High Pressure Group Research Articles

The Comparison of the Abdominal Leak Point Pressure and the 1-Hour Pad Test in Patients with Stress Urinary Incontinence

Purpose: The aim of this study was to determine whether or not the 1-hour pad test demonstrates the objective severity of female stress urinary incontinence. Materials and Methods: One hundred eighteen female patients with stress urinary incontinence symptom were prospectively evaluated with a 1-hour pad test as recommended by the International Continent Society and they also underwent videourodynamics to determine the ALPP. The patients were divided into 2 groups by the ALPP: group A (n=94) was the low leak point pressure group (ALPP≤100cmH2O), and group B (n=24) was the high leak point pressure group (ALPP>100cmH2O or no leakage). A pad gain ≤2g was considered a negative pad test. Student's t-test was done to evaluate the difference of urine leakage between the two groups. Results: The mean amount of urine leakage measured by the 1-hour pad test for groups A and B were 53.4±47.2 and 50.9±53.9g, respectively, and there was no statistically significant differences between two groups (p= 0.839). Eighteen (15.2%) women did not leak during the ALPP measurement and 6 (5.1%) women had a negative pad test. Among the 18 women with no leakage on the ALPP, 15 had a positive pad test and 3 had a negative pad test. Among the 6 women with a negative pad test, 3 had leakage and 3 had no leakage during the ALPP measurement. One hundred fifteen patients received an operation for stress urinary incontinence. The three patients who had no leak on the ALPP and who also had a negative pad test did not receive the operation. Conclusions: These data suggest that the 1-hour pad test did not demonstrate the objective severity of stress urinary incontinence. However, the 1-hour pad test was more sensitive to demonstrate leakage than the ALPP; therefore, in the case of no leakage during the ALPP measurement, the 1-hour pad test is needed to check the leakage. (Korean J Urol 2006;47: 847-851)

Growth history of Kilauea inferred from volatile concentrations in submarine-collected basalts

Major-element and volatile (H 2O, CO 2, S) compositions of glasses from the submarine flanks of Kilauea Volcano record its growth from pre-shield into tholeiite shield-stage. Pillow lavas of mildly alkalic basalt at 2600–1900 mbsl on the upper slope of the south flank are an intermediate link between deeper alkalic volcaniclastics and the modern tholeiite shield. Lava clast glasses from the west flank of Papau Seamount are subaerial Mauna Loa-like tholeiite and mark the contact between the two volcanoes. H 2O and CO 2 in sandstone and breccia glasses from the Hilina bench, and in alkalic to tholeiitic pillow glasses above and to the east, were measured by FTIR. Volatile saturation pressures equal sampling depths (10 MPa = 1000 m water) for south flank and Puna Ridge pillow lavas, suggesting recovery near eruption depths and/or vapor re-equilibration during down-slope flow. South flank glasses are divisible into low-pressure (CO 2 < 40 ppm, H 2O < 0.5 wt.%, S < 500 ppm), moderate-pressure (CO 2 < 40 ppm, H 2O > 0.5 wt.%, S 1000–1700 ppm), and high-pressure groups (CO 2 > 40 ppm, S > ∼1000 ppm), corresponding to eruption ≥ sea level, at moderate water depths (300–1000 m) or shallower but in disequilibrium, and in deep water (> 1000 m). Saturation pressures range widely in early alkalic to strongly alkalic breccia clast and sandstone glasses, establishing that early Kīlauea's vents spanned much of Mauna Loa's submarine flank, with some vents exceeding sea level. Later south flank alkalic pillow lavas expose a sizeable submarine edifice that grew concurrent with nearby subaerial alkalic eruptions. The onset of the tholeiitic shield stage is marked by extension of eruptions eastward and into deeper water (to 5500 m) during growth of the Puna Ridge. Subaerial and shallow water eruptions from earliest Kilauea show that it is underlain shallowly by Mauna Loa, implying that Mauna Loa is larger, and Kilauea smaller, than previously recognized.

Chronic pain is affected by atmospheric pressure or wind direction and is positively correlated with blood lactate levels

The effects of various meteorological factors were examined in chronic pain patients. Forty-three outpatients admitted periodically to our clinic for a total of 1856 times during 2000 were asked to grade the degree of pain. Atmospheric pressure was measured at each admission and divided into low (<1013 hPa) and high (≥1013 hPa). General weather conditions (clear or cloudy sky, rain, snow), atmospheric conditions (instability, stability), low temperature and 8 wind directions were also recorded. Another 21 outpatients were asked to grade the degree of pain, and atmospheric pressure and blood lactate level were measured at each pain evaluation. Although there was no correlation between the degree of pain and atmospheric pressure, the low pressure group showed a higher degree of pain than the high pressure group. Unstable atmospheric conditions were associated with a higher degree of pain. There was a weak correlation between the degree of pain and low temperature. Winds from a northeast-south directions were associated with a higher degree of pain. In the second group of patients, a weak correlation between the degree of pain and blood lactate levels was found.

