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Biomedical subjects

S Gabbay

Publications and source records attributed to S Gabbay.

9 recordsLinked to original sources
PubMed1992

Developmental changes in the heterocellular epidermis of Pelobates syriacus integument.

Changes in characteristic components of the skin epidermis of the large tadpole of Pelobates syriacus were studied throughout its development. The fate of two specific cells in the skin epidermis was followed, from the young tadpole to the adult was studied. It was found that flask-shaped type cells in the tadpole epidermis which are PAS-positive, stain with peanut lectin (PNA). There is no detectable band 3 in the premetamorphosed stages, and mitochondria-rich cells are very rare. This pattern of staining changes completely upon metamorphosis: the PAS-positive cells, specific to the tadpole epidermis disappear, and the mitochondria-rich (MR) cells in the adult skin epithelium react with polyclonal anti-band 3 antibody. Western blot analysis showed the presence of a band 3-like protein of about 95 kDa, only in the adult epithelial extract, corroborating the immunocytochemical observations. The finding of the presence of band 3-like protein in the MR cells of Pelobates, is similar to the observations made in the skin of other amphibian species. On the other hand, the binding of peanut lectin to MR cells is species-specific, since it does not react with the MR cells in the skin epithelium of Pelobates syriacus.

Animals↗
PubMed1979

Mechanism of reduction of mitral regurgitation with vasodilator therapy.

Acute mitral regurgitation was produced in six open chest dogs by excising a portion of the anterior valve leaflet. Electromagnetic flow probes were placed in the left atrium around the mitral anulus and in the ascending aorta to determine phasic left ventricular filling volume, regurgitant volume and stroke volume. The systolic pressure gradient was calculated from simultaneously measured high fidelity left atrial and left ventricular pressures. The effective mitral regurgitant orifice area was calculated from Gorlin's hydraulic equation. Infusion of nitroprusside resulted in a significant reduction in mitral regurgitation. No significant change occurred in the systolic pressure gradient between the left ventricle and the left atrium because both peak left ventricular pressure and left atrial pressure were reduced. The reduction of mitral regurgitation was largely due to reduction in the size of the mitral regurgitant orifice. Reduction of ventricular volume rather than the traditional concept of reduction of impedance of left ventricular ejection may explain the effects of vasodilators in reducing mitral regurgitation.

Animals↗
PubMed1979

Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area.

The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.

Angiotensin II↗
PubMed1979

In vitro hydrodynamic comparison of mitral valve bioprostheses.

With the use of the pulse duplicator built in our laboratory, the hydrodynamic characteristics of three sizes of the four commercially available mitral bioprostheses, Hancock, Carpentier-Edwards, Angell-Shiley, and Ionescu-Shiley, were studied and compared. A wide range of performance was found: for example, during pulsatile testing, at peak flow of 15 1/min (corresonding to a normal resting cardiac output) transvalvular gradients varied from as high as 20 mm Hg (Angell-Shiley) to 5 mm Hg(Ionescu-Shiley) in the 25 mm mounting diameter size. Effective orifice areas (EOA) are significantly different in valves of the same mounting size, e.g., at peak flows of 20 1/min, the Ionescu-Shiley 25 provides an EOA of 1.7 cm2 while the Angell-Shiley provides only 1.17 cm2. The EOAs of all bioprostheses have been found to increase with increasing flow (e.g., from 10--30 1/min peak flow, the Hancock 25 changed from 1.25 cm2 to 1.50 cm2). The Gorlin formula, as constituted for calculating the area of stenotic mitral valves, is inappropriate for prosthetic valves. But the discharge coefficients of the bioprostheses have been found to be around 1 when the planimetered area of the open valve orifice is determined at a given flow. By using this discharge coefficient, the Gorlin formula will give an excellent estimate of the true orifice area of mitral bioprostheses.

Bioprosthesis↗
PubMed1979

Dynamic changes in the canine mitral regurgitant orifice area during ventricular ejection.

