Physiological Stress Levels Research Articles

Fatigue of bone and bones: an analysis based on stressed volume.

The measured fatigue strength of a material can be affected by specimen size:tests using a large stressed volume may show a low fatigue strength due to the increased probability of finding weak regions. A Weibull analysis revealed an important size effect in bone and predicted this effect with an accuracy of 12%. This approach also explained apparent inconsistencies in the published data and made it possible to separate and quantify the effects of frequency, loading mode, and material source. The effect of frequency is the same for human and bovine bone, and the differences between different types of loading (tension, compression, and bending) are small (maximum: 12%). By extrapolating to the volume of whole bones, it is concluded that large bones will have a fatigue strength much lower, by a factor of 2-3, than that measured by conventional tests. Failure within 10(5) cycles is expected to occur at cyclic stresses of 23-30 MPa in human long bones and of 32-43 MPa in bovine bones. Repair is therefore needed to prevent failure at physiological stress levels.

Effect of prolonged pulsatile shear stress in vitro on endothelial cell seeded PTFE and compliant polyurethane vascular grafts

Compliance mismatch between graft and native artery, and failure of the graft to develop an endothelial lining are the two main factors in graft failure. The objective of this study was to assess a new compliant graft for effective cell attachment and cell retention at physiological levels of pulsatile shear stress over a 6-hour period of physiological pulsatile flow. Laboratory haemodynamic study. Human umbilical vein endothelial cells labelled with 111In-oxine were seeded on compliant polyurethane (CPU) and polytetrafluoroethylene (PTFE) vascular grafts. These were then exposed to varying shear stresses of up to 13.8 +/- 0.6 dyn/cm2 using a pulsatile flow model. Dynamic scintigraphy images were acquired using a gamma camera linked to an on-line computer during 6 h of perfusion and data presented as mean +/- standard error of mean. Mean seeding efficiencies were significantly different at 4,316 +/- 505 and 825 +/- 504 CPM/cm2 on the CPU and PTFE grafts, respectively (p = 0.018). The flow experiment showed a higher percentage of cells retained on the CPU graft after exposure to shear stress caused by pulsatile flow compared to PTFE with respect to time. After 6 h pulsatile perfusion there was a significantly higher proportion of initial cells attached to CPU graft compared to PTFE graft (73 +/- 8% vs 42 +/- 8%, p = 0.018). The areas under the time activity curves over the 6-hour period were 280 +/- 26.4 for CPU and 176.0 +/- 30.0 for PTFE, confirming a significant greater total cell loss from PTFE compared with CPU grafts (51 +/- 7.0% vs 23 +/- 8.3%, p = 0.018, Wilcoxon matched-pairs signed-ranks test). This flow model provides an effective method of assessing cell retention on graft materials under physiological conditions over a 6-hour period; CPU combines both excellent compliance and endothelial cell attachment rates after 6 h exposure to shear stress.

Shear stress induces spatial reorganization of the endothelial cell cytoskeleton

The morphology of endothelial cells in vivo depends on the local hemodynamic forces. Cells are polygonal and randomly oriented in areas of low shear stress, but they are elongated and aligned in the direction of fluid flow in regions of high shear stress. Endothelial cells in vitro also have a polygonal shape, but the application of shear stress orients and elongates the cells in the direction of fluid flow. The corresponding spatial reorganization of the cytoskeleton in response to the applied hemodynamic forces is unknown. In this study, we determined the spatial reorganization of the cytoskeleton throughout the volume of cultured bovine aortic endothelial cells after the cells had been exposed to a physiological level of shear stress for 0, 1.5, 3, 6, 12, or 24 h. The response of the monolayer to shear stress was not monotonic; it had three distinct phases. The first phase occurred within 3 h. The cells elongated and had more stress fibers, thicker intercellular junctions, and more apical microfilaments. After 6 h of exposure, the monolayer entered the second phase, where the cells exhibited characteristics of motility. The cells lost their dense peripheral bands and had more of their microtubule organizing centers and nuclei located in the upstream region of the cell. The third phase began after 12 h of exposure and was characterized by elongated cells oriented in the direction of fluid flow. The stress fibers in these cells were thicker and longer, and the heights of the intercellular junctions and microfilaments were increased. These results suggest that endothelial cells initially respond to shear stress by enhancing their attachments to the substrate and neighboring cells. The cells then demonstrate characteristics of motility as they realign. The cells eventually thicken their intercellular junctions and increase the amount of apical microfilaments. The time course of rearrangement can be described as a constrained motility that produces a new cytoskeletal organization that alters how the forces produced by fluid flow act on the cell and how the forces are transmitted to the cell interior and substrate. Cell Motil. Cytoskeleton 40:317–330, 1998. © 1998 Wiley-Liss, Inc.