The Use of Pressure Change on Standing as a Surrogate Measure of the Stiffness of a Compression Bandage

ObjectivesTo measure interface pressure and stiffness of short-stretch and long-stretch bandages applied with variable strength. These parameters have a deciding influence on the efficacy of compression therapy in chronic venous disease. DesignProspective experimental study. Materials and methodsCompression bandages constructed of different materials were applied with light, moderate and high pressure. Interface pressure was measured over the medial aspect of leg in 12 healthy individuals. Long-stretch bandages were compared to short-stretch bandages. The difference between standing and supine pressure was used to characterise stiffness. ResultsIn the low pressure range the median pressure of the final bandage in the supine position was between 18 and 30mmHg for the long-stretch and 25–33.5mmHg for the short-stretch bandages (p<0.01, Mann–Whitney U-test). The median differences between standing and supine pressure were between 2.0 and 8.5 for the long-stretch and 6.0–10.5mmHg for the short-stretch material.In the group of moderate pressure the median values in the supine position were in a range 33.0–58.0mmHg, for long-stretch and 39.0–49.5mmHg for short-stretch bandages, with an increase after standing of 6.0–7.0mmHg with long-stretch, and 14.0–21.0mmHg with short-stretch bandages (p<0.01, Mann–Whitney U-test).The median supine pressure values in the high pressure group were between 52.0 and 67.0mmHg for long-stretch and 59.5–67.0mmHg for short-stretch material. The median increase during standing ranged between 8.5 and 14.5mmHg in the elastic group and 23.0–33.0 in the inelastic group (p<0.01, Mann–Whitney U-test). ConclusionA bandage applied with light pressure corresponds to the moderate pressure category of stockings. The difference between the sub-bandage pressure from supine to standing can be used to characterise the stiffness of a bandage.

High central venous pressure is associated with prolonged mechanical ventilation and increased mortality after lung transplantation

Poor oxygenation might occur in transplanted lungs as a result of reperfusion injury and lack of lymphatic drainage. Low central venous and pulmonary capillary wedge pressures are advocated to reduce pulmonary edema and maximize oxygenation but might adversely affect cardiac index, circulation, and renal function. Histories, intensive care unit charts, and donor data on 118 lung transplantations performed between 1999 and 2002 were retrospectively assessed. Multiple logistic regression analysis was performed on donor, recipient, operative, and intensive care unit parameters to determine the relationship of filling pressure (central venous and pulmonary capillary wedge pressures) to prolonged mechanical ventilation and outcome. The mean central venous pressure was used to divide patients into high and low central venous pressure groups, which were then compared to determine differences in outcome and complication rates. A high central venous pressure was found to be associated with prolonged mechanical ventilation (odds ratio, 1.57; 95% confidence interval, 1.13-2.20; P = .008). After removing the effect of poor myocardial function by excluding patients with low cardiac index (< 2.2 L x min -1 x m(-2) ) and high inotrope requirement (> 10 microg/min), central venous pressure remained associated with prolonged mechanical ventilation (odds ratio, 2.31; 95% confidence interval, 1.31-4.07; P = .004). Duration of ventilation (P < .001), intensive care unit mortality (P = .02), hospital mortality (P = .09), and 2-month mortality (P = .02) were higher in patients with central venous pressures of greater than 7 mm Hg. There was no evidence of complications caused by hypovolemia in the low (< or = 7 mm Hg) central venous pressure group, who had lower inotrope requirements (P = .02) and lower creatinine levels (P = .013). Conclusions A high central venous pressure was associated with adverse outcomes after lung transplantation.

