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Biomedical subjects

B W Zweifach

Publications and source records attributed to B W Zweifach.

At least 19 recordsLinked to original sources
PubMed1991

Penetration of the systemic blood pressure into the microvasculature of rat skeletal muscle.

A series of arterial micropressure measurements in different skeletal muscles of the Wistar-Kyoto and spontaneously hypertensive rat is presented. The micropunctures were carried out with minimal surgical intervention through small skin incisions and the micropressures were recorded simultaneously with femoral artery pressures. The measurement sites were located at the entry points into the muscles for the proximal and distal supply arteries and at the midpoint of the arteriolar arcade bridge which directly connects these two supply arteries in the center of the muscle parenchyma. In contrast to feed artery pressure values from exteriorized muscles, which in the past have been reported to be as low as 40 mm Hg, the current mean pressure values are substantially higher and in the range between 70 and 100 mm Hg, equivalent to 70 to 90% of the mean systemic pressure. Systolic and diastolic values exhibit comparable trends to the mean pressures and they are similar in muscles at different locations in the body. Although in spontaneously hypertensive rats the absolute pressures were significantly higher compared with their controls, the normalized pressures were virtually identical at the locations used in this study. These data indicate that the absolute pressure in the central arteries of spontaneously hypertensive animals is reduced to a greater degree than in Wistar-Kyoto rats, while in both strains the major pressure reduction in skeletal muscle still occurs in the microcirculation.

Animals↗
PubMed1991

Leukocyte counts and activation in spontaneously hypertensive and normotensive rats.

The etiology for the progressive organ injury in hypertension is largely speculative. Recent studies have shown that leukocytes play a key role in several cardiovascular diseases. As an initial step toward investigating the role of leukocytes in hypertension, we measured leukocyte counts and spontaneous activation of granulocytes of freshly drawn unseparated blood samples in spontaneously hypertensive rats and in their normotensive counterpart, Wistar-Kyoto rats. The animals were derived from one breeder in the United States and from two breeders in Europe. Total leukocyte counts in young, mature, and old hypertensive rats were 50-100% above the controls. The number of granulocytes in mature and old spontaneously hypertensive rats in more than 100% elevated compared with control rats. In young hypertensive rats the mean granulocyte count was only slightly elevated. The number of spontaneously activated granulocytes, as detected by the nitroblue tetrazolium reduction, increases with age in both species; in mature spontaneously hypertensive rats, it is more than 300% above the values in the controls. Furthermore, in mature hypertensive rats the number of monocytes, activated monocytes, and the lymphocyte count are also significantly elevated over the values in the normotensive controls. It is proposed that these elevated leukocyte counts may constitute an enhanced risk for organ injury in the spontaneously hypertensive rat.

Animals↗
PubMed1991

Polymorphonuclear neutrophil contribution to induced tolerance to bacterial lipopolysaccharide.

The objective of this study was to investigate mechanisms by which polymorphonuclear neutrophils (PMNs) contribute to the tolerance induced by repeated lipopolysaccharide (LPS) injections. Tolerance was developed by daily intraperitoneal injections of sublethal doses of LPS for 4 days (LPS-tolerant group); controls were not pretreated (LPS-control group). Both groups were challenged with 9 mg/kg i.v. Escherichia coli LPS, a dose that resulted in 25% survival in LPS-control rats compared with 100% survival in LPS-tolerant rats. LPS injection caused an initial neutropenia in both groups. The neutropenia persisted throughout the experiment in LPS-control rats, whereas in LPS-tolerant rats the circulating PMN count increased dramatically; after 6 hours, the PMN count was 16-fold higher than that in LPS-control rats. Activation of circulating PMNs, PMN adhesion to nylon fibers, and tumor necrosis factor/cachectin activity were all increased in control rats given LPS. In contrast, LPS-tolerant rats had low activation of circulating PMNs, no trend for PMN adhesion to nylon fibers, and markedly reduced tumor necrosis factor activity. To determine whether neutropenia was associated with a trapping of PMNs in the microcirculation, we used a carbon perfusion technique 6 hours after LPS injection and examined histological sections of the myocardium. All of the arterioles and venules in both groups contained carbon; only capillaries showed evidence of obstruction. A significantly higher percentage of obstructed capillaries was observed in LPS-control rats than in LPS-tolerant rats. Obstruction of capillaries was consistently associated with trapped leukocytes. We conclude that PMN cytotoxicity induced by LPS involves microcirculatory entrapment and activation of PMNs. Repeated LPS pretreatment reduces dramatically circulating PMN activation and adhesion and is associated with an elevated circulating PMN count, a low degree of microvascular plugging, and survival after a normally lethal dose of LPS.

