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Osmotic pressure and hydrostatic pressure can be used effectively to probe the behavior of biologically important macromolecules and their complexes. Using the two techniques requires a theoretical framework as well as knowledge of the more common pitfalls. Both are discussed in this review in the context of several examples.
A direct relationship between renal arterial pressure (RAP) and renal interstitial hydrostatic pressure (RIHP) has been shown under conditions of efficient renal blood flow autoregulation. Experiments were performed in six anesthetized dogs to evaluate whether these RIHP responses to changes in RAP were modified during nitric oxide (NO) inhibition with nitro-L-arginine (NLA) or after administration of NO donor agents. A microtip catheter transducer was placed underneath the renal capsule to measure RIHP. Stepwise reductions in RAP (140 to 80 mm Hg) during control conditions resulted in decreases in RIHP from its basal value of 4.7+/-1.1 mm Hg with a slope of 0.04+/-0.026 mm Hg. mm Hg(-)(1) along with decreases in urinary nitrate/nitrite excretion rate (U(NOx)V). Renal cortical and medullary blood flows, measured by laser-Doppler flowmetry, exhibited high autoregulatory efficiency over this RAP range. The changes in RIHP during alterations in RAP were positively correlated (r=0.743; P:<0.001) with the changes in U(NOx)V but not with cortical or medullary blood flow. NLA infusion decreased RIHP to 1.9+/-0.5 mm Hg and also reduced U(NOx)V from 1.8+/-0.2 to 0.9+/-0.01 nmol. min(-)(1). g(-)(1). Infusion of NO donors restored RIHP (4.3+/-0.9 mm Hg) and U(NOx)V (1.5+/-0.2 nmol. min(-)(1). g(-)(1)). During NLA infusion, the RIHP responses to reductions in RAP were markedly attenuated and were not restored even during constant-rate infusion of NO donors. The results suggest that changes in RIHP in response to alterations in RAP are associated with changes in intrarenal NO, suggesting a direct effect of NO to regulate RIHP.
Since high hydrostatic pressure is becoming increasingly important in modern food preservation, its potential effects on microorganisms need to be thoroughly investigated. In this context, mild pressures (<200 MPa) have recently been shown to induce an SOS response in Escherichia coli MG1655. Due to this response, we observed a RecA- and LexA-dependent induction of lambda prophage upon treating E. coli lysogens with sublethal pressures. In this report, we extend this observation to lambdoid Shiga toxin (Stx)-converting bacteriophages in MG1655, which constitute an important virulence trait in Stx-producing E. coli strains (STEC). The window of pressures capable of inducing Stx phages correlated well with the window of bacterial survival. When pressure treatments were conducted in whole milk, which is known to promote bacterial survival, Stx phage induction could be observed at up to 250 MPa in E. coli MG1655 and at up to 300 MPa in a pressure-resistant mutant of this strain. In addition, we found that the intrinsic pressure resistance of two types of Stx phages was very different, with one type surviving relatively well treatments of up to 400 MPa for 15 min at 20 degrees C. Interestingly, and in contrast to UV irradiation or mitomycin C treatment, pressure was not able to induce Stx prophage or an SOS response in several natural Stx-producing STEC isolates.
The kidneys play a major role in the long-term regulation of extracellular fluid volume and arterial pressure. A central component of the feedback system for long-term control of arterial pressure is the pressure-natriuresis mechanism, whereby increases in renal perfusion pressure lead to decreases in sodium reabsorption and increases in sodium excretion. The specific intrarenal mechanism for the decrease in tubular reabsorption in response to increases in renal perfusion pressure appears to be related to increases in renal interstitial hydrostatic pressure (RIHP). Increases in renal perfusion pressure are associated with significant increases in RIHP. The mechanism whereby RIHP increases in the absence of discernible changes in whole kidney renal blood flow and peritubular capillary hydrostatic and/or oncotic pressures may be related to alterations in renal medullary hemodynamics. Several lines of investigation support an important quantitative role for RIHP in mediating pressure natriuresis. Preventing RIHP from increasing in response to increases in renal perfusion pressure markedly attenuates pressure natriuresis. Furthermore, direct increases in RIHP, comparable to increases measured in response to increases in renal perfusion pressure, have been shown to significantly decrease tubular reabsorption of sodium in the proximal tubule and increase sodium excretion. The exact mechanism whereby RIHP influences tubular reabsorption is unknown but may be related to alterations in tight junctional permeability to sodium in proximal tubules and/or release of renal autacoids such as prostaglandins.