Effects of L-NAME and inhaled nitric oxide on ventilator-induced lung injury in isolated, perfused rabbit lungs

To determine whether nitric oxide (NO) might modulate ventilator-induced lung injury. Randomized prospective animal study. Animal research laboratory in a university hospital. Isolated, perfused rabbit heart-lung preparation. Thirty-six isolated, perfused rabbit lungs were randomized into six groups (n = 6) and ventilated using pressure-controlled ventilation for two consecutive periods (T1 and T2). Peak alveolar pressure during pressure-controlled ventilation was 20 cm H2O at T1 and was subsequently (T2) either reduced to 15 cm H2O in the three low-pressure control groups (Cx) or increased to 25 cm H2O in the three high-pressure groups (Px). In the control and high-pressure groups, NO concentration was increased to approximately equal to 20 ppm (inhaled NO groups: CNO, PNO), reduced by NO synthase inhibition (L-NAME groups: CL-Name, PL-Name), or not manipulated (groups CE, PE). Changes in ultrafiltration coefficients (deltaKf [vascular permeability index: g.min(-1).cm H2O(-1).100 g(-1)]), bronchoalveolar lavage fluid 8-isoprostane, and NOx (nitrate + nitrite) concentrations were the measures examined. Neither L-NAME nor inhaled NO altered lung permeability in the setting of low peak alveolar pressure (control groups). In contrast, L-NAME virtually abolished the change in permeability (deltaKf: PL-Name (0.10 +/- 0.03) vs. PNO [1.75 +/- 1.10] and PE [0.37 +/- 0.11; p <.05]) and the increase in bronchoalveolar lavage 8-isoprostane concentration induced by high-pressure ventilation. Although inhaled NO was associated with the largest change in permeability, no significant difference between the PE and PL-NAME groups was observed. The change in permeability (deltaKf) correlated with bronchoalveolar lavage NOx (r2 =.6; p <.001). L-NAME may attenuate ventilator-induced microvascular leak and lipid peroxidation and NO may contribute to the development of ventilator-induced lung injury. Measurement of NO metabolites in the bronchoalveolar lavage may afford a means to monitor lung injury induced by mechanical stress.

HYPOTHERMIC MACHINE PERFUSION OF THE LIVER AND THE CRUCIAL BALANCE BETWEEN PERFUSION PRESSURES AND ENDOTHELIAL INJURY

P25 Aims: Hypothermic machine perfusion (HMP) provides better protection against cold-ischemic injury than cold-storage in marginal donor kidneys. Also, in liver transplantation a switch from static cold-storage to HMP could be beneficial as it would allow longer preservation times and the use of marginal donors. A critical question concerning application of HMP in liver preservation is the crucial balance between perfusion pressure and occurrence of endothelial injury. Methods: Rat livers were preserved using static cold-storage or continuous perfusion with the appropriate UW preservation solution. Cold-storage was compared to HMP preserved livers using an arterial perfusion pressure of 25 mmHg (mean) and a portal perfusion pressure of 4 mmHg (low pressure group), and to HMP at 50 mmHg and 8 mmHg perfusion, respectively (high pressure group). To stain for dead cells, the UW solution was enriched with 14.9 μM propidium iodide (PI), and with an additional 13.5 μM acridine orange, to stain for viable hepatocytes. After 24 h preservation the amount and anatomical localization of PI positive cells were assessed. Acridine orange (AO) used to stain viable hepatocytes, and the RECA-1 (rat endothelial cell antibody-1) and ED-1 (Kupffer cell marker) antibodies were used to identify which cells were PI positive. ATP levels were determined as a viability marker and to confirm that higher energy levels can be obtained with HMP than with cold-storage. Results: All livers in the cold-storage group and both HMP groups were completely perfused as shown with AO staining. Cold-storage preserved livers showed 75.1+/-6.2 dead PI positive cells per microscopic field. PI staining in the low-pressure group showed 64.4+/-7.8 and in the high-pressure group showed 93.4+/-5.9 PI positive cells per microscopic field. PI positive cells were non-parenchymal cells and correlated with the pattern found for RECA-1. The results for ED-1 staining did not correspond with the pattern found for PI positive cells. ATP levels were low after cold-storage (1.2 +/- 0.5) and significantly higher after HMP i.e. 44.5+/-5.9 (low-pressure) and 36.5+/-2.8 pmol/μg-protein (high-pressure), respectively. Conclusions: This study showed better ATP levels for HMP preserved livers in comparison to CS livers. The perfusion pressure showed a low PI-positive cell count in comparison to CS, when the HMP technique was used at a low perfusion pressure. A high HMP perfusion pressure resulted in more PI-positive cells compared to CS, indicating that the perfusion pressure is critical for HMP preservation of the liver. The PI-positive cells were found in the portal triad, sinusoids and central veins and were non-parenchymal in origin. The staining pattern with RECA-1 demonstrated that these non-parenchymal cells can be identified as endothelial cells. HMP preservation is effective for the liver with low-pressure perfusion and it is crucial to fine-tune the perfusion pressure to prevent endothelial injury.

