Biomedical subjects

W L Henry

Publications and source records attributed to W L Henry.

At least 19 recordsLinked to original sources

PubMed2001

HIF-1 expression in healing wounds: HIF-1alpha induction in primary inflammatory cells by TNF-alpha.

The expression of the hypoxia-responsive transcription factor hypoxia-inducible factor (HIF)-1 during acute inflammation was investigated in experimental wounds. HIF-1alpha mRNA was maximally expressed in wound cells 6 h after injury. HIF-1alpha protein was detectable in wound cells 1 and 5 days after injury. Cells from 1-day-old wounds were not hypoxic, as determined by lack of pimonidazole hydrochloride adduct formation. Tumor necrosis factor (TNF)-alpha, but not interleukin-1beta, increased the HIF-1alpha protein content of cells isolated 1 and 5 days after injury, and also of glycogen-elicited peritoneal cells, but not HIF-1alpha mRNA. HIF-1alpha did not accumulate in TNF-alpha-treated HeLa, NIH/3T3, NR8383, or RAW 264.7 cells. Nitric oxide from S-nitrosoglutathione did not induce HIF-1alpha accumulation or modulate the response to TNF-alpha. TNF-alpha did not increase oxygen consumption or result in the production of reactive oxygen intermediates by day 1 wound cells. Vascular endothelial growth factor mRNA in wound cells peaked 24 h after wounding. HIF-1 expression in early wounds may contribute to the regulation of inducible nitric oxide synthase and vascular endothelial growth factor, two HIF-1-responsive genes intimately related to the process of repair.

Animals↗

PubMed1999

Molecular and metabolic evidence for the restricted expression of inducible nitric oxide synthase in healing wounds.

Tissue injury initiates a temporally ordered sequence of local cellular and metabolic responses presumably necessary for successful repair. Previous investigations demonstrated that metabolic evidence for nitric oxide synthase (NOS) activity is detectable in wounds only during the initial 48 to 72 hours of the repair process. Present results identify the cell types contributing inducible NOS (iNOS) to experimental wounds in rats. iNOS antigen was expressed in most macrophages present in wounds 6 to 24 hours after injury, and these cells exhibited NAPDH diaphorase and NOS activity. Polymorphonuclear leukocytes contained little iNOS antigen and no NADPH diaphorase activity and were minimally able to convert L-arginine to L-citrulline. The frequency of iNOS-positive macrophages declined on days 3 and 5 after wounding. By day 10, most macrophages in the wound were negative for iNOS. These cells, however, acquired iNOS antigen and activity in culture. Wound fluids, but not normal rat serum, suppressed the induction of iNOS during culture. Findings indicate that the expression of iNOS in healing wounds is restricted to macrophages present during the early phases of repair and that components of wound fluid suppress the induction of iNOS in macrophages in late wounds. Polymorphonuclear leukocytes contribute little iNOS activity to the healing wound.

Animals↗

PubMed1999

Regulation of arginase isoforms I and II by IL-4 in cultured murine peritoneal macrophages.

Macrophages can express two arginase isoforms with distinct subcellular localization (cytosolic AI and mitochondrial AII). These isoforms are products of different genes and are capable of differential induction. Experiments were performed to identify the specific arginase isoforms induced by interleukin (IL)-4, a Th2 cytokine shown by others to increase arginase activity in macrophages, and serum. Results indicate IL-4, in concert with serum, increases AI, but not AII, mRNA in cultured murine macrophages. Moreover, they show serum to induce both arginase isoforms and to be required for maximal AI induction by IL-4. Together with the enhanced expression of AI, IL-4 induced the expression of the cationic amino acid transporter MCAT-2 and increased L-arginine transport into the cells. Present results confirm, then, specificity in the ability of macrophage arginase isoforms to be induced by different stimuli. Moreover, they suggest that a decrease in intracellular L-arginine concentration resulting from its consumption by arginase may be repaired by concurrent increases in L-arginine influx into the cell.