Hydrostatic pressure was measured within 10 single renal cysts during surgical exploration. The pressure ranged from 12.5 to 31.0 cm of water (average 22 cm). It seems that the persistently elevated hydrostatic pressure within renal cysts could be associated with their expansion.
The effect of hydrostatic pressure on the death of E. coli was studied in this paper. The results indicated that E. coli could be killed by hydrostatic pressure above 800 bar. At 2300 bar E. coli was totally killed in 30 minutes. The time course of E. coli death induced by pressure indicated that the most E. coli was killed in the first 10 minutes after the pressure was applied. It was also found that the lower temperature favored killing E. coli under pressure.
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The antibacterial working range of six lysozymes was tested under ambient and high pressure, on a panel of five gram-positive (Enterococcus faecalis, Bacillus subtilis, Listeria innocua, Staphylococcus aureus and Micrococcus lysodeikticus) and five gram-negative bacteria (Yersinia enterocolitica, Shigella flexneri, Escherichia coli O157:H7, Pseudomonas aeruginosa and Salmonella typhimurium). The lysozymes included two that are commercially available (hen egg white lysozyme or HEWL, and mutanolysin from Streptomyces globisporus or M1L), and four that were chromatographically purified (bacteriophage lambda lysozyme or LaL, bacteriophage T4 lysozyme or T4L, goose egg white lysozyme or GEWL, and cauliflower lysozyme or CFL). T4L, LaL and GEWL were highly pure as evaluated by silver staining of SDS-PAGE gels and zymogram analysis while CFL was only partially pure. At ambient pressure each gram-positive test organism displayed a specific pattern of sensitivity to the six lysozymes, but none of the gram-negative bacteria was sensitive to any of the lysozymes. High pressure treatment (130-300 MPa, 25 degrees C, 15 min) sensitised several gram-positive and gram-negative bacteria for one or more lysozymes. M. lysodeikticus and P. aeruginosa became sensitive to all lysozymes under high pressure, S. typhimurium remained completely insensitive to all lysozymes, and the other bacteria showed sensitisation to some of the lysozymes. The possible applications of the different lysozymes as biopreservatives, and the possible reasons for the observed differences in bactericidal specificity are discussed.
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We have used hydrostatic pressure to study the structural organization of actin in the sea urchin egg cortex and the role of cortical actin in early development. Pressurization of Arbacia punctulata eggs to 6,000 psi at the first cleavage division caused the regression of the cleavage furrow and the disappearance of actin filament bundles from the microvilli. Within 30 s to 1 min of decompression these bundles reformed and furrowing resumed. Pressurization of dividing eggs to 7,500 psi caused both the regression of the cleavage furrow and the complete loss of microvilli from the egg surface. Following release from this higher pressure, the eggs underwent extensive, uncoordinated surface contractions, but failed to cleave. The eggs gradually regained their spherical shape and cleaved directly into four cells at the second cleavage division. Microvilli reformed on the egg surface over a period of time corresponding to that required for the recovery of normal egg shape and stability. During the initial stages of their regrowth the microvilli contained a network of actin filaments that began to transform into bundles when the microvilli had reached approximately 2/3 of their final length. These results demonstrate that moderate levels of hydrostatic pressure cause the reversible disruption of cortical actin organization, and suggest that this network of actin stabilizes the egg surface and participates in the formation of the contractile ring during cytokinesis. The results also demonstrate that actin filament bundles are not required for the regrowth of microvilli after their removal by pressurization. Preliminary experiments demonstrate that F-actin is not depolymerized in vitro by pressures up to 10,000 psi and suggest that pressure may act indirectly in vivo, either by changing the intracellular ionic environment or by altering the interaction of actin binding proteins with actin.