Tomographic identification of neuroretinal rim loss in high-pressure, normal-pressure, and suspected glaucoma.

To identify progressive rim loss and describe patterns of regional change in various clinical presentations of glaucoma by scanning laser tomography (SLT). A previously described analytical approach was used to identify progressive rim area loss in SLT disc images of eyes of people with ocular hypertension (OHT, n = 97), early POAG (OHT converters; n = 30), asymmetric normal-pressure glaucoma (NPG, established and suspected in contralateral eyes; n = 26), and normal control subjects (n = 32). Analysis was performed longitudinally in individual image series, and cross-sectionally within groups at different time points. Reproducibly reduced rim area was detected in 2 (6.2%) of 32 normal control subjects, 11 (11%) of 97 OHT subjects, 27 (90%) of 30 OHT converters, 16 (58%) of 26 of suspected NPG eyes, and 15 (54%) of 26 of established NPG eyes (mean MD = -6.5 dB). Of 5 (19%) of 26 of suspected NPG eyes that converted on visual field testing, rim loss was detected in 3 of 5. In all groups, rim loss was common in the disc poles, especially inferiorly. Patterns of rim loss were similar within high-pressure and normal-pressure groups, whether or not eyes had field defects in each. In high-pressure groups, rim loss was more common nasally than temporally. Normal-pressure groups, unlike high-pressure groups, frequently had rim loss temporally. Suspected NPG eyes had more rim loss temporally and their rim area tended to be less compared with OHT and OHT converters, despite the three groups having equivalent baseline fields. There were similarities and differences in the pattern of rim loss in SLT disc images of high- and normal-pressure presentations of glaucoma. Progressive rim loss was detected in eyes without visual field defects, eyes that progressed to develop field defects, and eyes with established and more severe glaucoma.

Comparisons of Hemodynamic and Respiratory Parameters, and Outcomes between High and Low Cerebral Perfusion Pressure Groups in a Severe Head Injury

A secondary hypoxic brain injury is one of the most important determinants of a neurological outcome after a head injury. In the absence of a specific therapy to normalize cerebral blood flow (CBF), some advocators decided that one approach toward preventing cerebral ischemia was to monitor and maintain the cerebral perfusion pressure (CPP). To date, there is no evidence to support which level of CPP is needed to keep an adequate CBF in the management of severe head injuries. Furthermore, some studies suggested that side effects like acute respiratory distress syndrome (ARDS) or a respiratory complication with intentional CPP management therapy affected the patient's outcome. To examine the relationship between CPP and CBF, we analyzed CBF using the Kety-Schmidt N2O technique, and studied the patient's outcome and respiratory complications. We studied forty patients with severe head injuries (Glasgow Coma Scale<8), who were treated at the Musashino Red Cross Hospital between years 1999 to 2001. We divided the patients into the “high-CPP group (group-H), ” in which CPP was kept above 70mmHg as a threshold of CBF, and the “low-CPP group (group-L), ” in which CPP was kept from 50 to 70mmHg. We analyzed the patients' CBFs and their outcomes, and examined their cardiac indices (CI) and pulmonary arterial diastoric pressures with a thermo-dilution catheter. We also calculated the patients' cerebral vascular resistances (CVR) and compared the results in the two groups. There was no statistical significance concerning CBF, neurological outcomes, pulmonary hemodynamics, or the existence rate of pulmonary complications. The mean CVR in group-H was higher than that of group-L, and we considered that the CBF would be affected by both CVR and CPP. We concluded that the threshold of CPP at 70mmHg is not always appropriate for patients. CPP is affected by certain factors, such as the degree of pressure autoregulation. We should consider both CPP and CVR in the treatments of head injury patients. CPP management is one of the optional therapies that should be chosen with sufficient consideration.

Risk factors for coronary artery disease and the use of neural networks to predict the presence or absence of high blood pressure.

