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Dov Jaron

Publications and source records attributed to Dov Jaron.

8 recordsLinked to original sources
PubMed2005

Quantifying the L-arginine paradox in vivo.

NO and PO(2) microelectrodes were used to quantify the effects of increased availability of L-arginine in an exteriorized rat mesentery and small intestine microcirculatory preparation in n = 16 rats. During short periods of elevated L-arginine added to the superfusion bath, transient changes in perivascular NO or PO(2) were measured at 171 perivascular sites near intestinal arterioles and venules, simultaneously with tissue perfusion using laser Doppler flowmetry (LDF). Excess L-arginine increased perivascular NO over twofold, by 411 +/- 42 nM above the baseline of 329 +/- 30 nM (P < 0.0001), and increased tissue perfusion by 35.5 +/- 7.5% (P < 0.0001). No difference between arterioles and venules was observed in the magnitude or time course of the NO responses. Both increases and decreases in perivascular PO(2) were observed after excess L-arginine, with a similar increase in tissue perfusion by 42.0 +/- 12.3% (P < 0.0001). Our NO measurements confirm that increased bioavailability of L-arginine causes a significant increase in NO production throughout the microcirculation of this preparation, with increased tissue perfusion, and provides direct in vivo evidence for the L-arginine paradox.

Animals↗
PubMed2005

The influence of radial RBC distribution, blood velocity profiles, and glycocalyx on coupled NO/O2 transport.

The purpose of this investigation was to study the effect of the presence of red blood cells (RBCs) in the plasma layer near the arteriole wall on nitric oxide (NO) and oxygen (O2) transport. To this end, we extended a coupled NO and O2 diffusion-reaction model in the arteriole, developed by our group, to include the effect of the presence of RBCs in the plasma layer and the effect of convection. Two blood flow velocity profiles (plug and parabolic) were tested. The average hematocrit in the bloodstream was assumed to be constant in the central core and decreasing to zero in the boundary layer next to the endothelial surface layer. The effect of the presence or absence of RBCs near the endothelium was studied while varying the endothelial surface layer and boundary layer thickness. With RBCs present in the boundary layer, the model predicts that 1) NO decreases significantly in the endothelium and vascular wall; 2) there is a very small increase in endothelial and vascular wall Po2; 3) scavenging of NO by hemoglobin decreases with increasing thickness of the boundary layer; 4) the shape of the velocity profile influences both NO and Po2 gradients in the bloodstream; and 5) the presence of RBCs in the boundary layer near the endothelium has a much larger effect on NO than on O2 transport.

Arterioles↗
PubMed2004

Interactions between NO and O2 in the microcirculation: a mathematical analysis.

Biotransport of nitric oxide (NO) and of oxygen (O(2)) in the microcirculation are inherently interdependent, since all nitric oxide synthase (NOS) isoforms (eNOS, nNOS, and iNOS) require O(2) to produce NO. Furthermore, tissue O(2) consumption is reversibly inhibited by NO. To investigate these complex interactions, a mathematical model was developed for coupled mass transport of NO and O(2) around a cylindrical arteriole using finite element computational methods. Steady-state radial NO and O(2) gradients in the bloodstream, plasma layer, endothelium, vascular wall, and surrounding tissue were simulated for different conditions. Special cases of the model were solved, including O(2)-dependent NO production from eNOS alone, and with additional NO production from either nNOS or iNOS at specified locations. The model predicts that (a) concentration changes in one species can have significant effects on transport of the other species with the degree of interaction dependent on spatial gradients; (b) eNOS NO production rates required to maintain the concentration of NO in the vascular wall are more dependent on NO scavenging in blood than in tissue; (c) relatively low rates of NO production in tissue from either nNOS or iNOS can elevate vascular wall NO, compensating for possible reductions in NO production from eNOS; (d) depending on their physical location, nNOS and iNOS can be very sensitive to O(2); and (e) increased tissue NO can increase O(2) delivery to more distal regions by inhibiting O(2) consumption in other regions.