Shear stress induces spatial reorganization of the endothelial cell cytoskeleton.

The morphology of endothelial cells in vivo depends on the local hemodynamic forces. Cells are polygonal and randomly oriented in areas of low shear stress, but they are elongated and aligned in the direction of fluid flow in regions of high shear stress. Endothelial cells in vitro also have a polygonal shape, but the application of shear stress orients and elongates the cells in the direction of fluid flow. The corresponding spatial reorganization of the cytoskeleton in response to the applied hemodynamic forces is unknown. In this study, we determined the spatial reorganization of the cytoskeleton throughout the volume of cultured bovine aortic endothelial cells after the cells had been exposed to a physiological level of shear stress for 0, 1.5, 3, 6, 12, or 24 h. The response of the monolayer to shear stress was not monotonic; it had three distinct phases. The first phase occurred within 3 h. The cells elongated and had more stress fibers, thicker intercellular junctions, and more apical microfilaments. After 6 h of exposure, the monolayer entered the second phase, where the cells exhibited characteristics of motility. The cells lost their dense peripheral bands and had more of their microtubule organizing centers and nuclei located in the upstream region of the cell. The third phase began after 12 h of exposure and was characterized by elongated cells oriented in the direction of fluid flow. The stress fibers in these cells were thicker and longer, and the heights of the intercellular junctions and microfilaments were increased. These results suggest that endothelial cells initially respond to shear stress by enhancing their attachments to the substrate and neighboring cells. The cells then demonstrate characteristics of motility as they realign. The cells eventually thicken their intercellular junctions and increase the amount of apical microfilaments. The time course of rearrangement can be described as a constrained motility that produces a new cytoskeletal organization that alters how the forces produced by fluid flow act on the cell and how the forces are transmitted to the cell interior and substrate.

Suppression of apoptosis by nitric oxide via inhibition of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases.

Physiological levels of shear stress alter the genetic program of cultured endothelial cells and are associated with reduced cellular turnover rates and formation of atherosclerotic lesions in vivo. To test the hypothesis that shear stress (15 dynes/cm2) interferes with programmed cell death, apoptosis was induced in human umbilical venous cells (HUVEC) by tumor necrosis factor-alpha (TNF-alpha). Apoptosis was quantified by ELISA specific for histone-associated DNA-fragments and confirmed by demonstrating the specific pattern of internucleosomal DNA-fragmentation. TNF-alpha (300 U/ml) mediated increase of DNA-fragmentation was completely abrogated by shear stress (446 +/- 121% versus 57 +/- 11%, P <0.05). This anti-apoptotic activity of shear stress decreased after pharmacological inhibition of endogenous nitric oxide (NO)-synthase by NG-monomethyl-L-arginine and was completely reproduced by exogenous NO-donors. The activation of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like cysteine proteases was required to mediate TNF-alpha-induced apoptosis of HUVEC. Endothelial-derived nitric oxide (NO) as well as exogenous NO donors inhibited TNF-alpha-induced cysteine protease activation. Inhibition of CPP-32 enzyme activity was due to specific S-nitrosylation of Cys 163, a functionally essential amino acid conserved among ICE/CPP-32-like proteases. Thus, we propose that shear stress-mediated NO formation interferes with cell death signal transduction and may contribute to endothelial cell integrity by inhibition of apoptosis.