BackgroundThe Framingham Heart Study was initiated in 1948 as a long-term longitudinal study to identify risk factors associated with cardiovascular disease (CVD). Over the years the scope of the study has expanded to include offspring and other family members of the original cohort, marker data useful for gene mapping and information on other diseases. As a result, it is a rich resource for many areas of research going beyond the original goals. As part of the Genetic Analysis Workshop 13, we used data from the study to evaluate the ability of neural networks to use CVD risk factors as training data for predictions of normal and high blood pressure.ResultsApplying two different strategies to the coding of CVD risk data as risk factors (one longitudinal and one independent of time), we found that neural networks could not be trained to clearly separate individuals into normal and high blood pressure groups. When training was successful, validation was not, suggesting over-fitting of the model. When the number of parameters was reduced, training was not as good. An analysis of the input data showed that the neural networks were, in fact, finding consistent patterns, but that these patterns were not correlated with the presence or absence of high blood pressure.ConclusionNeural network analysis, applied to risk factors for CVD in the Framingham data, did not lead to a clear classification of individuals into groups with normal and high blood pressure. Thus, although high blood pressure may itself be a risk factor for CVD, it does not appear to be clearly predictable using observations from a set of other CVD risk factors.

Recruitment maneuver: Does it promote bacterial translocation?*

High peak airway opening pressures (Pao) are used routinely during recruitment maneuvers to open collapsed lung units. High peak Pao, however, can cause lung injury as evidenced by translocation of intratracheally inoculated bacteria. In this study we explored whether recruitment maneuvers that used high Pao could cause translocation of the intratracheally inoculated from the alveoli into the systemic circulation. Prospective, randomized, animal study. Experimental animal care laboratory. Eighteen male Sprague Dawley rats. INTERVENTIONS Rats were anesthetized, tracheostomized, and ventilated with 14 cm H2O peak Pao and 0 cm H2O positive end-expiratory pressure (PEEP) in pressure-controlled ventilation (frequency, 30 bpm; inspiratory/expiratory ratio, 1:2; Fio, 1). Intratracheal inoculation of 500 microL of saline containing 1 x 10 colony forming units/mL was performed before randomization into three groups (n = 6 in each): a low-pressure group (14 cm H2O peak Pao, 0 cm H2O PEEP), a high-pressure group (45 cm H2O peak Pao, 0 cm H2O PEEP), and a recruitment maneuver group (14 cm H2O peak Pao, 0 cm H2O PEEP, and a recruitment maneuver sustained inflation of 45 cm H2O continuous positive airway pressure for 30 secs every 15 mins). Blood samples for blood gas analysis were obtained before intratracheal instillation of bacteria and at the end of the experimental protocol (2 hrs). Blood cultures were obtained before and after bacterial instillation at 30-min intervals during the experiment. Blood samples were cultured directly in sheep blood, MacConkey, and Iso-Sensitest agars and were observed on the second day. Bacteremia was defined as the presence of one or more colonies of in 1 mL of blood. The blood cultures were positive for in only six rats in the high-pressure group and remained negative throughout the study period in the low-pressure and recruitment maneuver groups. Oxygenation deteriorated in all groups after intratracheal instillation of bacteria. In the high-pressure group, oxygenation decreased from 417 +/- 67 mm Hg to 79 +/- 20 mm Hg ( p=.004), whereas in the low-pressure and recruitment maneuver groups PaO2 decreased from 410 +/- 98 mm Hg and 383 +/- 78 mm Hg to 287 +/- 105 mm Hg ( p=.031) and 249 +/- 59 mm Hg (p =.11), respectively. Intermittent recruitment maneuvers applied as a sustained inflation superimposed on low-pressure ventilation with 0 cm H2O PEEP did not cause translocation of intratracheally inoculated.

The optimal pressure for initial flush with UW solution in heart procurement

Objective: University of Wisconsin (UW) solution is widely used in organ preservation. Some investigators have reported that high pressure during initial flush with UW solution may induce vasoconstriction and endothelial damage, because of its high potassium content and high viscosity. However, using lower pressure during the initial flush may lead to irregular distribution of the solution and incomplete flushing of blood components from coronary vascular beds. This experimental study evaluated the effects of a range of initial flush pressures during heart procurement, followed by orthotopic transplantation of the graft after 12 hours of preservation. Materials and methods: Twelve pairs of adult mongrel dogs, weighing 9 to 14 kg, formed the recipient–donor combinations. After determining hemodynamic status by measuring cardiac output, left ventricular pressure (LVP), and maximum positive and negative change in LVP (±LVdP/dt), donor hearts were excised. Coronary vascular beds were flushed with 4°C UW solution at a pressure of 60 mm Hg in the low-pressure group ( n = 6) and at 120 mm Hg in the high-pressure group ( n = 6). After 12 hours of cold preservation, orthotopic transplantation was performed using cardiopulmonary bypass (CPB). The hemodynamics of the transplanted graft were assessed by comparing recovery rates (%) from donor hearts 2 hours after weaning from CPB. Endothelin-1 (ET-1) levels were measured in the blood obtained from the coronary sinus 30 minutes after reperfusion. The transplanted grafts were then harvested for histologic study and measurement of adenosine triphosphate (ATP) content. Results: Cardiac output, LVP, LVdP/dt and myocardial tissue ATP content were significantly better ( p < 0.05) in the high-pressure group than in the low-pressure group. We found no significant differences in ET-1 levels between the groups. Transmission electron microscopic findings revealed that degeneration of the mitochondria was less extensive in the high-pressure group than in the low-pressure group. We observed no obvious ultrastructural damage to the endothelial cells in either group. Conclusion: When using UW solution in heart procurement, high pressure is better to completely wash out the blood components and distribute the solution.

