Increase In Hydrostatic Pressure Research Articles

Mechanics of human blastocyst hatching in vitro

Critical examination of 30 blastocysts by transmission electron microscopy at various stages of blastulation and hatching, has revealed the presence of specialized, plump, trophoblastic cells at the points of hatching, which seem to aid in initial breaking of the zona pellucida (ZP) and then widen its opening to permit the progressive emergence of the embryo in amoeboid fashion, when it acquires a characteristic dumb-bell shape. These cells are named ‘zona-breaker’ cells and their characteristics are described. Normally, trophoblast cells in expanding blastocysts are flattened (squamous), forming a continuous robust epithelium with specialized cell junctions. Bundles of tonofilaments anchor onto desmosomes, forming a terminal web. Proper expansion of blastocysts by intake of fluid into the blastocoele causes an increase in internal hydrostatic pressure that stretches the trophoblast epithelium leading to an enlargement of its volume two- to three-fold, consequently thinning the zona prior to hatching. This is an important prerequisite to normal hatching. The blastocysts usually hatch out at the pole opposite the inner cell mass (ICM), though a few hatch out at the embryonal pole or elsewhere. In all cases zona-breakers seem to play a vital role in the hatching process.

Multiple components of membrane retrieval in synaptic terminals revealed by changes in hydrostatic pressure.

Membrane retrieval following exocytosis in synaptic terminals is fast and compensatory, however, little is known about the factors that regulate or contribute to this special form of endocytosis. We used whole-terminal capacitance measurements to examine the effect of hydrostatic pressure on compensatory endocytosis in single synaptic terminals of retinal bipolar neurons. We report that a small increase in hydrostatic pressure reversibly inhibits compensatory endocytosis. Elevation in hydrostatic pressure does not block all membrane retrieval, however. A small, fast component of endocytosis persists, while a slower component is inhibited. When the hydrostatic pressure is then stepped back to a near-neutral setting, an even slower form of endocytosis is observed that restores the resting membrane capacitance to baseline. Thus even when endocytosis is temporally uncoupled from calcium entry and exocytosis, it can still be compensatory, indicating that presynaptic surface area is highly regulated. Our results suggest that at least two distinct mechanisms of membrane retrieval contribute to compensatory endocytosis. Given its dramatic inhibitory effect on membrane retrieval, we suggest that hydrostatic pressure be carefully controlled when studying endocytosis in the whole cell recording configuration.

An investigation of primary permeability in strata from a mine in the Eastern Transvaal Coalfield, South Africa

Excessive development of methane and water pressures were believed to be a contributory cause of roof fall in a coal mine in the Eastern Transvaal Coalfield. Accordingly, a laboratory investigation of the primary permeability of the strata enclosing the coal seam concerned was undertaken. The principal aim of the investigation was to see if there was a relationship between the various facies of the coal bearing strata and changes in permeability. In this way it may be possible to determine likely zones of pressure build-up. Permeability testing was carried out on drillholesamples using modified versions of the Ohle cell, the Bernaix cell and the Hoek triaxial cell. The use of the Hoek cell allowed testing to be carried out under different stress conditions. Nitrogen, methane and water were used as the permeating fluids. The liquid equivalent permeability of each sample was determined for the two gases. The permeability tended to decrease with increasing pressure when the two gases were used as the permeating fluid but not when water was used. In addition, the permeability was influenced by the grain size of the material tested and by the direction in which it was tested, that is, along or across the bedding. Hydraulic fracturing occurred in some specimens when tested at high water pressures in divergent flow in the Bernaix cell. An increase in hydrostatic pressure, confining pressure or axial pressure gave rise to a reduction in permeability in triaxial testing, the former giving rise to the greatest and the latter the least decrease. Staged loading showed that the greatest reduction in permeability occurred during initial loading. On cyclic loading the liquid equivalent permeability decreased with increasing applied stress and then increased with subsequent reduction in stress.

Alveolar epithelial fluid transport in acute lung injury: new insights.