Shear stress inhibits apoptosis of human endothelial cells

Physiological levels of shear stress alter the genetic program of cultured endothelial cells and reduce endothelial cell turnover in vivo. To test the hypothesis that shear stress interferes with programmed cell death, apoptosis was induced in human umbilical venous endothelial cells by growth factor withdrawal or incubation with tumor necrosis factor α(TNFα) for 18 h. Apoptosis was quantified by ELISA specific for histone-associated DNA fragments and confirmed by demonstrating the specific pattern of internucleosomal DNA fragmentation detected by electrophoresis and immunohistochemical staining. The TNFα (300 U/ml)-mediated increase in DNA fragmentation was completely abrogated by shear stress. Furthermore, shear stress dose-dependently reduced DNA fragmentation induced by growth factor withdrawal with maximal effect at 45 dyn/cm 2. Inhibition of the CPP32-like proteases with Ac-DEVD-CHO (100 μM) revealed similar anti-apoptotic effects. In contrast, CPP32-independent induction of endothelial cell apoptosis by C 2-ceramide (50 μM) was not prevented by shear stress. Thus, we propose that shear stress interferes with common cell death signal transduction involving the CPP32-like protease family and may contribute to endothelial cell integrity by inhibition of apoptosis.

Relation of RNA/DNA ratios to growth for the scallop Euvola (Pecten) ziczac in suspended culture

We examined the relation of RNA/DNA ratios to growth for three size groups of the tropical scallop Euvola ziczac maintained in suspended culture at 8, 21 and 34 m in depth in the Golfo de Cariaco, Venezuel. Various growth parameters indicated that production decreased with depth. This was more likely due to a decrease in seston quality with depth than to temperatures or seston abundance (which were similar at the various depths studied). The RNA/DNA ratio was correlated with the G-index of muscle growth for juveniles (r2=0.55). A much weaker correlation was observed for the maturing scallops (r2=0.18), probably because of the interaction between reproductive and somatic growth. In fully mature scallops, somatic growth was negligible and the RNA/DNA ratios appeared to be inversely related to the level of physiological stress of the scallops. Whereas RNA/DNA ratios are difficult to interpret for maturing E. ziczac, because an increased ratio can be due to either increased gonadal or somatic growth, they are useful in predicting growth in juveniles and physiological stress in fully mature scallops.

Effects of a Single Bout of Ultraendurance Exercise on Lipid Levels and Susceptibility of Lipids to Peroxidation in Triathletes

To determine the effects of a single bout of ultraendurance exercise, as a model for physiologic stress, on lipid and lipoprotein levels, and oxidative susceptibility of lipids in highly trained athletes. Observational trial. Thirty-nine volunteer subjects (26 mean, 13 women; mean age, 38 +/- 10 years) who competed in and completed the 1994 Hawaii Ironman World Championship Triathlon consisting of a consecutive 3.9-km (2.4-mi) swim, 180.2-km (112-mi) bike ride, and a 42.2-km (26.2-mi) run. Subjects answered questionnaires and had blood samples obtained 2 days prior to and within 15 minutes of completion of the triathlon. Prerace vs postrace changes in lipid and lipoprotein levels, and susceptibility of lipids to peroxidation. The mean duration of exercise was 753 +/- 128 minutes. With exercise, plasma volume-corrected levels of triglycerides decreased 39% from 1.58 +/- 0.83 to 0.97 +/- 0.68 mmol/L (139.6 +/- 73.6 to 85.8 +/- 60.5 mg/dL) (P < .001). Levels of total cholesterol decreased 9% from 4.94 +/- 0.88 to 4.50 +/- 0.79 mmol/L (190.8 +/- 33.8 to 173.8 +/- 30.6 mg/dL) (P < .001), low-density lipoprotein cholesterol decreased 11% from 2.59 +/- 0.77 to 2.30 +/- 0.86 mmol/L (100.1 +/- 29.9 to 88.7 +/- 33.3 mg/dL) (P = .02), and apolipoprotein B decreased 10% from 0.91 +/- 0.20 to 0.82 +/- 0.18 g/L (90.7 +/- 20.0 to 82.0 +/- 17.9 mg/dL) (P < .001). High-density lipoprotein cholesterol and apolipoprotein A-I increased with exercise but not significantly. The susceptibility of lipids to peroxidation decreased significantly (4.51 +/- 1.91 micromol/L, preexercise, vs 2.42 +/- 2.27 micromol/L, postexercise, P < .001), an effect that was not related to antioxidant use or levels of vitamins A, C, or E. Serum iron, a potential pro-oxidant, also decreased by 45% with exercise from 15.75 +/- 5.55 to 8.59 +/- 4.30 micromol/L (88 +/- 31 to 48 +/- 24 micrograms/dL) (P < .001), an effect that was weakly correlated with changes in lipid peroxidation (P = .05). These data suggest that a single bout of prolonged exercise can reduce lipid and lipoprotein risk factors for developing cardiovascular disease. Moreover, susceptibility of lipids to peroxidation is reduced by exercise, thereby adding to the benefits of physical activity. This effect appears to be independent of antioxidant supplement use and may be mediated by induction of endogenous antioxidants. These observations may explain in part the reduced risk of developing vascular and other diseases in individuals who are physically active.