Relation of insulin resistance to blood pressure in childhood.

To determine the relation between blood pressure and insulin resistance in children and the differences between fasting insulin and the insulin clamp in that relation. Children were randomly selected after blood pressure screening of 12 043 fifth--eigth grade Minneapolis, Minnesota, students, with stratification by systolic blood pressure (SBP) percentile [half from the upper 25th percentile (high blood pressure) and half from the lower 75th percentile (low blood pressure)]. Euglycemic insulin clamps were performed with an insulin infusion rate of 1 mU/kg per min and a variable infusion of 20% glucose to maintain plasma glucose at 5.6 mmol/l (100 mg/dl). Insulin sensitivity (Mlbm) is defined as the amount of glucose required to maintain euglycemia (mg glucose infused/kg lean body mass (LBM)/min. Diastolic blood pressure was not significantly correlated with any of the body measurements or laboratory data. SBP was significantly correlated with virtually all measures of body size in males and females. SBP and Mlbm were not significantly correlated in either sex. The correlation between SBP and fasting insulin was significant for boys and girls, but became non-significant after adjustment for BMI. All measures of body fatness were significantly greater in the high blood pressure group, and a significant clustering effect for fasting insulin, BMI, triglycerides, and HDL-C was related to blood pressure. The clustering effect was similar when Mlbm was substituted for fasting insulin and was similar for boys, girls, blacks and whites. These results suggest that level of blood pressure in children is mediated through body fat and that insulin resistance, as determined by the insulin clamp, does not play a primary role at this age of development. Nevertheless, the clustering effect of the risk factors according to SBP grouping is consistent with an early relation of blood pressure to the insulin resistance syndrome.

Glucocorticoid suppresses neutrophil activation in ventilator-induced lung injury.

To investigate, in a rat model, the role of the Mac-1/ICAM-1 pathway and the anti-inflammatory activity of steroid in ventilator-induced lung injury. Prospective, randomized controlled study. Animal investigation using Wistar rats. Rats in three randomly assigned groups of 18, a total of 54 animals, were subject to the following: Two groups received high peak inspiratory pressure (35 cm H2O) ventilation after pretreatment with methylprednisolone (high-methylprednisolone group) or pretreatment with methylprednisolone vehicle (high-vehicle group). The third group of animals received low peak inspiratory pressure (7 cm H2O) ventilation after pretreatment with methylprednisolone vehicle (low-vehicle group). Except for animals previously killed to establish baseline values, after 40 mins of mechanical ventilation, the animals in each group were killed. Some animals provided histological samples, and the rest received total lung lavage. We measured flow cytometry of lavage fluid, cell counts of tissue samples, and pressure-volume curves before and after mechanical ventilation. In the groups that received high peak inspiratory pressure ventilation, both the number of neutrophils that infiltrated the lungs and the expression of Mac-1 and ICAM-1 on neutrophils and macrophages increased significantly more than in the low-vehicle group. Static lung compliance was reduced in the high peak inspiratory pressure groups. In the high peak inspiratory pressure groups, there were significantly fewer neutrophils in samples from the high-methylprednisolone group (0.412 +/- 0.1 x 10(5)) than from the high-vehicle group (1.10 +/- 0.1 x 10(5); p < .05). The high-vehicle group showed greater expression of CD11b on neutrophils, but this was significantly decreased by methylprednisolone (mean fluorescence intensity: high-vehicle, 118.4 +/- 34.3; high-methylprednisolone, 25.8 +/- 4.2; p < .05). The lung mechanics measured by pressure-volume curve analysis were deteriorated less in the high-methylprednisolone group. Our study suggests that a neutrophil-endothelium interaction via the Mac-1/ICAM-1 pathway is involved in the activation and recruitment of neutrophils in ventilator-induced lung injury. Activation and recruitment of neutrophils were lessened by pretreatment with methylprednisolone, which might have contributed to the improvement of lung dysfunction after mechanical ventilation.