Animals↗
PubMed1990

Wall structure of arteries and arterioles feeding the spinotrapezius muscle of normotensive and spontaneously hypertensive rats.

Vessel wall structure in feed arteries and their hierarchical ramifications were investigated in a rat skeletal muscle. Emphasis was placed on the transition of wall structure elements from the axillary and thoracodorsal arteries to the feeder arteries and the arcade and transverse arterioles forming the microcirculation of the spinotrapezius muscle. Semi-thin sections, prepared for light microscopy, and ultra-thin sections for electron microscopy were used to compare mature (15-20 week old) normotensive and hypertensive animals. The results demonstrate a gradual transition of the elastica intima and the smooth muscle from the central arteries towards the arterioles, accompanied by an attenuation of the adventitia. The elastica intima in 60-40 microns arcade arterioles is reduced from a continuous sheet in the central arteries to single fibers oriented parallel to the vessel axis. The multiple layers of smooth muscle cells at the level of the feeder arteries are reduced in the majority of arcade arterioles and in transverse arterioles to a single smooth muscle coat. Comparisons of the smooth muscle mass per unit length of vessel at selected sites of normotensive and spontaneously hypertensive rats show evidence for some degree of wall hypertrophy in the axillary artery, but no evidence for wall hypertrophy in arterioles of the microcirculation. There is no evidence of a pressure-mediated structural medial wall hypertrophy along this peripheral vascular pathway.

Animals↗
PubMed1978

Endoneurial pressure in hexachlorophene neuropathy.

Increased endoneurial pressure of up to 17.0 cm H2O was recorded in the peripheral nerves of rats fed hexachlorophene in their laboratory diet. The pressure was measured using a micropressure transducer developed for recording pressure in the microcirculation. The results were correlated with morphologic findings. Teased nerve fibers and araldite-embedded specimens of hexachlorophene damaged sciatic nerve revealed the characteristic severe intramyelinic edema due to splits in the minor dense lines of compact myelin giving rise to wide interlamellar spaces as shown in previous studies. The endoneurial pressure of rats exposed to hexachlorophene for 11 days and subsequently fed a normal diet returned to normal (0.2-3.0 cm H2O) after 12 days, and morphologic examination showed few residual abnormalities. Prolonged exposure to hexachlorophene for up to 4 weeks caused widespread axonal degeneration in addition to intramyelinic edema. Animals treated with hexachlorophene for 21 days followed by a normal diet for 14 days showed degenerated axons, phagocytosis of myelin as well as interstitial edema and elevated endoneurial pressure. It is suggested that axonal degeneration in hexachlorophene neuropathy is caused by increased endoneurial pressure.

Animals↗
PubMed1978

The distribution of blood rheological parameters in the microvasculature of cat mesentery.

In vivo studies of the rheological behavior of blood in the microcirculation were conducted by direct in situ measurements in cat mesentery. Upstream to downstream pressure drops were measured in unbranched arterioles, capillaries, and venules, with diameters from 7 to 58 micrometer. Simultaneous measurements of red cell velocity and vessel geometry facilitated computation of bulk velocity, pressure gradient, apparent viscosity, wall shear stress, and resistance. Arteriovenous distributions of these parameters revealed the following. Maximum pressure gradient (0.015 cm H20/micrometer) occurs in the true capillaries (7 micrometer in diameter); intravascular wall shear stress averaged 47.1 dynes/cm2 in arterioles and 29.0 dynes/cm2 in venules. Extreme values as great as 200 dynes/cm2 were observed in a few shunting arterioles. Apparent viscosity averaged 3.59 cP in arterioles, 5.15 cP in venules, and 4.22 cP overall. Intravascular resistance per unit length of microvessel varied with luminal diameter as a power law function with exponents of -4.04 for arterioles, -3.94 for venules, and -3.99 for all vessels combined. This apparent maintenance of Poiseuille's law is attributed to the opposing processes of hematocrit reduction and decreasing shear rate as blood is dispersed in successive arteriolar segments, and the converse action of these processes in the venous confluences which lessen the extent of network variations in apparent viscosity. Reductions in bulk velocity from the normal flow state to below 0.5 mm/sec resulted in increases in apparent viscosity by a factor of 2 to 10, which are attributed primarily to obstruction of the lumen by leukocyte-endothelium adhesion.