Effects of food level and straw provision during pregnancy on sow performance and responses to an adrenocorticotrophic hormone challenge

In commercial practice, almost all pregnant sows are fed on restricted feeding regimes. Operant conditioning studies suggest that this results in the animals being food motivated for most of the day (Lawrence et at., 1988), a behavioural state which, in relatively barren environments, has been associated with the development of abnormal stereotypic behaviour (Spoolder et al., 1995). Straw provision reduces the development of stereotypies, possibly reflecting reduced (physiological) stress levels. In addition, it may result in lower nutritional requirements (Simmins et al., 1994).

Effects of food level and straw provision during pregnancy on sow performance and responses to an adrenocorticotrophic hormone challenge

In commercial practice, almost all pregnant sows are fed on restricted feeding regimes. Operant conditioning studies suggest that this results in the animals being food motivated for most of the day (Lawrence et at., 1988), a behavioural state which, in relatively barren environments, has been associated with the development of abnormal stereotypic behaviour (Spoolder et al., 1995). Straw provision reduces the development of stereotypies, possibly reflecting reduced (physiological) stress levels. In addition, it may result in lower nutritional requirements (Simmins et al., 1994).

Synergistic effects of fluid shear stress and cyclic circumferential stretch on vascular endothelial cell morphology and cytoskeleton.

The development of atherosclerosis is thought to be initiated by a dysfunctional state of the vascular endothelium. The proposal that mechanical forces play a role in the localization of this disease has led researchers to develop in vitro models to assess their effects on cultured endothelial cells. The arterial endothelium is exposed simultaneously to circumferential hoop stretch and wall shear stress, yet previous investigations have focused on the isolated effects of either cyclic stretch or shear stress. The influence of physiological levels of combined shear stress and hoop stretch on the morphology and F-actin organization of bovine aortic endothelial cells was investigated. Cells subjected for 24 hours to shear stresses higher than 2 dyne/cm2 or to hoop stretch greater than 2% elongated significantly compared with unstressed controls and oriented along the direction of flow and perpendicular to the direction of stretch. Exposure to more than 4% stretch significantly enhanced the responses to shear stress. Both shear stress and hoop stretch induced formation of stress fibers that were aligned with the cells' long axes. Simultaneous exposure to both stimuli appeared to enhance stress fiber size and alignment. These results indicate that shear stress and hoop stretch synergistically induce morphological changes in endothelial cells, which suggests that circumferential strain might modulate sensitivity of endothelial cells towards shear stress.

