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Biomedical subjects

R E Goldstein

Publications and source records attributed to R E Goldstein.

At least 109 records · Page 6Linked to original sources
PubMed1989

Finishing of composites and laminates.

Regardless of the color, shape or attention to detail, there must be sufficient time to adequately finish all restorations. Both esthetics and function can best be satisfied when the restoration acquires its maximal finish. In the final analysis, not only will the restoration look better, but it will look better for a longer period of time. Life expectancy of the restoration may, in fact, be directly dependent on just how well this task is accomplished.

Carbon↗
PubMed1989

Leukotriene D4 and hypoxia: differential effects on the pulmonary and systemic circulations in newborn piglets.

Hypoxia-induced release of cysteinyl leukotriene from pulmonary macrophages has been considered an important mechanism mediating hypoxic pulmonary vasoconstriction in the immature circulation. However, studies leading to this conclusion blocked hypoxic pulmonary vasoconstriction by relatively nonspecific LT antagonists. We have evaluated this hypothesis further by separate measurement of the hemodynamic effects of leukotriene D4 (LTD4) and hypoxia before and after administration of the highly specific leukotriene D4/E4 antagonist LY 171883 (LY). Anesthetized, open-chest newborn piglets were exposed to LTD4 0.1-3 micrograms/kg IV, or to hypoxia (12% 02 + 88% N2, for 3 min) prior and subsequent to LY 30 mg/kg IV (n = 7) or saline vehicle (n = 5). LTD4 administration before LY caused a 37% - 446% increase in pulmonary vascular resistance index (PVRI) (p less than 0.05). With LTD4 mean pulmonary artery pressure (PAP) rose 14% - 69% (p less than 0.05), left ventricular end-diastolic pressure (LVEDP) rose 18% - 160% (p less than 0.05) and systemic vascular resistance index (SVRI) increased 88% - 100% (p less than 0.05). Cardiac index (CI) and left ventricular shortening fraction (LVSF) fell only at peak LTD4 dose (92 +/- 7 to 49 +/- 8 ml/kg/min, 12 +/- 1 to 6 +/- 1%, both p less than 0.05). Hypoxia produced a 69% rise in PAP and a 122% increase in PVRI, both p less than 0.01. LY abolished LTD4-induced changes in PVRI, PAP, LVEDP, CI, SVRI, and LVSF, but had no effect on the hypoxic rise in PAP and PVRI. Thus, doses of LY which completely inhibited the substantial circulatory actions of LTD4 failed to alter hypoxic pulmonary vasoconstriction. The results suggest that acute hypoxic pulmonary vasoconstriction in newborn piglets is not attenuated by selective LTD4/E4 receptor antagonism.

Acetophenones↗
PubMed1988

Inhibition of eicosanoid-mediated coronary constriction during myocardial ischemia.

Thromboxane A2 and cysteinyl leukotrienes are highly effective microvessel constrictors in normally perfused myocardium. Their release during acute coronary thrombosis might augment myocardial underperfusion. The constrictor action of these substances could be modified substantially, however, by concomitant myocardial ischemia. We compared the effects of the two eicosanoid constrictors in normally perfused and ischemic myocardium of 24 open-chest, pentobarbital-anesthetized pigs. Left anterior descending coronary flow was measured after intracoronary bolus injections of the stable thromboxane A2 analog U46619 (1-10 micrograms) or leukotriene D4 (LTD4, 1-10 micrograms). Each dose was given before and during myocardial ischemia induced by a snare adjusted to produce 63 +/- 2% decrease in coronary flow for 10 min. Marked dose-independent inhibition of eicosanoid-induced coronary flow decrease occurred during ischemia. With 10 micrograms U46619, coronary flow decrease in the unoccluded state (25 +/- 2 from 55 +/- 4 ml/min pretreatment baseline) was virtually eliminated during snare occlusion (1 +/- 1 from 21 +/- 3 ml/min pretreatment baseline, P less than 0.001). Similar results occurred with LTD4. Distal coronary pressure during ischemia indicated a lack of microvessel responsiveness to the eicosanoids rather than a buffering of resistance change by the snare. U46619 and LTD4 did induce transient, small reductions in regional shortening fraction during ischemia. Our data suggest that eicosanoid-induced constriction of myocardial resistance vessels is not a likely complication of acute coronary thrombosis. However, eicosanoids could depress residual contractility in moderately ischemic regions.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1988

Metabolic role of the exercise-induced increment in epinephrine in the dog.