Amino Acid Transport Systems, Basic↗

PubMed1999

Vestigial respiratory burst activity in wound macrophages.

Macrophages from experimental wounds in rats were tested for their capacity to generate reactive oxygen intermediates. Measurements of superoxide and H2O2 release, O-2-dependent lucigenin chemiluminescence, oxygen consumption, hexose monophosphate shunt flux, and NADPH oxidase activity in cell lysates indicated, at best, the presence of a vestigial respiratory burst response in these cells. The inability of wound cells to release O-2 was not rekindled by priming with endotoxin or interferon-gamma in vivo or in vitro. NADPH oxidase activity in a cell-free system demonstrated that wound macrophage membranes, but not their cytosols, were capable of sustaining maximal rates of O-2 production when mixed with their corresponding counterparts from human neutrophils. Immune detection experiments showed wound macrophages to be particularly deficient in the cytosolic component of the NADPH oxidase p47-phox. Addition of recombinant p47-phox to the human neutrophil-cell membrane/wound macrophage cytosol cell-free oxidase assay, however, failed to support O-2 production. Present findings indicate an unexpected deficit of wound macrophages in their capacity to generate reactive oxygen intermediates.

Animals↗

PubMed1998

Distinct arginase isoforms expressed in primary and transformed macrophages: regulation by oxygen tension.

Experiments were performed to identify arginase isoforms expressed in primary and transformed rodent macrophages and to determine the molecular mechanisms for the previously observed increase in arginase activity in macrophages cultured in hypoxia or anoxia. Results demonstrate the following: 1) mRNA and protein for hepatic-type AI arginase are expressed in primary cultures of rat and mouse peritoneal macrophages and are enhanced seven- and nine-fold, respectively, by lipopolysaccharide (LPS). 2) mRNA for extrahepatic-type AII arginase is constitutively expressed in mouse, but not rat, peritoneal macrophages and is detected in RAW264.7 cells after LPS treatment; neither J774A.1 nor P388D1 cells contain arginase mRNA. 3) AI arginase mRNA, arginase activity in cell lysates, and L-arginine flux through arginase in intact cells are all increased in rat wound-derived and mouse peritoneal macrophages by hypoxic or anoxic culture; AII arginase mRNA is, in contrast, suppressed > 50% by O2 deprivation. 4) Expression of the L-arginine transporter mCAT-2 is increased greater than twofold by reduced O2 culture. These results demonstrate substantial variability in arginase isoform expression among primary and transformed rodent macrophages. They also identify AI and AII arginase and the mCAT-2 L-arginine transporter as O2-regulated genes.

Amino Acid Transport Systems, Basic↗

PubMed1996

B cell lymphoma-2 transfected P815 cells resist reactive nitrogen intermediate-mediated macrophage-dependent cytotoxicity.

Activated murine peritoneal macrophage cytotoxicity against P815 tumor cells has been shown to be mediated by the reactive nitrogen intermediates (RNI) produced by macrophages from L-arginine through nitric oxide (NO) synthase. Previous results from this laboratory indicated that NO-dependent killing of P815 fulfilled the criteria for apoptotic death. Work by others, in turn, demonstrated that the product of the bcl-2 gene confers protection against various inducers of apoptosis, including reactive oxygen intermediates. Experiments were performed to determine whether Bcl-2 could equally protect sensitive cells from RNI-dependent apoptosis within the context of a relevant biologic system such as the delivery of such RNI by activated macrophages. Results demonstrated that transfection of P815 cells with the human bcl-2 gene confers immunity from RNI-dependent, macrophage-mediated cytotoxicity. In contrast with wild-type or mock-transfected P815 cells, which do not contain detectable Bcl-2, bcl-2-transfected cells showed minimal DNA fragmentation and cell membrane failure when cocultured with activated macrophages. Additional findings indicate that Bcl-2 affords the transfected cells almost complete resistance to the DNA-fragmenting effects of chemically generated NO or H202 and partial protection from their cytolytic effects. These findings are consistent with the hypothesis that tumor cells expressing bcl-2 may escape destruction by macrophage-dependent immune surveillance mechanisms.