Intervertebral disc structures are exposed to wide ranges of intradiscal hydrostatic pressure during different loading exercises and are at their minimum during lying or relaxed sitting and at maximum during lifting weights with a round back. We hypothesize that these different loading magnitudes influence the intervertebral disc (IVD) by alteration of disc matrix turnover depending on their magnitudes. Therefore the aim of this study was to assess changes in gene expression of human nucleus cells after the application of low hydrostatic pressure (0.25 MPa) and high hydrostatic pressure (2.5 MPa). IVD cells isolated from the nucleus of human (n = 18) and bovine (n = 24 from four animals) disc biopsies were seeded into three-dimensional collagen type-I matrices and exposed to the different loading magnitudes by specially developed pressure chambers. The lower pressure range (0.25 MPa, 30 min, 0.1 Hz) was applied with a recently published device by using an external compression cylinder. For the application of higher loads (2.5 MPa, 30 min, 0.1 Hz) the cell-loaded collagen gels were sealed into sterile bags with culture medium and stimulated in a newly developed water-filled compression cylinder by using a loading frame. These methods allowed the comparison of loading regimes in a wide physiological range under an equal three-dimensional culture conditions. Cells were harvested 24 h after the end of stimulation and changes in the expression of genes known to influence IVD matrix turnover (collagen-I, collagen-II, aggrecan, MMP1, MMP2, MMP3, MMP13) were analyzed by real-time RT-PCR. A Wilcoxon signed-rank test(1) and a Wilcoxon 2-sample test(2) were performed to detect differences between the stimulated and control samples(1) and differences between low and high hydrostatic pressure(2). Multiple testing was considered by adjusting the p value appropriately. Both regimes of hydrostatic pressure influenced gene expression in nucleus cells with opposite tendencies for the matrix forming proteins aggrecan and collagen type-I in response to the two different pressure magnitudes: Low hydrostatic-pressure (0.25 MPa) tended to increase collagen-I and aggrecan expression of human nucleus cells (P < 0.05) but only to a small degree. High hydrostatic pressure (2.5 MPa) tended to decrease gene expression of all anabolic proteins with significant effects on aggrecan expression of nucleus cells (P = 0.004). Low hydrostatic pressure had no influence on the expression of matrix metalloproteinases (MMP1, MMP2, MMP3 and MMP13). In contrast, high hydrostatic pressure tended to increase the expression of MMP1, MMP3 and MMP13 of human nucleus cells with high individual-individual variations. The decreased expression of aggrecan (P = 0.008) and collagen type II (P = 0.023) and the increased MMP3 expression (P = 0.008) in response to high hydrostatic pressure could be confirmed in additional experiments with bovine nucleus cells. These results suggest that hydrostatic pressure as one of the physiological stimuli of the IVD may influence matrix turnover in a magnitude dependent way. Low hydrostatic pressure (0.25 MPa) has quite small influences with a tendency to anabolic effects, whereas high hydrostatic pressure (2.5 MPa) tends to decrease the matrix protein expression with a tendency to increase some matrix-turnover enzymes. Therefore, hydrostatic pressure may regulate disc matrix turnover in a dose-dependent way.