Biaxial mechanics of excised canine pulmonary arteries

A new method has been developed for measuring the stress-strain relationship in excised canine pulmonary arteries. Segments of dog main right pulmonary arteries were isolated by making two transverse cuts at each end of a segment near the bifurcations, yielding short cylinders, which were then cut radially, relieving the residual stress, causing the cylindrical shells to spring open to approximately flat rectangular slabs with dimensions approximately 1.0 x 3.0 x 0.1 cm. The specimens were then tested using a biaxial tensile testing machine. The resulting data show an approximately linear relationship between Kirchhoff stress and Lagrangian strain with very little hysteresis. The following pseudostrain energy function serves as a practical approximation for pulmonary arteries subjected to physiological levels of stress and strain: rho 0W(2) = 1/2(a1E2xx + a2E2yy + 2 a4ExxEyy), where rho 0 is the density of the wall (mass per unit volume), W is the energy per unit mass [superscript "(2)" indicates this is a 2-dimensional strain energy function], E is strain, a1, a2, and a4 are material constants with units of stress, and the subscripts x and y refer to the circumferential and axial axes, respectively, of the artery. To assess the physiological level of strain in the main right pulmonary artery, vessels were perfused in situ at physiological pressure (26 cmH2O) with silicone elastomer. The arteries were then excised and marked with small ink spots. Photographs of the spots on four tangent planes of the excised artery indicate a maximum circumferential strain of 21.5% and a maximum axial strain of 36.5% relative to the zero-stress state. These values are within the range of strain used in the biaxial tests. The relationship between Kirchhoff stress and Green's strain is approximately linear within the physiological range. The stress levels required to cause tissue failure are at least 10 times greater than the estimated normal physiological level.

Scientific basis and therapeutic regimens for use of antenatal glucocorticoids

The scientific basis for use of prenatal steroid therapy in preparing the human fetus for premature delivery is extensive and convincing. Studies in numerous animal species have documented precocious maturation of lung and other tissues after administration of glucocorticoids to the fetus, and ablation experiments indicate delayed organ maturation with a deficiency of endogenous corticosteroid. The timing of lung differentiation correlates well with the developmental increase in circulating corticosteroid, supporting the concepts that endogenous corticosteroids, interacting with other hormones, are important physiologic modulators of tissue maturation and that prenatal steroid therapy mimics the effect of endogenous glucocorticoids. In fetal lung the response to glucocorticoid involves induction of a limited number of proteins, including all the components of surfactant, as well as key lipogenic enzymes. These effects are mediated by glucocorticoid receptors, occur with physiologic concentrations of hormone, are primarily exerted at the level of gene activation, and are reversible on removal of hormone from cultured tissue. These various observations predict that a relatively brief exposure of the human fetus to glucocorticoid accelerates the normal developmental process in lung and other tissues and reduces disease resulting from developmental immaturity. Prenatal treatment with either betamethasone or dexamethasone at the recommended doses provides similar physiologic stress levels of glucocorticoid activity in fetal plasma sufficient to provide a near-maximal occupancy of receptors and induction of target proteins. Elevated glucocorticoid levels are maintained during the course of treatment and values return to normal by 2 days after the last dose. Treatment causes a transient suppression of maternal and fetal adrenal function; however, treated infants respond to newborn stress with a near-normal cortisol surge. However, there is little information, and reason for concern, regarding the safety of higher or repeated dose of prenatal steroid, and accordingly, routine retreatment of women who are not in active labor is not advised. The recommendation of the consensus panel that corticosteroid therapy is indicated for women at risk of premature delivery with few exceptions is thus well supported by evidence relating to glucocorticoid effects, mechanisms, and pharmacokinetics.

Methods and applications of stress research

The major health problems in the industrialized countries have a multifactorial etiology, where stress and other psychosocial factors seem to play an important role. Mental stress is not only induced by high demands, but also by demands that are too low, which happens in many repetitive and monotonous work situations and, e.g., in response to unemployment. For a long time, musculoskeletal disorders were mainly considered to be caused by physical conditions. However, accumulating evidence from several sources now indicate that psychosocial factors are also significantly associated with, e.g., back pain and shoulder problems. Studies of assembly line workers with a high incidence of back pain complaints indicate that the physical load on the spine at work is low, whereas psychophysiological stress levels are high and work satisfaction is low. Female assembly workers were found to have higher physiological arousal than men in traditional assembly line work, whereas their stress levels were lower in a more flexible and autonomous work organisation. In a recent laboratory experiment, both mental and physical stress was found to increase physiological stress levels and muscular tension. It was concluded, that data consistently support the assumption that mental stress is of importance for the development of musculoskeletal symptoms.