Pulmonary oedema is a life-threatening condition that frequently leads to acute respiratory failure. From a physiological perspective, pulmonary oedema develops either because of an increase in lung vascular hydrostatic pressure or an increase in lung vascular permeability. Resolution of alveolar oedema depends on the active removal of salt and water from the distal air spaces of the lung across the distal lung epithelial barrier. Much has been learned about the molecular and cellular basis for oedema fluid reabsorption, including the role of apical ion transporters for sodium (epithelial sodium channel) and chloride (cystic fibrosis transmembrane conductance regulator), as well as the central importance of the sodium pump. The rate of fluid clearance can be upregulated by both catecholamine-dependent and -independent mechanisms. Injury to the alveolar epithelium can disrupt the integrity of the alveolar barrier or downregulate ion transport pathways, thus, reducing net alveolar fluid reabsorption and enhancing the extent of alveolar oedema. Endogenous catecholamines upregulate alveolar fluid clearance in several experimental models of acute lung injury, but this upregulation may be short term and insufficient to counterbalance alveolar flooding. There is new evidence, however, that pharmacological treatment with beta2-adrenergic agonists and/or epithelial growth factors may influence a more sustained stimulation of alveolar fluid reabsorption and in turn facilitate recovery from experimental pulmonary oedema. Similar results have been achieved experimentally by gene transfer to enhance the abundance of sodium transporters in the alveolar epithelium. Clinical studies show that impaired alveolar fluid transport mechanisms contribute to the development, severity and outcome of pulmonary oedema in humans. Very recent data suggest that mechanisms that augment transepithelial sodium transport and enhance the clearance of alveolar oedema may lead to more effective prevention or treatment for some types of pulmonary oedema.

Effect of Hydrostatic Pressure on Photoluminescence Spectra from Structures with Si Nanocrystals Fabricated in SiO2Matrix

The effect of hydrostatic pressure applied at high temperature on photoluminescence of Si-implanted SiO 2 films was studied. A blue-shift of PL spectrum from the SiO 2 films implanted with Si + ions to total dose of 1.2× 10 1 7 cm - 2 with an increase in hydrostatic pressure was observed. For the films implanted with Si + ions to a total dose of 4.8 x 10 1 6 cm - 2 high temperature annealing under high hydrostatic pressure (12 kbar) causes a red-shift of photoluminescence spectrum. The red photoluminescence bands are attributed to Si nanocrystals while the blue ones are related to Si nanocrystals of reduced size or chains of silicon atoms or ≡Si-Si≡ defects. A decrease in size of Si nanocluster size occurs in result of the pressure-induced decrease in the diffusion of silicon atoms.

Update on ascites and hepatorenal syndrome

Ascites is the most common complication occurring during liver cirrhosis. Even if a significant decrease in renal clearance may be observed in the first step of chronic active liver disease, renal impairment, at times complicated by the typical signs of hepatorenal syndrome, occurs only in patients with ascites, especially when tense and refractory. Experimental and clinical data seem to suggest a primary sodium and water retention in the pathogenesis of ascites, in the presence of an intrahepatic increase of hydrostatic pressure, which, by itself, physiologically occurs during digestion. Abnormal sodium and water handling leads to plasma volume expansion, followed by decreased peripheral vascular resistance and increased cardiac output. This second step is in agreement with the peripheral arterial vasodilation hypothesis, depicted by an increase in total blood volume, but with a decreased effective arterial blood volume. This discrepancy leads to the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems associated with the progressive activation of the renal autacoid systems, especially, that of the arachidonic acid. During advanced cirrhosis, renal impairment becomes more sustained and renal autacoid vasodilating substances are less available, possibly due to a progressive exhaustion of these systems. At the same time ascites becomes refractory inasmuch as it is no longer responsive to diuretic treatment. Various pathogenetic mechanisms leading to refractory ascites are mentioned. Finally, several treatment approaches to overcome the reduced effectiveness of diuretic therapy are cited. Paracentesis, together with simultaneous administration of human albumin or other plasma expanders is the main common approach to treat refractory ascites and to avoid a further decrease in renal failure. Other effective tools are: administration of terlipressin together with albumin, implantation of the Le Veen shunt, surgical porto-systemic shunting or transjugular intrahepatic portosystemic stent-shunt, or orthotopic liver transplantation, according to the conditions of the individual patient.