The possible influence of serum colloid oncotic pressure (COP) and the gradient between COP and pulmonary capillary wedge pressure (COP-PCWP) on respiratory insufficiency and survival was studied prospectively in 77 critically ill surgical patients by daily simultaneous measurements of COP, PCWP, and intrapulmonary shunt (Qs/Qt). Mean ages of survivors (N = 51) and nonsurvivors (n = 26) were 46 +/- 3 years (survivors) and 58 +/- 4 years (nonsurvivors), respectively (p less than 0.01). Lowest value of COP was similar in survivors (15 +/- 1 torr) and in nonsurvivors (14 +/- 1 torr). Lowest value of COP-PCWP in survivors was 3 +/- 1 torr and -1 +/- 2 torr in nonsurvivors (p less than 0.05). The difference in COP-PCWP was secondary to a significantly greater PCWP in nonsurvivors (16 +/- 1 torr) than in survivors (12 +/- 1 torr) (p less than 0.01). For each patient, Qs/Qt measured at the time of lowest measured COP was not significantly different between survivors and nonsurvivors (0.18 +/- 0.01) in survivors and 0.20 +/- 0.01 in nonsurvivors) and measured at lowest COP-PCWP (0.18 +/- 0.01 in survivors, and 0.21 +/- 0.01 in nonsurvivors). No correlation was found between either lowest COP or lowest COP-PCWP and Qs/Qt. Progressive respiratory insufficiency was not a dominant factor in determining respiratory insufficiency was not a dominant factor in determining mortality. These data suggest that COP alone is not a critical factor in determining either survival or respiratory insufficiency as measured by Qs/Qt in critically ill surgical patients.
The effects of high hydrostatic pressure on the spontaneous contractile activity of isolated rat portal veins were studied. During compression, an increase of activity was seen, whereas stable elevated hydrostatic pressure gave a decrease of both frequency and time-integrated force. Decompression further reduced the activity, but all changes were reversible upon return to control pressure. During sustained high pressure the frequency of contractions was reduced by 15.9% at 25 atm, 26.4% at 50 atm, and 45.8% at 100 atm. The corresponding reductions in integrated active force were 13.7%, 16.7%, and 40.7%, respectively. Contractions caused by electrical stimulation of nerve endings left in the preparation were reduced by 44.1%, and potassium contractures were reduced by only 15.3% at 100 atm. It is concluded that inhibition of activity in rat portal vein at high hydrostatic pressure is due in part to effects on the smooth muscle membrane.
A procedure using high hydrostatic pressure without detergent has been applied in this study to subfractionate the components of the delta 6-desaturase system from the rat liver endoplasmic reticulum. Microsomes were suspended in a buffer containing liposomes made of phosphatidylcholine. The mixture was placed in a sealed pressure bomb and subjected to hydrostatic pressure of up to 1500 bars. Under these conditions the total desaturase activity was found in the liposomal fraction thus indicating that the three components of the desaturase system, namely NADH-cytochrome b5 reductase, cytochrome b5 and the delta 6-desaturase co-extracted. Size chromatography and FPLC of the released proteins followed by SDS-PAGE confirmed the independent release of the three components corresponding to the delta 6-desaturase, system. delta 6-Desaturase activity could be fully regenerated by mixing the aqueous dispersions of the three components without further purification. Our results indicate that these components are physically facing a similar lipid environment in the microsomal membrane.
In chondrocytes, a low-amplitude intermittent hydrostatic pressure induces production of extracellular matrix molecules, while high hydrostatic pressure inhibits it. High pressure increases cellular heat shock protein 70 level in a number of cell types on account of increased stabilisation of the heat shock protein 70 mRNA. In our experiments, only bovine primary chondrocytes, but not an immortalized chondrocytic cell line, could resist the induction of the stress response in the presence of continuous 30 MPa hydrostatic pressure. We have recently shown that protein synthesis is required for the stabilization. According to two-dimensional gel electrophoresis the synthesis of heat shock protein 90 was also increased in a chondrocytic cell line and in HeLa cells, and mass spectrometric analysis suggested that the induction was rather due to increase in heat shock protein 90beta than in heat shock protein 90alpha. The stress response was rather intense in HeLa cells, therefore, we investigated the effect of continuous 30 MPa hydrostatic pressure on the expression of the two heat shock protein 90 genes in HeLa cells using Northern and Western blot analyses. Heat shock protein 90beta mRNA level increased within 6 hours of exposure to 30 MPa hydrostatic pressure, while hsp90alpha level remained stable. At protein level there was a clear increase in the heat shock protein 90beta/heat shock protein 90alpha ratio, too. These results show a specific regulation of stress proteins in cells exposed to high hydrostatic pressure.
