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B W Zweifach

Publications and source records attributed to B W Zweifach.

At least 73 records · Page 4Linked to original sources

Microvascular pressure distribution in skeletal muscle and the effect of vasodilation.

In cats anesthetized with pentobarbital, 188 direct microvascular pressure and diameter measurements were made of the tenuissimus muscle. The microvascular pressure in arterioles of 70 mum in diameter or larger was proportional to the systemic arterial pressure (PA). The arterioles with diameter-s ranging from 35 to 20 mum have been shown to be the principa-l source of arteriolar resistance regulating micropressures downstream. Across the capillary bed proper, the drop in pressures was about 15% of PA. Micropressures in the smallest venules (8-15 mum) averaged 24 mmHg and reflect closely capillary blood pressure. With a background of basic microvascular data, the vasodilatory mechanism of papaverine (P) and isoproterenol (IPR) in the skeletal muscle was analyzed. Administration of IPR decreases both arteriolar and venular pressure, while P infusion decreased the pressure in arterioles wider than 20 mum in diameter; however, in smaller arterioles there was a substantial elevation in micropressure. The data establish two basically different vasodilatory effects on the terminal vasculature: one with increased capillary pressure and fluid filtration (P), a second with a decrease in capillary pressure enhancing absorption (IPR).

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Micromanipulation of pressure in terminal lymphatics in the mesentery.

The terminal lymphatics are a network of highly previous vessels that are distributed in a loose association with the blood capillary bed, in particular along with the collecting venules. The base-line pressure in these lymphatics is close to atmospheric, but after they converge to form valved collecting channels PL is increased with a pressure differential of 1-2 cmH20 built up across each valve. This increment in lymphatic pressure is clearly related to the presence of one-way valves, the contractile activity of the collecting channels, and the comparative impermeability of these channels. The pressure differential required to draw fluid from the interstitium into the lymphatics would appear to reside in the vasomotor activity of the collecting channels, although the data do not rule out changes in Pt coincident with net capillary filtration or absorption.

Animals↗

Vascular endothelium-leukocyte interaction; sticking shear force in venules.

To determine the shear force acting on a white blood cell sticking to the endothelium of a blood vessel, the flow field about a single white blood cell in a venule was determined by hign-speed motion picture photomicrography. The force acting on the white blood cell was then calculated according to the principles of fluid mechanics. In this paper, the calculation was made using an experimentally determined dimensionless shear force coefficient obtained from a kinematically and dynamically similar model. The large physical model of the hemodynamic system could be easily instrumented, and the shear force acting on the model cell and the flow field around it were measured. The data were then used to calculate a shear force coefficient. On the basis of dynamic similarity, this shear force coefficient was applied to the white blood cell in the venule. The shear force coefficient was strongly influenced by the hematocrit, so in vivo hematocrits were measured from electron micrographs. It was found that in the venules of the rabbit omentum a white blood cell sticking to the endothelial wall was subjected to a shear force in the range of 4 times 10--5 dynes to 234 times 10--5 dynes; the exact value depended on the size and motion of the white blood cell, the size of the blood vessel, the velocity of the blood flow, and the local hematocrit, which varied between 20% and 40% in venules of about 40 mum in diameter. The contact area between the white blood cell and the endothelial cell was estimated, and the shear stress was found to range between 50 dynes/cm-2 and 1060 dynes/cm-2. The normal stress of interaction between the white blood cell and the endothelium had a maximum value that was of the same order of magnitude as the shear stress. The accumulated relative error of the experimental procedure was about 49%. The instantaneous shear force was a random function of time because of random fluctuations of the hematocrit.

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