The mechanical properties of fresh and cryopreserved arterial homografts.
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OBJECTIVES: To assess the effect of cryopreservation on the elasticity and compliance of arterial allografts. MATERIALS AND METHODS: Iliofemoral segments of arteries and veins harvested from multiorgan donors were divided into two groups: fresh-control, tested for 24 hours after harvesting, and cryopreserved in liquid nitrogen after pretreatment with 20% dimethylsulphoxide and stored for an average time of 22 days. Vessel wall elastic properties were evaluated from the stress-strain relationship in a specially designed test cell fixed to the Instron Universal Testing Machine. RESULTS: The elastic modulus of the artery control group (1.54+/-0.33 MPa, n=20) was not significantly different from the cryopreserved group (1.69+/-0.61 MPa, n=15). Similarly, values for unfrozen veins (3.11+/-0.65 MPa, n=47) were not significantly different from those of frozen samples (2.71+/-0.85 MPa, n=38). Control compliance (6. 86+/-1.79x10(-5)%/Pa, for arteries; 3.84+/-0.81x10(-5)%/Pa, for veins) was similar to that of the cryopreserved group (6.66+/-1. 80x10(-5)%/Pa, for arteries; 4.16+/-1.21x10(-5)%/Pa, for veins). CONCLUSIONS: Cryopreservation maintains the important elastic properties of arterial and venous allografts during average storage time of 22 days. (+info)
Effects of temperature on the wall strength and compliance of frog mesenteric microvessels.
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In single perfused mesenteric microvessels of pithed frogs, we assessed wall strength from the critical pressure, PB, which has to be applied within the vessel in order to induce openings in the walls through which fluid and cells can extravasate. PB was determined in capillaries and venules of tissues at 12-20 The P(B) (mean +/- S.E.M.) in 22 vessels between 12 and 20 degrees C, P(B) was 92.0 +/- 7.40 cm H2O which was significantly higher than at room temperatures (P<0.001). The compliance of the vessel wall was estimated using both the red cell method and the oil meniscus technique. There was no measurable effect of temperature on wall compliance. The compliance of vessels from which the cells had been removed by previous perfusion with detergent solutions was very similar to that of intact vessels between 12 and 20 degrees C and between 0 and 5 degrees C. The negligible effects of temperature upon compliance suggest that microvessel walls have to be distended to a greater extent in cold tissue before P(B) is reached. This, together with their rapid closure, is consistent with the hypothesis that pressure-induced openings in microvascular walls are dependent on an active response of the endothelium rather than being the result of stress failure of the basement membrane. (+info)
Effects of microtubules and microfilaments on [Ca(2+)](i) and contractility in a reconstituted fibroblast fiber.
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We used a reconstituted fiber formed when 3T3 fibroblasts are grown in collagen to characterize nonmuscle contractility and Ca(2+) signaling. Calf serum (CS) and thrombin elicited reversible contractures repeatable for >8 h. CS elicited dose-dependent increases in isometric force; 30% produced the largest forces of 106 +/- 12 microN (n = 30), which is estimated to be 0.5 mN/mm(2) cell cross-sectional area. Half times for contraction and relaxation were 4.7 +/- 0.3 and 3.1 +/- 0.3 min at 37 degrees C. With imposition of constant shortening velocities, force declined with time, yielding time-dependent force-velocity relations. Forces at 5 s fit the hyperbolic Hill equation; maximum velocity (V(max)) was 0.035 +/- 0. 002 L(o)/s. Compliance averaged 0.0076 +/- 0.0006 L(o)/F(o). Disruption of microtubules with nocodazole in a CS-contracted fiber had no net effects on force, V(max), or stiffness; force increased in 8, but decreased in 13, fibers. Nocodazole did not affect baseline intracellular Ca(2+) concentration ([Ca(2+)](i)) but reduced ( approximately 30%) the [Ca(2+)](i) response to CS. The force after nocodazole treatment was the primary determinant of stiffness and V(max), suggesting that microtubules were not a major component of fiber internal mechanical resistance. Cytochalasin D had major inhibitory effects on all contractile parameters measured but little effect on [Ca(2+)](i). (+info)
In vitro system to study realistic pulsatile flow and stretch signaling in cultured vascular cells.
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We developed a novel real-time servo-controlled perfusion system that exposes endothelial cells grown in nondistensible or distensible tubes to realistic pulse pressures and phasic shears at physiological mean pressures. A rate-controlled flow pump and linear servo-motor are controlled by digital proportional-integral-derivative feedback that employs previously digitized aortic pressure waves as a command signal. The resulting pressure mirrors the recorded waveform and can be digitally modified to yield any desired mean and pulse pressure amplitude, typically 0-150 mmHg at shears of 0.5-15 dyn/cm(2). The system accurately reproduces the desired arterial pressure waveform and cogenerates physiological flow and shears by the interaction of pressure with the tubing impedance. Rectangular glass capillary tubes [1-mm inside diameter (ID)] are used for real-time fluorescent imaging studies (i. e., pH(i), NO, Ca(2+)), whereas silicon distensible tubes (4-mm ID) are used for more chronic (i.e., 2-24 h) studies regarding signal transduction and gene expression. The latter have an elastic modulus of 12.4. 10(6) dyn/cm(2) similar to in vivo vessels of this size and are studied with the use of a benchtop system. The new approach provides the first in vitro application of realistic mechanical pulsatile forces on vascular cells and should facilitate studies of phasic shear and distension interaction and pulsatile signal transduction. (+info)
The PDE inhibitor zaprinast enhances NO-mediated protection against vascular leakage in reperfused lungs.