Animals↗
PubMed2004

Impact of the Fåhraeus effect on NO and O2 biotransport: a computer model.

Nitric oxide (NO) and oxygen (O2) transport in the microcirculation are coupled in a complex manner, since enzymatic production of NO depends on O2 availability, NO modulates vascular tone and O2 delivery, and tissue O2 consumption is reversibly inhibited by NO. The authors investigated whether NO bioavailability is influenced by the well-known Fåhraeus effect, which has been observed for over 70 years. This phenomenon occurs in small-diameter blood vessels, where the tube hematocrit is reduced below systemic hematocrit as a plasma boundary layer forms near the vascular wall when flowing red blood cells (rbcs) migrate toward the center of the bloodstream. Since hemoglobin in the bloodstream is thought to be the primary scavenger of NO in vivo, this might have a significant impact on NO transport. To investigate this possibility, the authors developed a multilayered mathematical model for mass transport in arterioles using finite element numerical methods to simulate coupled NO and O2 transport in the blood vessel lumen, plasma layer, endothelium, vascular wall, and surrounding tissue. The Fåhraeus effect was modeled by varying plasma layer thickness while increasing core hematocrit based on conservation of mass. Key findings from this study are that (1) despite an increase in the NO scavenging rate in the core with higher hematocrit, the model predicts enhanced vascular wall and tissue NO bioavailability due to the relatively greater resistance for NO diffusion through the plasma layer; (2) increasing the plasma layer thickness also increases the resistance for O2 diffusion, causing a larger P(O2) gradient near the vascular wall and decreasing tissue O2 availability, although this can be partially offset with inhibition of O2 consumption by higher tissue NO levels; (3) the Fåhraeus effect can become very significant in smaller blood vessels (diameters <30 microm); and (4) models that ignore the Fåhraeus effect may underestimate NO concentrations in blood and tissue.

Biological Transport↗
PubMed2003

Modeling the influence of superoxide dismutase on superoxide and nitric oxide interactions, including reversible inhibition of oxygen consumption.

A mathematical mass transport model was constructed in cylindrical geometry to follow coupled biochemical reactions and diffusion of oxygen, nitric oxide, superoxide, peroxynitrite, hydrogen peroxide, nitrite, and nitrate around a blood vessel. Computer simulations were performed for a 50 microm internal diameter arteriole to characterize mass transport in five concentric regions (blood, plasma layer, endothelium, vascular wall, perivascular tissue). Steady state gradients in nitric oxide, oxygen partial pressure, superoxide, and peroxynitrite, and associated production of hydrogen peroxide, nitrite, and nitrate were predicted for varying superoxide production rates, superoxide dismutase concentrations, and other physiological conditions. The model quantifies how competition between superoxide scavenging by nitric oxide and superoxide dismutase catalyzed removal varies spatially. Reversible inhibition of oxygen consumption by nitric oxide, which causes increased tissue oxygenation at deeper locations, was also included in the model. The mass transport model provides insight into complex interactions between reactive oxygen and nitrogen species in blood and tissue, and provides an objective way to evaluate the relative influence of different biochemical pathways on these interactions.

Arteries↗
PubMedDate not supplied

Healthcare technology, economics, and policy: an evolving balance.

Economic and policy issues increasingly influence healthcare technology solutions as we wrestle with keeping healthcare quality high while keeping costs under control. The healthcare system is also undergoing rapid change brought about by managed care, shifting care to team providers in an outpatient or home environment. The development of health technologies under new market arrangements needs to be examined so that quality of care and cost are not at cross roads. As these issues continue to evolve in the public forum, it is critical for engineers and contributors to technology in healthcare to understand the dynamics that influence technology need and and adoption in the healthcare market. We hope that this special issue will provide a basis for initial understanding of these issues and stimulate further involvement by the bioengineering community at large, for the improvement of healthcare across all of society.

Biomedical Engineering↗