1. Effects of hydrostatic pressure (range 0.1-10 MPa) on the isometric tension of skinned (rabbit psoas) muscle fibres were examined at 12 degrees C and at different levels of Ca2+ activation (pCa range 4-7); the effects on both the steady tension and the tension transients induced by rapid pressure release (< 1 ms) are described. 2. The steady tension was depressed by increased pressure (approximately 1% MPa-1) at a high level of Ca2+ activation (pCa approximately 4) whereas it was potentiated at lower Ca2+ levels (pCa > 6); the effects were reversible. 3. At maximal Ca2+ activation, the tension recovery following pressure release (10 MPa to atmospheric) consisted of a fast (approximately 30 s-1) and a slow (2-3 s-1) phase; the rate and the normalized amplitude (normalized to the steady tension at atmospheric pressure for a particular pCa) of the fast phase were invariant with changes in Ca2+ level. 4. The effects of changing Ca2+ level on the slow phase were complex; its positive amplitude at high Ca2+ levels changed to negative and the rate decreased to approximately 1 s-1 at low Ca2+ levels (pCa > 6.0). 5. Results are discussed in relation to previous studies on the effect of pressure on intact muscle fibres and the actin-myosin interaction. This work supports calcium regulation of cross-bridge recruitment rather than calcium regulation of the rate of a specific step in the cross-bridge cycle.
The effects of oxygen gas tensions and hydrostatic pressure on intracellular calcium, [Ca2+]i, response to a flow stimulus in endothelial cells were investigated. Cultured bovine aortic endothelial cells (BAECs) were exposed to a hydrostatic pressure of 100 mmHg under low oxygen gas tensions and were subsequently subjected to a 1 minute mechanical stimulation of fluid shear stress of 20 dynes/cm2. The [Ca2+]i response in BAECs was measured using a fluorescent indicator, Calcium Green-1. The maximum intensity for low oxygen tension was significantly lower than that for normal oxygen tension, which provides evidence that low oxygen tension regulates cellular functions downward. Moreover, preloading of hydrostatic pressure also reduced the increases in [Ca2+]i. These results suggest that BAECs in venous system, where oxygen tension and hydrostatic pressure are lower than those in arterial system, may be less sensitive to fluid flow. A separate observation showed that low oxygen tension did not significantly affect the cell morphology. In contrast, BAECs exposed to hydrostatic pressure showed marked elongation with no predominant orientation and the F-actin filament distributions were rearranged, indicating centrally located thick stress fibers. For better understanding of endothelial cell physiology, it is very important to elucidate the effect of oxygen gas tensions together with mechanical environment on endothelial cell responses.
Increased intraarticular hydrostatic pressure (Pia) may inhibit juxtaarticular muscle function, obstruct blood supply to joint structures and promote anoxic joint destruction in chronic arthritis. Joint capsular stiffness together with synovial fluid volume determines Pia at rest. Seventeen knee joints with effusive arthritis and different degrees of radiological cartilage involvement in 13 patients with chronic arthritis were examined. Since capsular elastance was difficult to standardize, we introduce a measure of joint capsular stiffness where the intraarticular volume yielding a pressure of 50 mm Hg (V50) is used. After normalization of injected volumes according to the V50, pressure volume curves became similar. Intraarticular hydrostatic pressure and maximal voluntary isometric extensor torque were measured simultaneously, while altering the intraarticular fluid volume in 9 knee joints. In 5 of these, quantified electromyography (EMG) of the vastus medialis and lateralis portion of the quadriceps muscle was also monitored. Progressive inhibition of extensor torque and EMG was found as the intraarticular pressure volume was increased in both intact and destroyed joints. No difference in inhibition was found for the 2 portions of quadriceps muscle tested. Increased intraarticular hydrostatic pressure Pia levels between 200 and 1150 mm Hg were observed during maximal voluntary activation of extensor muscles. The reproducibility was good for all variables studied. In a few instances evidence of intraarticular compartmentalization was found at low volumes. We conclude that the V50 is a convenient expression of capsular stiffness. Furthermore, increasing Pia caused by joint effusion inhibits knee extensor muscle function and impairs synovial blood flow. Awareness of these relations will facilitate more rational therapeutic approaches in chronic arthritis.