Effects of Pressure and Measurement Time on the Fluid Filtration Method in Endodontics

The purpose of this study was to evaluate the influence of the measurement time and the pressure on the outcome of a fluid filtration test. Thirty-six roots were prepared with a Profile device and filled with Thermafil. The leakage along the filling material was recorded under a 15 cm H2O pressure (n = 18) or a 150 cm H2O pressure (n = 18) at 3 min, 1 h, and 24 h. The fluid flow expressed as microl min(-1) decreased with an increased measurement time (p = 0.001) and was higher in the high pressure group (p = 0.001). The fluid flow of this study, where all of the teeth were filled with the same technique, ranged from 3.8 x 10(-5) microl min(-1) cm H2O(-1) to 43 x 10(-5) microl min(-1) cm H2O(-1), depending on the pressure and measurement time. This shows the need for standardization to compare the results from various studies.

The management of the elderly with hypertension.

JRAAS 2001;2:11–3 Although much effort is spent in trying to define hypertension by identifying a level of blood pressure (BP) above which subjects are at increased risk,hypertension is best defined as the level of BP above which treatment does more good than harm. This information cannot come from epidemiological or clinical observations,but from the results of randomised controlled trials. At the beginning of year 2001, we know that, at ages up to the late seventies, it is worth treating a systolic blood pressure (SBP) >160 mmHg and/or a diastolic blood pressure (DBP) ≥90 mmHg. A randomised controlled trial assesses outcome in at least two equivalent groups. In the traditional comparison of active hypertensive treatment with placebo, the only difference between the active and placebo-treated groups is the treatment. In observational studies, any benefits from active treatment may be due to selection of subjects with confounding factors, such as high social class, low blood sugars and cholesterol, a tendency to take exercise, not to smoke nor to drink alcohol in excess. Although the randomisation trials tell us when to treat, we do not know the lowest level of BP at which treatment confers an overall benefit. It is unlikely that those with low levels of BP would benefit, as few would gain by having cardiovascular events prevented, yet all are at risk of the adverse effects of treatment. While awaiting trial results, there is speculation that treatment should be started at, say, a systolic pressure of 140–159 mmHg. Even if this is true, adverse effects may outweigh advantages in certain groups, for example the very elderly (over 80 years) and those whose BP is high when lying but low on standing. Adverse consequences may also apply to those with a high BP when first seen but normal pressures thereafter and those who always have a high BP in the clinic but not outside (white coat hypertensives). The benefit: risk comparison for those over the age of 80 and for those with postural hypotension, is not yet known and the problem of the over 80s is considered later in this editorial. Transient hypertension, at least in men, appears to confer an excess cardiovascular risk although this risk may not be reversible with treatment,a problem that was examined in the Syst-Eur trial. In this trial of 4695 patients, followed for an average of two years,717 had ambulatory BP monitoring at baseline. All patients were over the age of 60, had isolated systolic hypertension, with systolic pressure in the clinic of more than 160 mmHg, and their standing SBP had to be more than 140 mmHg. They were divided into three groups according to the average ambulatory daytime systolic pressure of ≥160 mmHg,140–159 mmHg and <140 mmHg, and the reduction in cardiovascular events was 50%, 20% and 60% in the three groups, respectively. Events were few in the low pressure group and the 60% reduction did not achieve statistical significance. However, the 50% reduction in the high pressure group approached statistical significance and this group had a 70% reduction in stroke incidence with active treatment (p=0.03).These data provide some evidence to support the concept that the higher the sustained levels of BP, the greater the benefits of active treatment and presumably the more favourable benefit: risk comparison. We need to determine the sustained level of BP. At age 65–79 years, randomised trials have shown that a sustained systolic pressure ≥160 mmHg should be treated, irrespective of DBP. It is also probable (but not proven) that a diastolic pressure of ≥90 mmHg should be treated, irrespective of systolic pressure. The pressure should be measured at least three times on separate occasions over a period of time. The period of time should be at least two months, to agree with the evidence from the trials, and the BP should be taken in the sitting position but with a standing systolic pressure of at least 140 mmHg. Thus, we have an evidence base for treatment in subjects under age 80, but, having decided on ‘treatment’, what should this be and what target BP should we aim for?