Animals↗

PubMed1995

Macrophage activation by culture in an anoxic environment.

The extracellular amino acid composition of experimental wounds in rats during peak macrophage infiltration bears the imprint of the elevated arginase activity present in wound fluid: L-arginine is found in this space in concentrations markedly lower, and L-ornithine in concentrations markedly higher, than those that are detectable in plasma. No evidence, in the form of L-citrulline or NO2- accumulation, can be found at this time for nitric oxide synthase (NOS) activity. Wound-derived macrophages, however, metabolize L-arginine through both arginase and NOS in culture. Given the requirements of NOS for O2 and the reduced O2 tension in wounds, experiments were performed to determine the role of O2 availability on the metabolism of L-arginine by wound-derived macrophages. Results demonstrated that, beyond inhibiting NOS, culture of wound-derived macrophages in an anoxic environment provided an activation signal, markedly increasing total L-arginine metabolism, arginase activity, NOS protein content, and the release of TNF-alpha and IL-6. Neither resident nor Corynebacterium parvum-elicited peritoneal macrophages responded to anoxic culture with increases in L-arginine utilization, arginase activity or, in the case of resident macrophages, in NOS protein content. The enhanced TNF-alpha and IL-6 release induced by anoxia in wound-derived macrophages was also found in resident peritoneal macrophages. Anoxia appears to act, then, as an inducer of activation-associated traits in macrophages obtained from different sites.

Animals↗

PubMed1993

Calculation of volume flow rate by the proximal isovelocity surface area method: simplified approach using color Doppler zero baseline shift.

OBJECTIVES: The goal of this study was to develop an accurate, simplified proximal isovelocity surface area (PISA) method for calculating volume flow rate using lower blue-red interface velocity produced by a color Doppler zero baseline shift technique. BACKGROUND: The Doppler color proximal isovelocity surface area method has been shown to be accurate for calculating the volume flow rate (Q) across a narrowed orifice by the formula Q = PISA x Blue-red interface velocity. A hemispheric model is generally used to calculate proximal isovelocity surface area (PISA = 2 pi a2, where a = the radius corresponding to the blue-red interface velocity). Although a hemispheric model is simple, requiring measurement of one radius, it may underestimate the actual volume flow rate because, in the general case, the shape of a proximal isovelocity surface area is hemielliptic. Although a hemielliptic model is generally more accurate for calculating proximal isovelocity surface area, it is more complex, requiring measurement of two orthogonal radii. METHODS: Sixteen in vitro constant flow model studies were performed using planar circular orifices (diameter range 6 to 16 mm). The blue-red interface velocity was changed from 3 to 54 cm/s using color Doppler zero baseline shift. RESULTS: 1) With decreasing blue-red interface velocity, the size of the proximal isovelocity surface area was increased, and its shape changed from hemielliptic to hemispheric. 2) With the blue-red interface velocity in the range 11 to 15 cm/s, the proximal isovelocity surface area became nearly hemispheric; however, it was difficult to determine the blue-red interface radius at a blue-red interface velocity < 10 cm/s because of interface fluctuations. 3) Calculated volume flow rate using the hemispheric proximal isovelocity surface area model with a single radius was relatively accurate at a blue-red interface velocity of 11 to 15 cm/s (mean percent difference from actual volume flow rate was -3.6%). CONCLUSIONS: Because the shape of the proximal isovelocity surface area is nearly hemispheric at a blue-red interface velocity of 11 to 15 cm/s, volume flow rate can be accurately calculated in this proximal isovelocity surface area interface velocity range (produced by zero baseline shift) by measuring a single-interface radius. This approach should be clinically useful for calculating the volume flow rate across stenotic and regurgitant valves and across shunt defects.