We designed this study to test the hypothesis that in acute mitral regurgitation the mitral regurgitant area (MRA) is a dynamic quantity which varies with the time variation of ventricular volume. Mitral insufficiency was created in five open-chest dogs in which a portion of the anterior leaflet was excised. Phasic aortic and mitral flows were measured electromagnetically, along with left atrial and ventricular pressures. Filling, regurgitant, and stroke volumes, and systolic pressure gradient were determined by digital methods. MRA was calculated from the fluid dynamic equation of motion to give the temporal mean and the instantaneous value at three instants of time and at the time of peak flow (when inertia is negligible). Mean regurgitant fraction was 42 +/- 12% with no indication of left ventricular failure due to volume overload. MRA decreased monotonically with time to 59% of its initial value and closely paralleled the decrease in ventricular volume during systole. In a control study using a tilting-disc prosthesis with a hole 5 mm in diameter in the occluder, the calculated MRA was time invariant and equal to the measured area for regurgitation. We conclude that in acute mitral regurgitation the MRA is a function of ventricular volume.

Animals↗
PubMed1978

In vitro hydrodynamic comparison of mitral valve prostheses at high flow rates.

A pulse duplicator system for evaluating the hemodynamic performance of mitral prostheses is described. Under conditions stimulating normal resting physiology, all valves tested had measurable but acceptably small pressure drops. Under conditions simulating exercise, all were moderately to severely stenotic. Valves with nearly equal mounting diameters were compared. The Hancock, Beall, and Starr-Edwards valves (Group A) were found to be significantly more stenotic than the Björk-Shiley, Cutter-Cooley, Ionescu-Shiley, and Lillehei-Kaster valves (Group B). In the 29 to 30 mm. mounting diameter size at cardiac outputs of 5 and 9 L. per minute, Group A had average pressure drops of 3.2 and 10.5 mm. Hg and Group B, pressure drops of 1.6 and 5.3 mm. Hg, respectively. In the 24 to 26 mm. mounting diameter size, at cardiac outputs of 9 L. per minute, all the valves had critically large pressure drops (9 to 17.6 mm. Hg). The standard Gorlin formula is inappropriate for computing the orifice area of prosthetic valves. The discharge coefficient for a valve (a measure of how well the valve uses its primary flow area) and a performance index (a measure of how well the valve uses its mounting area) have been computed from a knowledge of the orifice size, without the necessity of assuming a value for the discharge coefficient required by the Gorlin formula. The biological valves (Hancock and Ionescu-Shiley) provide an efficient orifice for fluid flow at the free leaflet margins and have large discharge coefficients. On the basis of the fluid dynamic equation of motion, steady flow, root mean square (RMS) flow, and peak flow, combined with the appropriate transvalvular gradients, were all shown to yield equally accurate characterizations of valvular hydrodynamic performance. Mean flow, unfortunately the only value obtainable clinically, yielded effective orifice areas 10 percent smaller than either of the other three flow values.

Bioprosthesis↗
PubMedDate not supplied

A system for in-vitro characterization of heart valve bioprostheses under accelerated fatigue conditions and under physiologic conditions.

An accelerated fatigue testing system and a pulse duplicator (heart simulator) were used in a set-up in which pressure differences and pulsatile flow rates across prosthetic heart valves, as well as machine rates, could be measured using a real-time on-line data-acquisition system. With this information available, an immediate in-vitro characterization of the fluid dynamics of prosthetic heart valves could be obtained under both physiologic and accelerated conditions. In addition to the fatigue tester and the pulse duplicator, a signal conditioner, a DC amplifier, an analog-to-digital converter, and a digital microcomputer comprised the essential hardware. For the purpose of this study, special acquisition software was developed. By means of the same computational algorithms, all quantitative fluid dynamics data could be calculated using information from both the pulse duplicator and the fatigue tester, so that direct comparisons and correlations could be approached. Pressure difference-flow rate relationships for the two machines were comparable.

Bioprosthesis↗