, p less than 0.001) and incidence (p less than 0.05) of VT. Thus nicergoline reduced severity of ischemia and afforded protection against arrhythmias induced by myocardial ischemia and reperfusion. The observed reduction in heart rate may have contributed importantly to these beneficial effects. Clinical investigation of this potentially useful vasodilator seems warranted.

Animals↗
PubMed1983

Cardiopulmonary toxicity in patients with breast carcinoma during plasma perfusion over immobilized protein A. Pathophysiology of reaction and attenuating methods.

Tumoricidal reactions in dogs with spontaneous breast carcinoma occur after perfusion of plasma over protein A derived from Staphylococcus aureus and immobilized in collodion charcoal. When this treatment was extended to humans with breast cancer, hemodynamic and physiologic changes were noted. The evolution and spectrum of these reactions were evaluated during 47 plasma infusions in five patients. Initial treatment conditions consisting of rapid perfusion of plasma over high quantities of immobilized protein A were employed for 12 treatments in two patients. Within 30 minutes after treatments were begun, mean blood pressure, systemic vascular resistance, and stroke volume increased, as did heart rate, cardiac output, and rectal temperature; however, mean pulmonary artery pressure and total pulmonary resistance did not change. At 90 minutes, hypotension developed (lowest mean blood pressure was 59 +/- 14 mm Hg) that was associated with a decrease in systemic vascular resistance and total pulmonary resistance (536 +/- 66 and 146 +/- 44 dynes . second . cm-5, respectively). Cardiac output increased, tachycardia developed, stroke volume decreased, and rectal temperature increased. During the hypotensive phase, values of creatinine clearance and fractional excretion of sodium diminished. Noncardiogenic pulmonary edema appeared occasionally, with bronchospasm noted once. No hemodynamic changes were seen when saline solution was passaged over protein A immobilized in collodion charcoal or when autologous plasma was given without passage over protein A immobilized in collodion charcoal. Treatment conditions were modified by diminishing protein A quantity and plasma volume and slowing plasma perfusion rate, which resulted in significant attenuation of all cardiopulmonary responses. This report, then, defines for the first time the physiologic basis of the cardiopulmonary toxicity in humans after plasma perfusion over immobilized protein A.

Breast Neoplasms↗
PubMed1983

Attenuation of experimental retrograde amnesia through pretraining administration of a dissimilar amnestic agent.

Experiment 1 found that pretraining administration of electroconvulsive shock (ECS) attenuated ECS-induced amnesia of one-trial passive avoidance training in rats. Similarly, pretraining injections of cycloheximide (CXM) attenuated the amnestic effects of CXM at training. Experiment 2 demonstrated the ability of pretraining ECS to attenuate CXM-induced amnesia and pretraining CXM to attenuate ECS-induced amnesia. These studies join others in observing comparable behavioral effects of ECS-like amnestic agents and antimetabolite-like amnestic agents despite their different means of primary action. Collectively, these studies support the view that the two families of amnestic agents produce amnesia through a common mechanism.

Animals↗
PubMed1983

Comparative metabolism and disposition of ethylene glycol monomethyl ether and propylene glycol monomethyl ether in male rats.

Male Fischer 344 rats were given a single po dose of approximately 1 or 8.7 mmol/kg of [14C]EGME (ethylene glycol monomethyl ether) or [14C]PGME (propylene glycol monomethyl ether). After dosing, expired air, excreta, and tissues were analyzed for 14C; metabolites in urine were isolated and identified. There were pronounced differences in the metabolism and disposition of [14C]EGME and [14C]PGME. Approximately 50 to 60% of the administered 14C was excreted in urine, and about 12% was eliminated as 14CO2 within 48 hr after a single po dose of [14C]EGME. For PGME, only 10 to 20% of the administered 14C was excreted in urine, while 50 to 60% was eliminated as 14CO2 within 48 hr. Methoxyacetic acid was identified as the primary urinary metabolite of EGME, accounting for 80 to 90% of the total 14C in urine. PGME, propylene glycol(1,2-propanediol), and the sulfate and glucuronide conjugates of PGME were identified in urine of rats given PGME. Since methoxyacetic acid causes the same spectrum of toxicity as EGME in male rats, it is likely that the adverse effects of EGME are the result of its in vivo bioactivation to methoxyacetic acid. Hence, differences in routes of metabolism and types of metabolites appear to be the underlying basis for the remarkably different toxicologic properties of EGME and PGME, respectively.

Animals↗
PubMed1983

Analysis of ambulatory electrocardiograms in 15 patients during spontaneous ventricular fibrillation with special reference to preceding arrhythmic events.