Blood Flow Velocity↗

PubMed1993

Direct myocardial effects of cocaine.

OBJECTIVE: The aim was to determine whether cocaine has a direct effect on the myocardium which is independent of coronary vasospasm. METHODS: Cocaine was introduced into the perfusate of the isolated rabbit ventricular septal preparation in the concentration range 10(-5) to 10(-3)M while holding coronary flow of oxygenated Krebs solution constant at 3.0 ml.min-1 by a perfusion pump. The septa were obtained from white male New Zealand rabbits and were paced at 48 beats.min-1. Mechanical and enzymatic measurements were performed. RESULTS: Developed tension (T), maximum contraction velocity (+dT/dt), and maximum relaxation velocity (-dT/dt) were all depressed to approximately the same degree at each different cocaine concentration and averaged 4, 48, and 95% at 10(-5), 10(-4), and 10(-3)M cocaine respectively, with an ED50 = 9 x 10(-5)M. Relaxation time (tR/T) was prolonged, but the ED50 was greater (by 1.5 times) than for the other mechanical parameters. Simultaneously, an increase in excitation threshold dysrhythmia developed which resulted in 17, 50, and 90 beats missed per 100 stimulations at 10(-5), 10(-4), and 10(-3)M cocaine respectively. Resting tension (RT) was not altered. Coronary flow rate was not reduced in presence of cocaine because of the constant delivery pump. T, +dT/dt, -dT/dt and modulation of the excitation threshold completely recovered after washout of cocaine. CONCLUSIONS: Cocaine has acute direct, though reversible, depressant effects on the myocardium, including depression of function and modulation of excitation threshold, which are independent of its effect on coronary flow.

Animals↗

PubMed1991

Nitric oxide production is required for murine resident peritoneal macrophages to suppress mitogen-stimulated T cell proliferation. Role of IFN-gamma in the induction of the nitric oxide-synthesizing pathway.

Lymphocyte proliferation in Con A- or LPS-stimulated murine splenic cell (SC) cultures was suppressed by the addition of excess macrophages. In Con A-stimulated cultures, suppression was associated with the expression of nitric oxide-synthesizing pathway (NOSP) activity as demonstrated by the accumulation of nitrite, a degradation product of nitric oxide (NO), in the culture supernatants. That NO, a cytotoxic and anti-proliferative metabolite of l-arginine, or other reactive nitrogen intermediates generated through the NOSP mediated the suppressive effect was suggested by the reversal of suppression brought about by the addition of a specific inhibitor of the NOSP (NG-monomethyl-l-arginine acetate) to the culture media. No NOSP activity was detectable in LPS-stimulated SC/macrophage cocultures. The role of T cell-derived IFN-gamma in the induction of the NOSP was investigated by the use of anti-IFN-gamma-mAb. Antibody-treated Con A supernatants failed to induce the NOSP in macrophages, and the addition of the mAb to Con A-stimulated SC/macrophage cocultures obviated the suppressive effects. Indomethacin and catalase only partially restored proliferation in Con A-stimulated SC/macrophage cocultures but were remarkably efficient in preventing macrophage-dependent suppression when LPS was used as the mitogenic stimulus. These results demonstrate a regulatory system of potential relevance in sites of predominant macrophage infiltration by which T cell-derived IFN-gamma activates the production of the mediator, NO, that suppresses T cell proliferation. In addition, these data demonstrate that, although the suppressive effects of excess macrophages appear to be expressed nonspecifically toward both T and B cells, suppression is mediated through a different mechanism in each case.

Animals↗

PubMed1991

Suppression of lymphocyte proliferation through the nitric oxide synthesizing pathway.