The role of the exercise-induced increment in epinephrine was studied in five adrenalectomized (ADX) and in six normal dogs (C). Experiments consisted of an 80-min equilibration period, a 40-min basal period, and a 150-min exercise period. ADX were studied with epinephrine replaced to basal levels during rest and to increased levels during exercise to simulate its normal rise (HE) and on a separate day with epinephrine maintained at basal levels throughout the study (BE). Cortisol was replaced during rest and exercise in ADX so as to simulate the levels seen in C. Glucose was infused as needed in ADX to maintain the glycemia evident during exercise in C. Glucose production (Ra) and utilization (Rd) were assessed isotopically. In C, epinephrine had risen by 95 +/- 25 pg/ml by the end of exercise. In HE, the increment in epinephrine (117 +/- 29 pg/ml) was similar to that seen in C, whereas in BE epinephrine fell by 18 +/- 9 pg/ml. Basal norepinephrine levels were 139 +/- 9, 260 +/- 25, and 313 +/- 33 pg/ml in C, HE, and BE, respectively. In response to exercise, norepinephrine increased by nearly twofold in all protocols. Basal and exercise-induced changes in plasma glucagon and insulin were similar in C and ADX. Ra increased similarly in C (5.3 +/- 0.6 mg.kg-1.min-1) and HE (4.9 +/- 0.6 mg.kg-1.min-1). In BE, Ra rose normally for the initial 90 min but then declined resulting in a rise of only 2.9 +/- 0.5 mg.kg-1.min-1 after 150 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1987

Serial acquisition of data to predict one-year mortality rate after acute myocardial infarction.

Eight hundred sixty-six patients with acute myocardial infarction (AMI) were enrolled in a prospective study to determine optimal predictors of long-term prognosis. During 12-month (mean) follow-up there were 65 cardiac deaths and 21 nonfatal repeat AMIs. Twenty-nine variables (from the history, physical examination, serum chemistries, ambulatory monitor, radionuclide ventriculogram and exercise test) were arranged into in 5 sequential groups according to the time at which results became available during hospitalization. Multivariate analysis (logistic regression) and receiver-operator characteristic curves were used to assess improvement in prediction of mortality or repeat AMI by addition of each group of variables. The first group of independent predictors included rales, left bundle branch block and symptom status at 1 month before admission. Addition of information from ambulatory monitoring or serum chemistry did not improve prediction. Radionuclide ejection fraction made a statistically significant, independent contribution to mortality prediction. Of the final group the only exercise test variable that contributed independently to prediction was whether the patients took the test. However, receiver-operator characteristic curves showed that improvement in sensitivity and specificity by addition of information from the radionuclide scan and exercise test was clinically insignificant. Our results imply that costly tests after AMI should be reserved for specific indications and not applied universally for prognosis. Although these tests were highly predictive individually, each test generally added little to preexisting prognostic information.

Follow-Up Studies↗
PubMed1987

Calcitonin gene-related peptide: a potent modulator of coronary flow.

Calcitonin gene-related peptide (CGRP) has been identified in nerve fibers innervating cardiovascular elements and particularly in coronary arteries (CA). To investigate its potential role in modulating coronary blood flow, we injected rat-CGRP into the CA of pentobarbital anesthetized, open chest pigs. Significant dose-related increments in coronary flow were observed. The rise in coronary flow was characterized by unusually, slow onset, late peak and prolonged duration. Arterial pressure, heart rate (HR) and myocardial contractility were unchanged, except at the highest dose (3.0 nmol), which produced mild systemic hypotension and sinus tachycardia. Coronary levels of catecholamines and 6-keto-PGF1 alpha were unchanged by CGRP. The direct, sustained, and potent dilatory activity of CGRP, in coronary arteries of the pig together with anatomical CGRP localization in this site suggest a role for this neuropeptide in hemodynamic regulation.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Cardiac and coronary consequences of intracoronary platelet activating factor infusion in the domestic pig.

