Biomedical subjects

I R Weinstein

Publications and source records attributed to I R Weinstein.

17 recordsLinked to original sources

PubMed1987

Pseudo-retrograde ventriculoatrial conduction and mid-diastolic filling waves noted on echocardiogram.

Explore the source record for details and available documents.

Aged↗

PubMed1983

Identification and properties of myocardial myoglobin as a binder of iodothyronines.

Gel filtration of dog myocardial cytosol previously incubated with [125I]T4 or [125I]T3 revealed hormone binding in three fractions, one of which, M-2, was presumptively identified as myoglobin by absorbance maximum, molecular weight and specific immunodiffusion. Gel chromatography of purified horse or dog myoglobins incubated with labeled T3 or T4 resulted in coelution of the myoglobin and iodothyronine peaks. Excess unlabeled thyroid hormone displaced no more than 25% of tracer bound to myoglobin. Acid-acetone fractionation of myoglobin into heme and globin, and subsequent precipitation of the heme, localized hormone binding to the heme moiety. Hematin (ferric state heme) in solution was also shown to bind thyroid hormone. Added to human sera which were then subjected to T3 or T4 radioimmunoassay, myoglobin reduced detectable, endogenous iodothyronine by 77 and 26%, respectively. The myoglobin effect was concentration dependent. Heart myoglobin, like hemoglobin in the erythrocyte, is a cytoplasmic heme protein responsible for a major fraction of binding of intracellular iodothyronine. The nature of the interaction between iodothyronines and the heme prosthetic group is unclear.

Animals↗

PubMed1983

Ultrasonic assessment of the St. Jude prosthetic valve: M mode, two-dimensional, and Doppler echocardiography.

To determine whether the flow characteristics of aortic and mitral St. Jude Medical valves could be defined noninvasively, we analyzed Doppler transprosthetic flow velocity spectra in 23 relatively asymptomatic patients. Results were interpreted in the framework of M mode and two-dimensional echocardiographic data and were compared with Doppler transvalvular flow velocity spectra from native valves of healthy subjects. Although the morphologic characteristics of Doppler spectra were similar, peak and mean transprosthetic mitral flow velocities were higher than values obtained across native valves (1.38 +/- 0.3 m/sec and 0.73 +/- 0.1 m/sec vs 0.78 +/- 0.1 m/sec and 0.35 +/- 0.06 m/sec, respectively; p less than .001). However, calculated pressure half-times were not different (61.2 +/- 16.9 msec vs 57.2 +/- 13.2 msec; p greater than .05) and calculated transprosthetic mitral gradients were small (2.3 +/- 0.9 mm Hg). Similarly, the morphologic characteristics of aortic Doppler flow spectra in St. Jude and native valves were analogous. However, prosthetic valves exhibited higher peak and mean velocities (p less than .01) and slightly prolonged time-to-peak flow (p = .02). M mode and two-dimensional studies did not show useful quantitative measures of prosthetic function and did not demonstrate evidence of paravalvular leaks, which were detected in four cases by Doppler techniques. Thus Doppler echocardiography provides quantitative information about transprosthetic flow characteristics in patients with implanted St. Jude valves and is useful in identifying patients with prosthetic dysfunction.

Adult↗

PubMed1981

Zero-flow pressures and pressure-flow relationships during single long diastoles in the canine coronary bed before and during maximum vasodilation. Limited influence of capacitive effects.

The proposal that diastolic coronary flow is regulated by an intramyocardial "back-pressure" that substantially exceeds coronary venous and ventricular diastolic pressures has been examined in an open-chest canine preparation in which instantaneous left circumflex pressure and flow could be followed to cessation of inflow during prolonged diastoles. Despite correlation coefficients consistently >0.90, pressure-flow data during individual diastoles were concave to the flow axis before and during pharmacologically induced maximum coronary vasodilation. Data were better fitted (P < 0.01) by second-order equations than by linear equations in >90% of cases. Second-order pressure-axis intercepts (P(f=0))(1) averaged 29+/-7 (SD) mm Hg before vasodilation and 15+/-2 mm Hg during vasodilation; left and right atrial pressures were always substantially lower (8+/-3 and 5+/-2 mm Hg before vasodilation and 8+/-2 and 4+/-1 mm Hg during dilation). Values of P(f=0) before vasodilation varied directly with levels of coronary inflow pressure. A modification of the experimental preparation in which diastolic circumflex pressure could be kept constant was used to evaluate the suggestion that P(f=0) measured during long diastoles are misleadingly high because of capacitive effects within the coronary circulation as inflow pressure decreases. Decreases in P(f=0) attributable to capacitive effects averaged only 5.9+/-3.0 mm Hg before vasodilation and were smaller during dilation. We conclude that P(f=0) is a quantitatively important determinant of coronary driving pressure and flow, resulting from both factors related to, and independent of, vasomotor tone. Adjustments of flow during changing physiological situations may involve significant changes in P(f=0) as well as in coronary resistance.

Animals↗

PubMed1974