The amino acid L-arginine can be metabolized through a nitric oxide-synthesizing pathway (NOSP) to produce L-citrulline and reactive nitrogen intermediates. Among these nitrogen intermediates, NO has been implicated as the mediator of a variety of biological effects including vasodilatation, inhibition of platelet aggregation, tumor cytotoxicity and microbiostasis by activated macrophages and generalized suppression of macrophage functions. Work reported here demonstrated that the NOSP is expressed in Con A-stimulated rat splenic cell (SC) cultures and is associated with a profound suppression of lymphocyte proliferation. Inhibition of the NOSP by NG-monomethyl-L-arginine (N-MMA) or binding of its products by hemoglobin, either free in solution or contained in RBC, markedly promotes rat SC mitogenic response to Con A. Mouse SC do not express the NOSP under the conditions used in these experiments. Consequently, their mitogenic response to Con A is not affected by N-MMA or hemoglobin. These data confirm and expand the apparent role of NO as a regulator of immune responses while indicating potentially important species differences.

Animals↗

PubMed1991

Doppler color flow "proximal isovelocity surface area" method for estimating volume flow rate: effects of orifice shape and machine factors.

Previously described Doppler color flow mapping methods for estimating the severity of valvular regurgitation have focused on the distal jet. In this study, a newer Doppler color flow technique, focusing on the flow proximal to an orifice, was used. This method identifies a proximal isovelocity surface area (PISA) by displaying an aliasing interface. Volume flow rate (cm3/s) can be calculated as PISA (cm2) x aliasing velocity (cm/s). For planar circular orifices, a hemi-elliptic model accurately approximated the shape of PISA. Clinically, however, orifice shapes may be noncircular. In vitro flow experiments (n = 226) using orifices of various shapes (ellipse, square, triangle, star, rectangle) were performed. Volume flow rate calculated using a hemi-elliptic model for PISA was accurate, with average percent differences from actual flow rate = +4.3% for a square, -4.2% for a triangle, -4.7% for a star, -4.5% for an ellipse and -2.8% for a rectangle. However, average percent differences for calculated volume flow rates using a hemispheric model for PISA shape ranged from -11.6% (square) to -34.8% (rectangle). In addition, to evaluate whether PISA is influenced by machine factors, in vitro studies (n = 83) were performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗

PubMed1991

A comparison of excimer laser, thermal probe, and mechanical devices for recanalizing occluded human arteries.

To evaluate the mechanism of excimer laser recanalization and compare the results with those of laser-assisted thermal probe recanalization and mechanical recanalization, a total of 42 human atherosclerotic totally occluded arterial segments (2-15 cm long) were recanalized by excimer laser with a 400-800 micron quartz fiber pulsed at 20 Hz with 50 mJ/mm2 of energy (n = 21), an Argon heated thermal probe at 10-12 watts (n = 11), a guidewire directed through a 6 Fr multipurpose catheter, or an angioplasty balloon catheter (n = 10). On histologic examination, the excimer laster created a single round lumen or multiple lumens ("Swiss-cheese" like appearance) with no evidence of thermal injury at the perimeter of the lumen. The incidence of perforation in vitro was less with an excimer laser catherter (8/21 or 38%) than with the thermal prove (10/11 or 91%) (p less than 0.01). However, serial histologic cross-sectional examination showed that the pathway of the devices were essentially the same in all recanalization procedures. The pathway of the device was located outside the atheroma but proximal to the internal elastic membrane in 13 arteries with the excimer laser (62%), in 10 arteries with the thermal probe (91%), and 8 arteries with mechanical devices (80%). These results indicate that although the eximer laser could recanalize human atherosclerotic arteries without thermal injury, the fiber frequently deflected around firm atherosclerotic plaque and advanced in a dissection plane between the plaque and media. A similar course was noted for the thermal probe or during mechanical recanalization with a guidewire and catheter. To insure the safety of an excimer fiber or a thermal probe to reopen complete occlusions, better guidance systems must be developed.