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Disruption of endothelial barrier properties with development of noncardiogenic pulmonary edema is a major threat in lung ischemia-reperfusion (I/R) injury that occurs under conditions of lung transplantation. Inhaled nitric oxide (NO) reduced vascular leakage in lung I/R models, but the efficacy of this agent may be limited. We coadministered NO and zaprinast, a cGMP-specific phosphodiesterase inhibitor, to further augment the NO-cGMP axis. Isolated, buffer-perfused rabbit lungs were exposed to 4.5 h of warm ischemia. Reperfusion provoked a transient elevation in pulmonary arterial pressure and a negligible rise in microvascular pressure followed by a massive increase in the capillary filtration coefficient and severe lung edema formation. Inhalation of 10 parts/million of NO or intravascular application of 100 microM zaprinast on reperfusion both reduced pressor response and moderately attenuated vascular leakage. Combined administration of both agents induced no additional vasodilation at constant microvascular pressures, but additively protected against capillary leakage paralleled by a severalfold increase in perfusate cGMP levels. In conclusion, combining low-dose NO inhalation and phosphodiesterase inhibition may be suitable for the maintenance of graft function in lung transplantation by amplifying the beneficial effect of the NO-cGMP axis and avoiding toxic effects of high NO doses. (+info)
Structure and mechanical properties of resistance arteries in hypertension: role of adhesion molecules and extracellular matrix determinants.
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Abnormalities of resistance arteries may play a role in the pathogenesis and pathophysiology of hypertension in experimental animals and humans. Vessels that, when relaxed, measure <400 microm in lumen diameter act as the major site of vascular resistance and include a network of small arteries (lumen approximately 100 to 400 microm) and arterioles (<100 microm). Because increased peripheral resistance is generated by a narrowed lumen diameter, significant effort has been focused on determining the mechanisms that reduce lumen size. Three important vascular components are clearly involved, including alterations of vascular structure, mechanics (stiffness), and function. Structural abnormalities comprise a reduced lumen diameter and thickening of the vascular media, resulting in an increased media-lumen ratio. Changes in the mechanical properties of an artery, particularly increased stiffness, may also result in a reduced lumen diameter. These vascular abnormalities may be caused or influenced by the expression and/or topographic localization of extracellular matrix components, such as collagen and elastin, and by changes in cell-extracellular fibrillar attachment sites, such as adhesion molecules like integrins. This article discusses the abnormalities of resistance arteries in hypertension and reviews the evidence suggesting an important role for adhesive and extracellular matrix determinants. (+info)
Methods for assessing hepatic distending pressure and changes in hepatic capacitance in pigs.
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The equilibrium pressure obtained during simultaneous occlusion of hepatic vascular inflow and outflow was taken as the reference estimate of hepatic vascular distending pressure (P(hd)). P(hd) at baseline was 1.1 +/- 0.2 (mean +/- SE) mmHg higher than hepatic vein pressure (P(hv)) and 0.7 +/- 0.3 mmHg lower than portal vein pressure (P(pv)). Norepinephrine (NE) infusion increased P(hd) by 1. 5 +/- 0.5 mmHg and P(pv) by 3.7 +/- 0.6 mmHg but did not significantly increase P(hv). Hepatic lobar vein pressure (P(hlv)) measured by a micromanometer tipped 2-Fr catheter closely resembled P(hd) both at baseline and during NE-infusion. Dynamic pressure-volume (PV) curves were constructed from continuous measurements of P(hv) and hepatic blood volume increases (estimated by sonomicrometry) during brief occlusions of hepatic vascular outflow and compared with static PV curves constructed from P(hd) determinations at five different hepatic volumes. Estimates of hepatic vascular compliance and changes in unstressed blood volume from the two methods were in close agreement with hepatic compliance averaging 32 +/- 2 ml. mmHg(-1). kg liver(-1). NE infusion reduced unstressed blood volume by 110 +/- 38 ml/kg liver but did not alter compliance. In conclusion, P(hlv) reflects hepatic distending pressure, and the construction of dynamic PV curves is a fast and valid method for assessing hepatic compliance and changes in unstressed blood volume. (+info)
Vascular compliance in normal pressure hydrocephalus.
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BACKGROUND AND PURPOSE: Normal pressure hydrocephalus (NPH) is considered to be a combination of altered CSF resorption and a reversible form of cerebral ischemia. The hypothesis tested in this study was that a reduction in venous compliance in the territory drained by the superior sagittal sinus (SSS) is associated with NPH and cerebral ischemia. METHODS: This prospective study involved 27 patients without evidence of hydrocephalus. This group was subdivided into those with normal MR findings and those with evidence of ischemia or atrophy. Ten patients with NPH then underwent MR flow quantification studies of the cerebral vessels. Five of these patients had the same studies performed after CSF drainage. Vascular compliance was measured in the SSS and straight sinus territory by use of MR flow quantification with net systolic pulse volume (NSPV) and arteriovenous delay (AVD) as markers. RESULTS: Vascular compliance of patients with ischemia or atrophy was significantly higher than that of healthy subjects (mean NSPV in the SSS, 417 microL and 274 microL, respectively). Patients with NPH showed lower compliance than that of the healthy subjects in the SSS (mean NSPV, 212 microL and 274 microL, respectively; mean AVD, 42 ms and 89 ms, respectively). After intervention, the NPH group showed compliance approximating the group with ischemia/atrophy. CONCLUSION: Vascular compliance is significantly different in the brains of healthy subjects as compared with that in patients with ischemia/atrophy or NPH. (+info)