Fifteen patients sustained ventricular fibrillation during ambulatory electrocardiographic recording in a period of 3.5 years over which time 16,500 ambulatory electrocardiograms were analyzed (prevalence = 0.09% or 1/1,100). Eight patients died, and seven survived cardiopulmonary resuscitation. Quantitative analysis of hourly ventricular arrhythmias prior to ventricular fibrillation revealed an increased frequency of premature ventricular beats and ventricular tachycardia, especially in the 2 hours immediately before ventricular fibrillation. Ventricular fibrillation was initiated by ventricular tachycardia in all 15 cases. These runs of ventricular tachycardia were characterized by their unusual length (mean = 560 +/- 536 beats) and their rapid rate (241 +/- 45 beats/min). Although an R on T premature ventricular beat initiated ventricular tachycardia and ventricular fibrillation occasionally, the mean prematurity index of the initiating premature ventricular beat was not early (mean = 1.27 +/- 0.28). QT prolongation was present in only 3 of the 15 patients (mean QTc interval = 0.42 +/- 0.06). Left ventricular dysfunction (mean left ventricular ejection fraction = 34.9 +/- 9.9%) and coronary artery disease were nearly always present. The cardiac medications most frequently associated with these patients at the time of ventricular fibrillation were digitalis and quinidine.

Aged↗
PubMed1983

Signaled tailshock is perceived as similar to a stronger unsignaled tailshock: implications for a functional analysis of classical conditioning.

Water-deprived rats given fixed-electrode, variable-intensity tailshock at random times rated each trial by pressing either a "high-aversiveness" or "low-aversiveness" lever in order to obtain water. Trials on which a warning signal preceded tailshock resulted in more "high-aversiveness" leverpressing than did otherwise equivalent unsignaled trials. The magnitude of this effect increased and decreased as a function of several parameters including signal-shock interval, signal duration, and range and absolute value of shock intensities but was never reversed despite efforts to achieve such a reversal. Variation in the size of the effect as a function of signal parameters as well as lick suppression scores indicated that the signal had acquired aversive characteristics, which suggests that the effect of the signal on lever choice was due largely to the aversiveness of the signal summating with the aversiveness of the tailshock. Several hypotheses concerning factors that might have either masked or prevented classically conditioned preparatory responses elicited by the signal from reducing tailshock aversiveness were tested and rejected. Despite the greater aversiveness of the signaled condition, when given the choice of receiving or not receiving the signal, the animals displayed a preference for signaled tailshock. Implications for the role of preparatory responding both in the preference-for-signaled-shock phenomenon and in classical conditioning are discussed.

Animals↗
PubMed1983

Program to disseminate information on new hospital pharmacy practices.

A five-year program to stimulate interest in contemporary pharmacy practices and disseminate information to pharmacists and other health professionals in community hospitals throughout the State of Maine is described. Pharmacists from the New England Medical Center in Boston and the Maine Medical Center in Portland conducted a program from 1973 to 1978 that included consultative services, drug information, and continuing-education components. Pharmacy consultants visited about 50% of the hospitals in the state and met with the director of pharmacy, administrator, and director of nursing who received written reports of all findings and suggestions. Most frequently, hospitals requested recommendations on drug-distribution systems, design and use of medical profiles, and design of physician order forms. Surveys at the beginning and at the end of the program indicated that the number of hospitals with unit dose systems and i.v. admixture programs increased during the life of the program; pharmacy staffing levels also increased. The program successfully brought consultative services, drug information, and educational programs to pharmacists and other health professionals in community hospitals in Maine.

Boston↗
PubMed1982

Argyrophilic cell hyperplasia and an atypical carcinoid tumor in chronic ulcerative colitis.

An unusual case of chronic ulcerative colitis, is presented in which an atypical carcinoid tumor was seen. Many areas of the mucosa showed glandular changes of chronic injury and dysplasia, and in these areas, argyrophilic cell hyperplasia was identified. Data is presented describing the evolution of argyrophilic cell hyperplasia as a reaction to injury, the evolution of carcinoid tumors in argyrophilic cell hyperplasia, and the relationship of the proliferating argyrophilic cells to the proliferating glandular cells in ulcerative colitis.

Adult↗
PubMed1982

Importance of preoperative hypertrophy, wall stress and end-systolic dimension as echocardiographic predictors of normalization of left ventricular dilatation after valve replacement in chronic aortic insufficiency.