Cellular pathophysiology of pulmonary hypertension

Zusammenfassung Die pulmonale Hypertonie umfasst eine Gruppe von Erkrankungen heterogener Ätiologie, die mit einem Anstieg des hydrostatischen Druckes in der Lungenstrombahn einhergehen. Während sich die sekundäre pulmonale Hypertonie zumeist als direkte Folge eines akuten oder chronischen linksventrikulären Pumpversagens entwickelt, resultieren die primären Formen häufig aus charakteristischen Gendefekten oder typischen Auslösemechanismen. Trotz ihrer unterschiedlichen Pathogenese weisen jedoch die verschiedenen Formen der pulmonalen Hypertonie ähnliche pathophysiologische Veränderungen und zelluläre Reaktionsmuster in der pulmonalen Mikrozirkulation auf. Die Dysfunktion der pulmonalvaskulären Endothelzellen, die den hämodynamischen Veränderungen unmittelbar exponiert sind, ist die treibende Kraft des pathophysiologischen Geschehens. Die endotheliale Dysfunktion bewirkt durch eine verminderte Freisetzung vasodilatierender, anti-proliferativer Mediatoren bei gleichzeitig vermehrter Produktion vasokonstriktiver, proliferativer Substanzen nicht nur eine zunehmende pulmonale Vasokonstriktion, sondern unterstützt auch die pathologischen Umbauprozesse in Gefäßintima und -media. Darüber hinaus trägt das pulmonale Endothel durch die Rekrutierung von Thrombozyten und Leukozyten wesentlich zur Freisetzung zusätzlicher vasokonstriktiver, proliferativer Faktoren und zur Bildung charakteristischer Gefäßthromben bei. Diese endothelial initiierten Pathomechanismen verstärken sich zudem wechselseitig, führen zu einem weiteren Anstieg des pulmonalen Strömungswiderstandes und fixieren schließlich die pulmonale Hypertonie. Die pulmonale Hypertonie beschreibt folglich nicht nur eine Änderung der Lungenhämodynamik, sondern umfasst ein komplexes zelluläres Geschehen, an dem parenchymatöses Lungengewebe und korpuskuläre Blutbestandteile gleicherweise beteiligt sind. Bei der Entwicklung neuer Therapiekonzepte ist dieser multifaktorielle Charakter der Erkrankung zu berücksichtigen.

Electrical resistivity of CeNiSn underuniaxial and hydrostatic pressures

We present measurements of the electrical resistivityρ(T) on high-quality single-crystalline CeNiSnunder both hydrostatic pressure up to 1 GPa and uniaxialpressure up to 0.25 GPa. At ambient pressure, ρ(T) along the orthorhombic a-axis (b-axis) shows twomaxima at TL = 12 K (14 K) and TH = 74 K (40 K),respectively, which arise from the Kondo scattering of conduction electrons by the crystal-field ground state andexcited states. With increasing hydrostatic pressure, bothTL and TH increase linearly, and for P⩾0.8 GPa, the anisotropy in ρ(T) for I∥aand I∥b almost vanishes as a result of increasedhybridization between the 4f electrons and the conductionelectrons. Under P∥a, both TL and TH in ρ(I∥b) increase similarly to underhydrostatic pressure. Under P∥c, however, the depressionof TL in ρ(I∥a) and ρ(I∥b) suggests that the c-f hybridization in thecrystal-field ground state is weakened in the a-b plane ofCeNiSn.

Modification of ureteral motility and promotion of urine flow around an intraureteral obstruction by CL‐316243, phenylephrine, and furosemide in dogs

The aim of this study was to evaluate the effects of a beta3-adrenoceptor (AR) agonist (CL-316243), an alpha1-AR agonist (phenylephrine), and a loop diuretic (furosemide) on the spontaneous rhythmic contractions of the isolated canine ureter and on an acute ureteral obstruction produced by inflation of a balloon catheter in anesthetized dogs. In the isolated ureter, CL-316243 concentration dependently reduced both the amplitude and frequency of the rhythmic contractions (pD(2): 7.19 +/- 0.33), whereas phenylephrine significantly enhanced both variables (pD(2): 5.26 +/- 0.09) and furosemide reduced them only slightly. In the acute ureteral obstruction model, the intraureteral pressure (IUP) gradually rose to reach a plateau of 58.9 mm Hg after inflation of a balloon catheter within the lower ureter. Intravenous administration of CL-316243 (0.3 microg/kg) significantly reduced the elevated IUP and the resumed urine flow (UF), leading to a sustained reduction in the IUP. In contrast, the IUP continued to increase above the plateau level for 10 minutes after phenylephrine administration (10 microg/kg) and for 30 minutes after furosemide administration (1,000 microg/kg). In the phenylephrine group, the UF resumed when the IUP reached 75.8 mm Hg, and thereafter the IUP gradually decreased in parallel with the increase in the UF. From these results, we conclude that in dogs, CL-316243 reduces the IUP by allowing the UF to resume as a result of a relaxation of ureter at the obstruction site, whereas with phenylephrine, the reduction in the IUP is secondary to a resumption in the UF resulting from an induced contraction of ureter that causes an increase in hydrostatic pressure above the obstruction site.