A scaling law for wall shear rate through an arterial stenosis.

Atherosclerosis of the human arterial system produces major clinical symptoms when the plaque advances to create a high-grade stenosis. The hemodynamic shear rates produced in high-grade stenoses are important in the understanding of atheromatous plaque rupture and thrombosis. This study was designed to quantify the physiologic stress levels experienced by endothelial cells and platelets in the region of vascular stenoses. The steady hemodynamic flow field was solved for stenoses with percent area reductions of 50, 75, and 90 percent over a range of physiologic Reynolds numbers (100-400). The maximum wall shear rate in the throat region can be shown to vary by the square root of the Reynolds number. The shear rate results can be generalized to apply to a range of stenosis lengths and flow rates. Using dimensions typical for a human carotid or coronary artery, wall shear rates were found to vary from a maximum of 20,000 s-1 upstream of the throat to a minimum of -630 s-1 in the recirculation zone for a 90 percent stenosis. An example is given which illustrates how these values can be used to understand the relationship between hemodynamic shear and platelet deposition.

Role of calcium and calmodulin in flow-induced nitric oxide production in endothelial cells

These experiments demonstrate that exposure of cultured endothelial cells (EC) to well-defined laminar fluid flow results in an elevated rate of NO production. NO production was monitored by release of NOx (NO2- + NO3(2-) and by cellular guanosine 3',5'-cyclic monophosphate (cGMP) concentration. NO synthase (NOS) inhibitor blocked the flow-mediated stimulation of both NOx and cGMP, indicating that both measurements reflect NO production. Exposure to laminar flow increased NO release in a biphasic manner, with an initial rapid production consequent to the onset of flow followed by a less rapid, sustained production. A similar rapid increase in NO production resulted from an increase in flow above a preexisting level. The rapid initial production of NO was not dependent on shear stress within a physiological range (6-25 dyn/cm2) but may be dependent on the rate of change in shear stress. The sustained release of NO was dependent on physiological levels of shear stress. The calcium (Ca2+) or calmodulin (CaM) dependence of the initial and sustained production of NO was compared with bradykinin (BK)-mediated NO production. Both BK and the initial production were inhibited by Ca2+ and CaM antagonists. In contrast, the sustained shear stress-mediated NO production was not affected, despite the continued functional presence of the antagonists. Dexamethasone had no effect on either the initial or the sustained shear stress-mediated NO production. An inducible NOS does not, therefore, explain the apparent Ca2+/CaM independence of the sustained shear stress-mediated NO production.(ABSTRACT TRUNCATED AT 250 WORDS)

Platelet-derived growth factor B chain promoter contains a cis-acting fluid shear-stress-responsive element.

The endothelial lining of blood vessels is constantly exposed to fluid mechanical forces generated by flowing blood. In vitro application of fluid shear stresses to cultured endothelial cells influences the expression of multiple genes, as reflected by changes in their steady-state mRNA levels. We have utilized the B chain of platelet-derived growth factor (PDGF-B) as a model to investigate the mechanisms of shear-stress-induced gene regulation in cultured bovine aortic endothelial cells (BAECs). Northern blot analysis revealed elevated endogenous PDGF-B transcript levels in BAECs, after exposure to a physiological level of laminar shear stress (10 dynes/cm2; 1 dyne = 100 mN) for 4 h. A transfected reporter gene, consisting of a 1.3-kb fragment of the human PDGF-B promoter coupled to chloramphenicol acetyltransferase (CAT), indicated a direct effect on transcriptional activity. Transfection of a series of PDGF-B-CAT deletion mutants led to the characterization of a cis-acting component within the PDGF-B promoter that was necessary for shear-stress responsiveness. In gel-shift assays, overlapping oligonucleotide probes of this region formed several protein-DNA complexes with nuclear extracts prepared from both static and shear-stressed BAECs. A 12-bp component (CTCTCAGAGACC) was identified that formed a distinct pattern of complexes with nuclear proteins extracted from shear-stressed BAECs. This shear-stress-responsive element does not encode binding sites for any known transcription factor but does contain a core binding sequence (GAGACC), as defined by deletion mutation in gel-shift assays. Interestingly, this putative transcription factor binding site is also present in the promoters of certain other endothelial genes, including tissue plasminogen activator, intercellular adhesion molecule 1, and transforming growth factor beta 1, that also are induced by shear stress. Thus, the expression of PDGF-B and other pathophysiologically relevant genes in vascular endothelium appears to be regulated, in part, by shear-stress-induced transcription factors interacting with a common promoter element.