Arteries↗

PubMed1991

Effects of heart rate and pulmonary artery pressure on Doppler pulmonary artery acceleration time in experimental acute pulmonary hypertension.

Chronic pulmonary hypertension in humans is characterized by shortening of the pulmonary artery acceleration time as measured by Doppler echocardiography, such that the higher the pulmonary artery pressure, the shorter the pulmonary acceleration time. Increases in heart rate are also known to produce decreases in the pulmonary artery acceleration time. To explore the relationship between mean pulmonary artery pressure, heart rate, and Doppler pulmonary artery acceleration time, experimental acute pulmonary hypertension was created in nine Duroc swine, either by infusion of Sephadex beads with embolization of the pulmonary arterial circulation or by partially occluding the main pulmonary artery 8 to 10 cm distal to the pulmonic valve. Pulmonary artery Doppler flow velocity recordings and invasive pressure measurements were made at baseline and at paced atrial rates ranging from 60 to 160 beats per minute, in 20-beat increments. The results in this acute animal model reveal that increases in heart rate produced significant decreases in Doppler pulmonary artery acceleration time at mean pressures below 25 mm Hg. However, with mean pulmonary artery pressures greater than 25 mm Hg, both heart rate and increases in pulmonary artery pressure had no significant effect on acceleration time.

Acute Disease↗

PubMed1991

Bovine coronary artery endothelium: culture, characterization, angiogenesis and sensitivity to laser photodynamic treatment modalities.

Culture, characterization and sensitivity to laser and photosensitizers of bovine coronary artery endothelium is presented. Endothelial cells from bovine coronary artery specimens obtained after sacrifice were successfully cultured. Endothelial cells were obtained from the anterior descending coronary artery. Cells were grown in RPMI-1640 with 20% fetal bovine serum. Preconditioned medium was required to enhance the efficiency of the initial inoculum. The resulting cultures could be passed for up to 15 times and maintained a stable, normal karyotype throughout this period. The culture reached a stable confluency packing density by two to three weeks (5 x 10(5) to 10(6) cells/cm2). When cultures were maintained at the confluency packing density for three to four weeks, the cells had the unique tendency to assume capillary-like networks of cell cords around which neighboring cells showed polar orientation and migration towards the apparent tube-like structures without the need for added extracellular matrix. All cultured cells were stained positive with mouse anti-human factor VIII monoclonal antibody tagged with either Texas red-streptavidin or fluorescein isothiocyanate (FITC). All cultures were negative for staining with mouse monoclonal antibody to alpha actin tagged with FITC, suggesting absence of smooth muscle cells or fibroblasts. Cells were negligibly sensitive to argon laser irradiation at wave lengths 620 nm at 37 J/cm2. Cultured cells showed dose dependent sensitivity to both unactivated HPD and phycocyanin with minimal cytotoxicity (less than 20%) at concentrations below 0.5 and 50 micrograms/ml, respectively. Laser activation of the photosensitizers at these concentrations resulted in similar but significant cell death, 40% and 41% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Modulation of serotonin-induced vasospasm by endothelium and monoamine oxidase.

Endothelial modulation of flow induced by intraluminal serotonin (5-HT) in isolated and perfused bovine coronary artery segments was studied. A constant-pressure continuous perfusion apparatus was utilized. Control coronary arteries were perfused with a fixed volume of serotonin-containing solution followed by a serotonin-free solution, and flow-rate changes during onset and relaxation of vasospasm were measured. Both monoamine oxidase inhibition by iproniazide and endothelium disruption by collagenase increased the rate of onset and magnitude of vasospasm. When the endothelium was intact the vasospasm continued to increase, reaching maximum well after the end of the serotonin perfusion, followed by slow relaxation toward baseline. This contrasted with de-endothelialized vessels in which the increase in contractile response terminated abruptly at the end of the serotonin perfusion and returned rapidly to baseline. Coronary arteries stimulated with prostaglandin F2 alpha responded similarly to de-endothelialized vessels stimulated by 5-HT, although further de-endothelialization of F2 alpha-stimulated vessels showed increased rates of onset and relaxation of vasospasm, suggesting a physical barrier role for the endothelium towards unmetabolized agents. These observations are consistent with the hypothesis that endothelial cells are capable of taking up, storing and subsequently releasing serotonin. The results suggest a protective role of the endothelium as a metabolic and physical barrier. This may represent an anatomical substrate favouring the development of localized vasospasm at sites where the endothelium is injured.