硬脆機能材料の高静水圧環境における延性モード切削 第２報 高静水圧環境における種種の硬脆材料の切削実験

This paper reports results of machining tests under high hydrostatic pressure, 400MPa, done on four kinds of hard brittle materials; soda glass, quarts glass, quarts, silicon. They were examined by a newly developed machining device that consists of a pressure vessel in which a turntable and a tool stage mechanisms are installed. In the machining tests, end surface of the specimens were machined with a single point diamond tool, and tangential cutting force was measured. The examined specimens were observed with a laser microscope, and profiles of machined grooves and the crack ratio were measured. Results show that external hydrostatic pressure is effective to decrease machining defects and to increase the critical groove section area, which indicates limit of machining volume where no machining fracture arises. Tested materials were separated into two groups based on characteristics of the machining fracture; one is soda glass and quartz glass, the other is quartz and silicon. The former group of materials show steep increase of crack ratio by the increase of groove cross section area, but show small increase of the critical groove section area with the increase of external hydrostatic pressure. Besides the latter material group shows gradual increase of the crack ratio, but large increase of the critical groove section area. The difference of these characteristics depends on difference of crystalline structure. Variation of tangential cutting force was also studied, and results show that cutting force increases with hydrostatic pressure. Magnitude of the effect differs with material.

Delamination characteristics of multi‐directional carbon fiber/epoxy composites under high pressure

AbstractIt was shown in a previous study that for unidirectional (0‐deg) graphite/epoxy composites, the fracture toughness under hydrostatic pressure increased 38% as hydrostatic pressure increased from 0.1 MPa to 200 MPa. This work investigates the compressive delamination behavior of multi‐directional graphite/epoxy laminated composites subjected to various hydrostatic pressures. Compressive delamination tests were performed under four hydrostatic pressure levels: 0.1, 100, 200, and 300 MPa Eighty‐eight‐ply dog‐bone type specimens with a single delamination at the center of the specimen were used. The stacking sequence applied was [0°/±45°/90°]lls. The compliance and fracture load were determined from load‐displacement curves as a function of hydrostatic pressure.The results show that the compliance decreases with increasing pressure while fracture load increases with increasing pressure. The compressive delamination toughness, Gc, was determined from the compliance method as a function of applied hydrostatic pressure. The results also show that Gc is significantly affected by hydrostatic pressure and increases from 2.11 kJ/m2 to 3.04 kJ/m2 (44% increase) as hydrostatic pressure increased from 0.1 MPa to 300 MPa. Visual examination of the fractured surface revealed that the increase of Gc is due to the suppression of micro‐cracks With increasing pressure. It was also found from SEM examination of delaminated surface that the Gc increase is due to more epoxy adhering to the fibers and more plastic deformation of epoxy material as applied hydrostatic pressure increases.

Obesity and the kidney connection

The importance of the functional and structural changes that occur in the kidneys in association with obesity was discussed previously in the medical literature.1-4 These studies suggested that the kidneys are involved in the development of obesity-induced hypertension. This involvement is explained by an abnormal tubular sodium handling and by deposition of cells or matrix in the renal medulla that causes an increase in the renal interstitial fluid hydrostatic pressure.3,5

Epithelial Na(+) channels are regulated by flow.

Na(+) absorption in the renal cortical collecting duct (CCD) is mediated by apical epithelial Na(+) channels (ENaCs). The CCD is subject to continuous variations in intraluminal flow rate that we speculate alters hydrostatic pressure, membrane stretch, and shear stress. Although ENaCs share limited sequence homology with putative mechanosensitive ion channels in Caenorhabditis elegans, controversy exists as to whether ENaCs are regulated by biomechanical forces. We examined the effect of varying the rate of fluid flow on whole cell Na(+) currents (I(Na)) in oocytes expressing mouse alpha,beta,gamma-ENaC (mENaC) and on net Na(+) absorption in microperfused rabbit CCDs. Oocytes injected with mENaC but not water responded to the initiation of superfusate flow (to 4-6 ml/min) with a reversible threefold stimulation of I(Na) without a change in reversal potential. The increase in I(Na) was variable among oocytes. CCDs responded to a threefold increase in rate of luminal flow with a twofold increase in the rate of net Na(+) absorption. An increase in luminal viscosity achieved by addition of 5% dextran to the luminal perfusate did not alter the rate of net Na(+) absorption, suggesting that shear stress does not influence Na(+) transport in the CCD. In sum, our data suggest that flow stimulation of ENaC activity and Na(+) absorption is mediated by an increase in hydrostatic pressure and/or membrane stretch. We propose that intraluminal flow rate may be an important regulator of channel activity in the CCD.

Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 +/- 1 mmHg, P < 0.05) and less during WI + NS (4 +/- 1 mmHg) and NS (3 +/- 1 mmHg). The decrease in heart rate (HR) by 13 +/- 1 beats/min (P < 0.05) and the increase in arterial pulse pressure (PP) by 17 +/- 4 mmHg (P < 0.05) during supine was more pronounced (P < 0.05) than during WI + NS (10 +/- 2 beats/min and 7 +/- 2 mmHg, respectively) and WI (8 +/- 2 beats/min and 6 +/- 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS (P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change.

Arterial stiffness and gradient of blood pressure at essential hypertension

The two major causes of increased large artery stiffness are aging and high blood pressure. This study was designed to assess the modifications in large artery elastic properties and their hemodynamic resistance at essential hypertension (EH). The pulse wave velocity (PWV) was evaluated in the following distance: carotid-femoral artery, femoral-posterior tibial artery and carotid-radial artery by piezoelectric detectors. The gradient of arterial pressure (AP) was analyzed in the distance: brachial-finger artery and brachial-posterior tibial artery applying auscultatory method (using acoustic system), and, simultaneously, the gradient of systolic AP was evaluated according to volume oscillations. Data were analyzed in supine position, when intravascular pressure was modified by rising and lowering the extremity referring to the heart level, and when subjects was passively tilted up to 70° with and without unilateral thigh arterial occlusion for 5 min. Group of 78 patients with EH (38-57 yrs aged men) and 31 age and gender matched controls were studied. Antihypertensive treatment, if any, was interrupted 8 days before the examination. In EH pts mean AP gradient in the distance of brachial-finger artery was increased (14.1±1.4 vs. 8.7±1.7 mmHg; P<0.02), whereas systolic and pulse pressure on tibial artery comparing to brachial artery was increased (Franc's phenomenon) and this increase was more expressed in EH pts (35.2±5.4 vs. 18.5±2.3 mmHg; P<0.02) and related (r=0.63; P<0.01) to systemic AP level. Upper extremity lowering and subjects tilting was related with less than expected (calculated hydrostatic pressure) increase of AP in distal parts. This difference disappeared on background of unilateral reactive hyperemia. At upper extremity elevation, decrease of finger AP corresponded to expected hydrostatic pressure decrease in both groups. In all analyzed distances PWV values were increased in EH pts comparing to controls (P<0.001) and were related to systemic arterial (brachial) pressure level (r=0.51-0.59; P<0.01). Modifications in regional AP caused by hydrostatic effect was related with corresponding PWV changes (r=0.8 in EH pts and r=0.72 in controls). This study suggests that alongside increased wall stiffness the hemodynamic resistance of large arteries is increased at EH and modifications in smooth muscle tone maintain important role in systemic and regional hemodynamic reactions.

Pathogenetic mechanisms of venous congestion after the Fontan procedure.

The hemodynamic status after a Fontan type procedure for definitive palliation of functionally univentricular hearts is dominated by a high central venous pressure, which seems to be one of several factors responsible for venous congestion appearing as a frequent complication in the early and late postoperative course. The purpose of our study was to find other hemodynamic parameters correlating with the presence of venous congestion and effusions in these patients. We compared the hemodynamic data of 18 patients who had an uneventful long-term course after a Fontan type procedure with the respective data of 10 patients who developed symptoms of venous congestion in the immediate postoperative period. Based on a theoretical model, we developed an algorithm to calculate mean hydrostatic capillary pressure from mean arterial pressure, systemic vascular resistance index and central venous pressure. Pulmonary vascular resistance index (2.1 +/- 1.0 mmHg L-1 min m2), mean left atrial pressure (9.7+/-4.0 mmHg) and cardiac index (3.6+/-0.6 l/min/m2) are mainly normal in patients with venous congestion in the immediate postoperative period, but mean hydrostatic capillary pressure is significantly higher compared to patients without venous congestion (24.3+/-3.1 vs 18.3+/-4.0 mmHg). Lower mean hydrostatic capillary pressures in these patients are due to a highly significant increase of systemic vascular resistance index (18.6+/-4.2 versus 33.6+/-6.6 mmHg L-1 min m2) and a concomitant decrease of cardiac index to 2.4+/-0.3 l/min/m2. The increase of mean hydrostatic capillary pressure, caused by high central venous pressures but also by relatively low systemic vascular resistance indexes, seems to be the hemodynamic key parameter responsible for venous congestion and effusions in patients after a Fontan type procedure in the immediate postoperative period.