Disaster Education, Household Preparedness, and Stress Responses Following Hurricane Hugo

This study examines the impact of disaster education and household preparedness activities on stress responses among adults in the Charleston, South Carolina area following Hurricane Hugo. Two samples, composed of 198 adults who had participated in special disaster education workshops sponsored by the Earthquake Education Center (EEC) at Charleston Southern University, and a general sample of 511 adults in the Charleston area were interviewed by telephone. The data reveal that (a) those who had participated in disaster education programs generally (other than the EEC programs) reported higher levels of stress than did those who did not participate in such programs, although this relationship was not significant; (b) engaging in household preparedness activities resulted in higher levels of stress; and (c) controlling for other pertinent variables, the EEC workshop sample reported significantly higher levels of both physiological and psychological stress than did the general sample. Possible reasons for these unexpected findings are discussed.

Endothelium-derived Relaxing Factor Inhibits Shear Stress-induced Platelet Aggregation

The effect of endothelium-derived relaxing factor (EDRF) and related compounds on platelet aggregation in response to physiological and pathological levels of arterial wall shear stress (30-120 dyne/cm(2)) was investigated. Platelets in plasma, or washed platelets, aggregated markedly in response to shear stresses generated by a cone-plate viscometer. Pre-treatment of platelets with the S-nitrosothiol compounds S-nitroso-N-acetylcysteine or S-nitrosocysteine, or with nitric oxide (NO) or SIN-1 (which is non-enzymatically metabolized to NO), resulted in decreased platelet aggregation in response to shear stress. Non-hydrolyzable analogues of cyclic guanosine 3',5'-monophosphate (cGMP) also inhibited shear stress-induced platelet aggregation, and specific pharmacological manipulations of NO and cGMP (with methylene blue or the cGMP phosphodiesterase inhibitor M&B 22 984) resulted in alterations of intraplatelet levels of cGMP that correlated with the degree of inhibition of shear stress-induced platelet aggregation. These results demonstrate that EDRF and related compounds inhibit platelet aggregation that is initiated by shear stress, and suggest that this physiologically relevant mechanism of platelet aggregation may be regulated by intraplatelet cGMP.

The Effectiveness of Ligating or Detaching Ceca as an Alternative to Cecectomy

Cecectomy (the surgical removal of ceca) is a technique that has been used to explore the nutritional and osmoregulatory role of the ceca in domestic fowl and other birds. The operation imposes a high level of physiological stress on a bird. The current study describes the effectiveness of ligating or detaching the ceca in young turkeys as an alternative to complete removal of the organ.Birds with ligated ceca showed less postsurgical depression and initiated feeding and other normal activities sooner than birds with detached ceca. Birds with detached ceca also had a significantly slower rate of weight gain 1 wk after surgery. Both surgically treated groups were more depressed than were sham-operated turkeys. Post-mortem examinations revealed that cecal detachment was more successful in actually separating the ceca from the rectum and in preventing flow of digesta in and out of the ceca. Evidence of growth of cecal stumps that remained attached to the rectum was found following both ligation and detachment.Post-mortem examinations revealed that in four birds both ligated or detached ceca left in the abdominal cavity became enlarged and filled with a dark, pasty, odorous substance. This increase in cecal size and volume of contents with time apparently indicates that some microbial metabolic activity continued in the cecal lumen. If so, this might have negative implications for studies that assume that such ceca are no longer functional.