Animals↗
PubMed1977

Contractile stimuli in collecting lymph vessels.

Contractility was investigated in collecting lymph vessels of rat and guinea pig mesentery. Lymphatic diameter and micropressure were simultaneously recorded under normal conditions and during micromanipulation of intralymphatic pressure. Spontaneous activity involved characteristic changes in intralymphatic pressure coincident with opening and closure of upstream and downstream valves. Contractions were irregular but still predictable by noting the trend of intraluminal pressure as it approached a threshold level. Mechanical obstruction upstream of lymph vessels reduced lymph pressure and contraction frequency. Microinjection or withdrawal of fluid caused contraction frequency. Microinjection or withdrawal of fluid caused contraction frequency to rise and fall, respectively. Contraction rate was not affected by the level of general anesthesia. Lymphatic wall tension, as calculated from pressure-radius variables, correlated well with contraction frequency, suggesting a myogenic origin for the contractile mechanism. However, lymphatic smooth muscle may be inherently unstable since some contractility persists despite an absence of pressure stimuli.

Animals↗
PubMed1977

A method for determining segmental resistances in the microcirculation from pressure-flow measurements.

On the basis of an electrical analog, open circuit impedance functions were used to analyze the microcirculation. No specific structure need be assumed except a two-port, two-terminal network in which the major artery and vein supplying the tissue represent the input port and the two ends of the microvessel under study are the output port. The open circuit measurements were made by occluding microvessels in the exteriorized omentum of anesthetized rabbits. The pressure upstream and downstream to the occlusion defines the source pressure of a Thévenin's equivalent circuit. The equivalent resistance value was calculated by plotting the flow through a given microvessel against the pressure developed during a gradual occlusion. The changes in pressure vs. the changes in flow during a progressive occlusion were found to be linearly related. The Thévenin's equivalent resistance was maximum downstream to an occluded artery and upstream to the occluded vein. Within the capillary network, source pressures consistently were within a narrow range. Topically applied norepinephrine resulted in marked changes in source resistance and no changes in source pressures. Threshold doses of norepinephrine given intravenously resulted in changes in source pressures, but minimal changes in source resistance, even though a substantial change in vascular resistance was indicated when calculated on the basis of arterial pressure minus micropressure divided by microvessel flow. The present method defines the functional characteristics of the distributing vessels in terms of two pressures and two equivalent resistances and is relatively easy to perform. The technique can be used to determine the vascular components involved in the response to particular stimuli.

Administration, Topical↗
PubMed1977

Quantitative studies of microcirculatory structure and function. III. Microvascular hemodynamics of cat mesentery and rabbit omentum.

We made simultaneous measurements of intravascular pressure and red blood cell velocity for vessels which make up the modular configuration of microvascular networks in mesentery and omentum. An analysis of these variables and the computed volumetric flow rates is presented for arterioles which had a maximum diameter of 56 micrometer through the "true capillaries" (typically 7 micrometer for mesentery and 8 micrometer for omentum) to 56-micrometer venules. The spatial variance of pressure and flow is related to topographical features of each network. Vascularization statistics for each network are presented and demonstrate a unique ratio of potential microvascular exchange area to module planar area, with values of 0.71 +/- 0.22 (SD) for omentum and 0.19 "/- 0.03 (SD) for mesentery. Analysis of the volumetric flow rate for each module demonstrates a linear relationship to the planar area of tissue serviced by each modular network. In situ perfusion rates of 1180 ml/min per 100 g and 105 ml/min per 100 g were determined for omentum and mesentery, respectively. The hemodynamic resistance of the omental and mesenteric circuitry was evaluated, and in the case of the omentum, found to be inversely proportional to the planar area of the module. The arterial to venous distribution of pressure and flow for the mosaic of contiguous modules in omentum and mesentery is described and related to the deployment of parallel and serial microvessels of each network.

Animals↗