Fonction pulmonaire et solutés de remplissage vasculaire

The formation of the pulmonary edema is dependent upon the intra- versus extravascular hydrostatic pressure gradient and on permeability alterations of the alveolocapillary membrane. The colloid-oncotic pressure gradient could be protective. It has been known for a long time that intravascular fluid loading does considerably worsen any pulmonary lesion. Whether colloids could be protective against pulmonary edema compared to crystalloids has long been discussed. The increase in hydrostatic pressure generated by colloids, however, may not always be compensated by the increase in oncotic pressure. In addition, in the case of a lesion of the membrane, leakage of colloids into the interstitium may be deleterious. It is difficult to recommend one type of solutes, since the main determinant of edema seems to be the capillary hydrostatic pressure level.

Oedema in childhood.

Oedema is a common childhood problem with important public health implications. It is an abnormal accumulation of fluid in the interstitial space which might result from a decrease in intravascular oncotic pressure, an increase in intravascular hydrostatic pressure, an increase in capillary permeability or impaired lymphatic drainage. Renal sodium retention is an important factor in generalised oedema. This article reviews the pathophysiology and aetiology of oedema in children and suggests an approach to evaluation, diagnosis and management of the problem.

Hydrostatic Pressure Effect on the Fracture Toughness of Unidirectional (0-deg) Graphite/Epoxy Laminated Composites

Previous studies show that hydrostatic pressure affects elastic modulus, strength, and strain of fiber-reinforced composites. However, no work has been done to understand the compressive fracture behavior of laminated composites under hydrostatic pressure. This work is an experimental study of the hydrostatic pressure effects on the compressive fracture behavior of fiber-reinforced composites. Compressive fracture tests were conducted under various hydrostatic pressures from 0.1 MN/m2 (atmospheric pressure) to 200 MN/mi2 (2 Kbar). Test specimens used were unidirectional (0-deg) graphite/epoxy laminated composites with a single delamination at the center of specimen. First, compression load-displacement curves were determined as a function of hydrostatic pressure and delamination length. Second, the compressive fracture toughness was determined from the compliance method based on the load-displacement curves as a function of hydrostatic pressure. The results showed that compliance, fracture load, and fracture toughness were significantly influenced by hydrostatic pressure. The fracture load increases as hydrostatic pressure increases. The compliance decreases linearly with increasing pressure. Particularly, fracture toughness increased from 3.45 N-mm/mm2 to 4.53 N-mm/mm2 (32% increase) as hydrostatic pressure increased from 0.1 MN/mm2 to 200 MN/mm2. Apparently the increase of fracture toughness is due to the suppression of local delamination with increasing hydrostatic pressure.

Hydrostatic Pressure Dependence of Transformation Temperatures of Ti-Ni-Cu Alloys

The transformation start temperatures of shape memory Ti 50 Ni 50-x Cu x (x = 2, 3, 5, 12.5) alloys under hydrostatic pressures were obtained by resistivity measurements, and their thermodynamical analysis was made by using Clausius-Clapeyron equation. The obtained results are the followings. (1) As hydrostatic pressure increases, transformation temperatures (M s and A f ) of the B2 ↔B19' transformation increase linearly for the 2Cu and 3Cu alloys, but decrease linearly for the 5Cu alloy. (2) For the 12.5Cu alloy, M s and A f of B2↔B19 transformation increase but those of B19↔B19' transformation decrease as pressure increases. (3) The copper content dependence of volume change associated with martensitic transformation, which is calculated by Clausius-Clapeyron equation, suggests that the 5Cu alloy transforms in two steps B2→B19→B19' although it is believed to transform in one step.