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In these experiments, we tested the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell oxygen levels following blood flow reduction. This hypothesis predicts that if the fall in parenchymal cell PO₂ during stimulation can be minimized, escape should be reduced. To test this prediction, we studied the behavior of superficial arterioles of the cat sartorius muscle during 3 minutes of sympathetic nerve stimulation. The muscle was covered with silicone oil equilibrated with 0%, 5% and 10% oxygen. During stimulation under 0% oxygen, 90% of visible arterioles showed a significant secondary relaxation (escape). The relaxation averaged 55% of the initial constriction. Under 5% oxygen, resting arteriolar diameter was reduced by an average of 12% and escape was significantly reduced throughout the arteriolar network. Under 10% ambient oxygen, there was an additional 5% reduction in resting diameter and a further reduction of escape. Escape was not attenuated when control diameter was reduced to the same degree with arginine vasopressin, suggesting that the effect of oxygen was specific rather than secondary to an increase in vascular tone. The above observations are also consistent with the hypothesis that escape is mediated through a fall in vascular wall PO₂. To evaluate this possibility, periarteriolar and parenchymal tissue PO₂ were measured with oxygen microelectrodes during sympathetic stimulation under 0% and 10% oxygen suffusion of the muscle. In the proximal arterioles, the periarteriolar PO₂ during control and during stimulation was identical under 0% and 10% oxygen yet escape was reduced by 75% under 10% oxygen. Similarly, escape was reduced 90% in the distal arterioles under 10% oxygen but periarteriolar PO₂ was very nearly the same as that measured under 0% oxygen. In contrast, mean parenchymal tissue PO₂ fell to low levels during stimulation under 0% oxygen but did not fall below normal levels during stimulation under 10% oxygen. These findings argue against the hypothesis that a fall in vascular wall PO₂ is responsible for escape. The findings are consistent with the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell PO₂. (Abstract shortened with permission of author.)

Evidence suggests different sections of the arteriolar network supplying muscle can respond independently and this may provide a mechanism for the localized distribution of blood flow. This hypothesis was tested in the microcirculation of the cat sartorius muscle by measurement of arteriolar diameter changes during muscle contraction and sympathetic nerve stimulation in each consecutive section of the network. The diameter changes were referenced to the initial distribution of resistance across the network, as determined from arteriolar pressure measurements and morphometric data. This led to an estimate of the change in network resistance. Unlike previous reports, the most distal arterioles dilated little during muscle contraction and our resistance estimate indicates these vessels play an insignificant role in functional hyperemia. The more proximal, third order arterioles dilated proportionately more than other arteriolar orders and made the largest single contribution to resting resistance. Similarly, these vessels were the largest single site of resistance change during sympathetic stimulation. Together, these findings suggest the third order arterioles play a dominant role in regulating flow to the capillaries that each supplies. Antagonism of sympathetic control during muscle contraction has been attributed to direct inhibition of vascular smooth muscle contraction and to inhibition of sympathetic neurotransmission. Evidence to support the latter mechanism comes from the observation that functional dilation is reduced with exogenous norepinephrine as compared to sympathetic stimulation. However, exogenous norepinephrine may bind to both alpha-1 and alpha-2 adrenergic receptors, whereas that released by sympathetic stimulation may bind primarily to alpha-1 receptors. Since this difference could be significant, functional dilation after systemic injection of norepinephrine or phenylephrine, a selective alpha-1 agonist, was compared to that during sympathetic stimulation. In contrast to the findings with norepinephrine, functional dilation after phenylephrine did not differ from that observed during sympathetic stimulation. This indicates the dilator substance(s) released during exercise may selectively inhibit alpha-1 mediated vasoconstriction but less effectively inhibit vasoconstriction mediated by alpha-2 receptors. Furthermore, these findings suggest that the vasodilator mechanism may act primarily at the level of the vascular smooth muscle, without appreciable pre-junctional inhibition of sympathetic nerves.

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Thesis (M.Sc. (Applied Mathematics)) -- University of Limpopo, 2008 / Understanding the effects of blood viscosity variation plays a very crucial role in hemodynamics, thrombosis and inflammation and could provide useful information for diagnostics and therapy of (cardio) vascular diseases. Blood viscosity, which arises from frictional interactions between all major blood constituents, i.e. plasma, plasma proteins and red blood cells, constitutes blood inherent resistance to flow in the blood vessel. Generally, blood viscosity in large arteries is lower near the vessel wall due to the presence of plasma layer in this peripheral region than the viscosity in the central core region which depends on the hematocrit. In this dissertation, the flow of blood in a large artery is investigated theoretically using the fluid dynamics equations of continuity and momentum. Treating artery as a rigid channel with uniform width and blood as a variable viscosity incompressible Newtonian fluid, the basic flow structure and its stability to small disturbances are examined. A fourth-order eigenvalue problem which reduces to the well known Orr–Sommerfeld equation in some limiting cases is obtained and solved numerically by a spectral collocation technique with expansions in Chebyshev polynomials implemented in MATLAB. Graphical results for the basic flow axial velocity, disturbance growth rate and marginal stability curve are presented and discussed. It is worth pointing out that, a decrease in plasma viscosity near the arterial wall has a stabilizing effect on the flow.

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