Animals↗

PubMed1990

Temporal expression of different pathways of 1-arginine metabolism in healing wounds.

Arginine can be metabolized by inflammatory cells through at least two pathways. One is an oxidative l-arginine deiminase (OAD) that results in the formation of citrulline and reactive nitrogen intermediates. The other is arginase, which determines the production of ornithine and urea. The temporal expression of these pathways in an experimental wound model (s.c. implanted polyvinyl alcohol sponges in the rat) was investigated by examining the concentrations of amino acids and of nitrite in fluids obtained from the sponges 6 h to 15 day after implantation. These analyses revealed two distinct periods during which the arginine concentration in the fluids was markedly below plasma levels. During the early period (less than 3 days after sponge implantation) wound fluid contained more citrulline and nitrite than at any other time, suggesting OAD activity. In contrast, ornithine accumulated in the fluids during the late decrease in arginine concentration that extended beyond day 3, during which time the wound fluid also contained a high arginase activity. This time-dependent expression of different pathways of arginine metabolism in wounds was confirmed in sponge cultures containing [guanido-14C]-l-arginine. Cells contained in sponges harvested less than 48 h after implantation metabolized labeled arginine mainly to labeled citrulline, whereas labeled urea was produced during culture of sponges harvested after this time. The low arginine content of wound fluid did not appear to be rate limiting for the expression of OAD in late sponges because no OAD activity was evidenced when 4 mM arginine was added to the cultures. These results indicate that the OAD pathway is expressed in this model predominantly during the early, polymorphonuclear leukocyte-predominant, phase of repair. At this time, the reactive nitrogen intermediates resulting from the metabolism of arginine may mediate some of the events characteristic of early inflammation, including microbiostasis, vasodilation, and inhibition/reversal of platelet aggregation. In turn, the late suppression of this pathway and the catabolism of arginine through arginase may promote macrophage function within wounds.

Animals↗

PubMed1990

Effect of machine parameters on variance display in Doppler color flow mapping.

In color Doppler flow studies, "variance" is an important display modality for diagnosing stenotic, regurgitant, and shunt lesions. Variance, a mathematical calculation based on the variation in the Doppler signal frequencies, has been reported to reflect the degree of flow disturbance. A wide-band pulsed Doppler spectrum results in a larger degree of variance. It has been suggested that variance area (green color or mosaic area) might provide useful quantitative information regarding the severity of stenotic, regurgitant, and shunt lesions. Since ultrasound machine settings may affect the color Doppler variance image, we evaluated in 101 free jet experiments the effect of packet size (eight versus four samples per line), pulse repetition frequency (3.9 versus 5.2 kHz), frame rate (11 versus 22 frames per second), system gain (+15 dB versus -15 dB), transmit power (high versus low), and moving target indicator (MTI) filter setting (high versus low) on variance display. The variance area was planimetered using an image analysis computer. The following machine parameters were inversely correlated with variance area: (1) packet size (p less than 0.01), (2) pulse repetition frequency (p less than 0.001), and (3) frame rate (p less than 0.05). Both system gain (p less than 0.001) and wall filter setting (p less than 0.01) showed a direct correlation with variance area. We conclude that machine factors must be standardized in evaluating stenotic, regurgitant, and shunt lesions by color Doppler variance display imaging.

Analysis of Variance↗