In previous studies we have shown that platelet-activating factor (PAF) is a potent vasoactive substance with deleterious effects on coronary blood flow (CBF) and myocardial performance. The present study further investigates the effects of PAF during its sustained intracoronary infusion in the blood-perfused domestic pig (n = 16). PAF infusion (1-9 nmol/min) produced triphasic changes in CBF (n = 7): an initial brief phase of coronary dilation (14 +/- 2% above baseline), followed by severe reduction in CBF due to increase in coronary vascular resistance and a third phase of escape that was characterized by return of CBF towards baseline in spite of continuing PAF infusion. In 9 remaining pigs PAF infusion had a biphasic response: the first phase of coronary dilation rapidly turned into severe coronary constriction accompanied by severe systemic hypotension and death within a few min. PAF infusion caused a profound rise in systemic arterial and coronary venous thromboxane B2 levels, while 6-keto-PGF1 alpha and leukotriene C4-immunoreactivity levels were not changed. Indomethacin completely blocked the rise in thromboxane level during PAF infusion and abolished the constrictor effect of PAF on the coronary vessels. These data suggest that PAF might play a detrimental role on the coronary circulation and cardiac function, primarily through thromboxane A2 mediated mechanism.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Interaction of amiodarone and desethylamiodarone with solubilized nuclear thyroid hormone receptors.

The mechanisms of action of the potent antiarrhythmic drug amiodarone are unknown. However, amiodarone and its abundant metabolite, desethylamiodarone, bear a striking structural resemblance to thyroid hormones. In addition, certain cardiac electrophysiologic effects of amiodarone treatment are similar to those of hypothyroidism. These facts suggest that amiodarone or desethylamiodarone could be acting, in part, by blocking thyroid hormone action. Because thyroid hormones are known to act through nuclear receptor proteins, the binding of amiodarone and desethylamiodarone was measured to nuclear extracts derived from human lymphocytes, bovine atrium and ventricle and rat liver. The capacity of increasing concentrations of amiodarone and desethylamiodarone nuclear extracts to block receptor binding of radiolabeled triiodothyronine (T3) in a standard in vitro competition assay was tested. Nuclear extracts demonstrated only minimal binding to amiodarone. However, all receptor preparations had substantial affinities (KD) for the desethyl analog: lymphocyte, 8.6 microM; atrium, 35.0 microM; ventricle, 26.9 microM and liver, 8.6 microM. Desethylamiodarone accumulates in very large quantities in parenchymatous organs during long-term amiodarone treatment. Taking its usual therapeutic serum level (about 4 microM or 2.7 micrograms/ml) as an estimate of intranuclear concentration, desethylamiodarone would partially saturate nuclear thyroid hormone receptors in several different tissues, including the heart. Thus, amiodarone treatment may exert some of its electrophysiologic effects by metabolic conversion to desethylamiodarone. This metabolite may then exclude thyroid hormone from nuclear receptor sites within the myocardium.

Amiodarone↗
PubMed1987

Estimating left ventricular offset volume using dual-frequency conductance catheters.

The measurement of left ventricular volume by the conductance-catheter technique has many advantages, but it is difficult to determine absolute volumes with this method. Current procedure requires that a bolus of concentrated hypertonic saline be injected to measure absolute volume. It also demands that the subject be in a steady state and that measurements only be made at discrete intervals. The saline bolus may affect the cardiovascular state of the subject. This paper describes a new technique for estimating absolute volume utilizing the conductance catheter that relies on the different frequency responses of blood and muscle. Good correlation between the salt-injection method and the dual-frequency method was found in nine closed-chest pigs anesthetized with pentobarbital sodium (r = 0.922). Further refinements may extend the utility of the dual-frequency approach.

Animals↗
PubMed1987

Bleaching teeth: new materials--new role.

Today, bleaching alone can be effective in restoring appearance to teeth stained from various causes. Moreover, bleaching can be combined with other restorative treatment to produce results not otherwise possible. Bleaching requires careful diagnosis and techniques but offers a relatively simple, safe, and successful way to significantly improve appearance. In the future, bleaching will be a routine, conservative treatment option.

Dental Restoration, Permanent↗
PubMed1986

Tachykinin modulation of coronary blood flow.

In pentobarbital anesthetized, open chest pigs, coronary blood flow (CBF), myocardial contractility and systemic hemodynamic variables were monitored during intracoronary injections of substance P (SP), neurokinin A (NA) or neurokinin B (NB). SP was most potent in increasing CBF although NA was also active in high doses while NB had absolutely no effect. SP was also more potent than NA in producing systemic hypotension. The data suggests that SP and its receptors might be potentially important modulators of CBF.

Animals↗