To define and compare predictors of postoperative normalization of diastolic left ventricular dimension after aortic valve replacement, echocardiographic indexes of left ventricular size, function, degree of hypertrophy and systolic wall stress were examined in 43 patients with chronic and 14 with acute aortic insufficiency. In all of the latter 14 patients, left ventricular diastolic dimension returned to normal (mean 5.2 +/- 0.4 cm) in the postoperative follow-up period (mean 8.0 months). In contrast, of those with chronic insufficiency, 28 (group A) had postoperative normalization of diastolic dimension whereas the remaining 15 (group B) had persistent enlarged diastolic dimension. Preoperative end-systolic dimension, diastolic radius/thickness ratio, mean radius/thickness ratio, mean wall stress and end-systolic stress were 84 to 93 percent accurate in predicting normalization versus persistence of left ventricular dilatation postoperatively, and were superior to preoperative end-diastolic dimension and shortening fraction. Postoperatively, group A had complete normalization of end-systolic dimension and of mean and end-systolic wall stresses with persistence of a normal shortening fraction. Group B continued to have increases in end-systolic dimension, mean wall stress and end-systolic stress with a reduction in shortening fraction. Postoperatively there was a 43 and 29 percent incidence rate of heart failure and death by heart failure, respectively, in group B versus none in group A (p less than 0.01). These findings support the concept that inappropriate hypertrophy in chronic aortic insufficiency is associated with progressive increases in wall stress and end-systolic dimension and a reduction in shortening fraction that eventually result in irreversible cardiac dilatation and failure. Accurate and clinically relevant determination of reversible and irreversible alterations in left ventricular size and function may be obtained with these echocardiographic indexes.

Adolescent↗
PubMed1982

Pulsed doppler echocardiographic detection of mitral regurgitation in mitral valve prolapse: correlation with cardiac arrhythmias.

The incidence of mitral regurgitation in mitral valve prolapse was studied retrospectively in 88 consecutive hospital based patients with mitral valve prolapse using pulsed Doppler echocardiography. Pulsed Doppler findings of turbulence in the left atrium were predictive of angiographic findings of mitral regurgitation in 31 patients. On 24-hr Holter monitoring, patients with mitral valve prolapse and mitral insufficiency had a higher prevalence of ventricular arrhythmias than patients without mitral insufficiency (61 vs 22%; P less than 0.02). Detection of mitral insufficiency identified individuals with mitral valve prolapse who are at higher risk of ventricular arrhythmias.

Adolescent↗
PubMed1982

Effect of cardiac surgery on ventricular septal motion: assessment by intraoperative echocardiography and cross-sectional two-dimensional echocardiography.

Echocardiographic evidence of paradoxical septal motion frequently occurs after cardiac surgery. To assess possible etiologic factors 17 patients were studied preoperatively, intraoperatively, and 7 days after surgery. Preoperative septal motion was normal in 14 and paradoxical in three (two with previous cardiac surgery, one with atrial septal defect [ASD]). Intraoperative septal motion prior to surgical procedure was normal in 16 and paradoxical in one (ASD). Septal motion (excursion and thickening fraction) was normal in all patients prior to chest closure. Echocardiograms of adequate quality were obtained at 7 days post surgery in 15 patients; septal motion was paradoxical in nine (group A) and normal in six (group B). No significant differences were seen between the two groups in ischemic time or in the preoperative to postoperative change in left ventricular (LV) and right ventricular diastolic dimension, shortening fraction, or septal and posterior wall thickening fraction. A significant postoperative decrease in septal excursion was seen in group A but not in group B; significant postoperative increases in posterior wall excursion were seen in both groups. Cross-sectional two-dimensional echocardiograms performed in 20 patients (8 normal, 12 postoperative paradoxical septal motion) were analyzed. In normal controls no significant change was detected in the LV centroid position during systole. In contrast, the 12 postoperative patients showed significant anterior displacement of the LV centroid and right septum during systole. Thus, paradoxical septal motion after cardiac surgery appears to relate to excessive anterior cardiac mobility due to pericardiotomy rather than to myocardial ischemia resulting from cardiopulmonary bypass.

Adult↗
PubMed1982

Effect of nifedipine on exercise-induced left ventricular dysfunction and myocardial hypoperfusion in stable angina.

To assess the effects of nifedipine on left ventricular function and regional myocardial perfusion, exercise radionuclide ventriculography was performed in 15 men (median age 59 years) and exercise thallium-201 scintigraphy was done in 11 of them, before and 90 minutes after the oral administration of 20 mg of nifedipine. All patients had stable angina and angiographically proved coronary artery disease without evidence of spasm. Exercise tolerance after administration of nifedipine increased from 343 +/- 42 seconds to 471 +/- 50 seconds (p less than 0.01), whereas the peak exercise double product remained essentially unchanged (difference not significant). Ejection fraction improved significantly at rest (from 49 +/- 3.6% to 52 +/- 3.3%, p less than 0.05) and at peak exercise (42 +/0 3.3% to 47 +/- 3.7%, p less than 0.05). Nifedipine also resulted in an improved segmental wall motion score (4.3 +/- 2.3 to 3.0 +/- 2.3, p less than 0.05; 0 = normal and 4 = worst degree of dysfunction). The ejection fraction increased by more than 5% in one third of the patients at rest, and in more than half of the patients at peak exercise. Improved exercise myocardial perfusion occurred in 5 of 11 patients (45%) and in 7 of 28 segments (25%) with reversible hypoperfusion. Thus, nifedipine produces significant improvement in global and regional left ventricular function in patients with coronary artery disease and stable angina. This may be accounted for, at least in part, by improvement in myocardial perfusion.

Aged↗