Ventilator-Induced Lung Injury Is Associated with Neutrophil Infiltration, Macrophage Activation, and TGF-β1 mRNA Upregulation in Rat Lungs

Activated neutrophils contribute to the development of ventilator-induced lung injury (VILI) caused by high-pressure mechanical ventilation. However, exact cellular and molecular mechanisms have not been conclusively studied. Our investigation aimed to examine expression of adhesion molecules by both neutrophils and macrophages in lung lavage fluids of rats with VILI. Further, involvement of proinflammatory (tumor necrosis factor-α) and profibrogenetic (transforming growth factor-β1) mediators was analyzed at mRNA level in lung tissue. Wistar rats were ventilated by high pressure (45 cm H2O of peak inspiratory pressure, n = 23) or low pressure (7 cm H2O, n = 13) with 0 positive end-expiratory pressure. After 40 min of comparative ventilation, lung lavage was performed in 20 rats from the experimental group and 10 from the control for immunofluorescence analysis with anti-Mac-1 and anti-ICAM-1 monoclonal antibodies. The lung tissues from remaining rats were subjected to pathological and reverse transcription-polymerase chain reaction examinations. Although there was no significant change of Pao2 in the low-pressure group, Pao2 was decreased in the high-pressure group. The high-pressure group also had greater neutrophil infiltration into alveolar spaces, upregulation of CD54 and CD11b on alveolar macrophages, and more transforming growth factor-β1 mRNA in lung tissues. Tumor necrosis factor-α was not involved in the pathogenesis of the severe VILI observed. Histologic findings also demonstrated more infiltrating neutrophils, destructive change of the alveolar wall, and deposition of matrix in the high-pressure group. These results suggest that a series of proinflammatory reactions and profibrogenetic process may be involved in the course of VILI. Implications High-pressure ventilation demonstrated, in the early phase, not only proinflammatory processes, including neutrophil infiltration and adhesion molecules upregulation on macrophages, but profibriogenetic processes, including transforming growth factor-β1 mRNA expression in the lung tissue. These immunological alterations may be involved in the progress of ventilator-induced lung injury.

Effect of high transcapillary pressures on capillary ultrastructure and permeability coefficients in dog lung

To determine the correlation between ultrastructural and physiological changes in blood-gas barrier function in lungs transiently exposed to very high vascular pressures, we increased capillary transmural pressure (Ptm) of 6 canine isolated perfused left lower lung lobe preparations (high-pressure group) to 80.3 Torr for 3.8 min and then determined the capillary filtration (K(fc)) and osmotic reflection (sigma(d)) coefficients at a Ptm of 19.1 Torr in the ventilated lung lobes. This was followed by perfusion fixation of the lobes at a Ptm of 20.5 Torr for ultrastructural analysis. These data were compared with those obtained in six lobes in which Ptm was not transiently elevated before K(fc), sigma(d), and ultrastructural evaluation. K(fc) was higher [0.249 +/- 0.042 (SE) vs. 0.054 +/- 0.009 g. min(-1). Torr(-1). 100 g(-1); P < 0.01] and sigma(d) was lower (0.52 +/- 0.07 vs. 0.85 +/- 0.08; P < 0.01) in the high-pressure group. In contrast, although endothelial and epithelial breaks were occasionally observed in some experiments, their incidence was not increased in the high-pressure group. These data suggest that the increased transvascular water and protein flux occurred through pathways of a size not resolvable by electron microscopy after vascular perfusion-fixation at a Ptm of 20.5 Torr.

Ventilator-induced lung injury is associated with neutrophil infiltration, macrophage activation, and TGF-beta 1 mRNA upregulation in rat lungs.

Activated neutrophils contribute to the development of ventilator-induced lung injury (VILI) caused by high-pressure mechanical ventilation. However, exact cellular and molecular mechanisms have not been conclusively studied. Our investigation aimed to examine expression of adhesion molecules by both neutrophils and macrophages in lung lavage fluids of rats with VILI. Further, involvement of proinflammatory (tumor necrosis factor-alpha) and profibrogenetic (transforming growth factor-beta 1) mediators was analyzed at mRNA level in lung tissue. Wistar rats were ventilated by high pressure (45 cm H(2)O of peak inspiratory pressure, n = 23) or low pressure (7 cm H(2)O, n = 13) with 0 positive end-expiratory pressure. After 40 min of comparative ventilation, lung lavage was performed in 20 rats from the experimental group and 10 from the control for immunofluorescence analysis with anti-Mac-1 and anti-ICAM-1 monoclonal antibodies. The lung tissues from remaining rats were subjected to pathological and reverse transcription-polymerase chain reaction examinations. Although there was no significant change of PaO(2) in the low-pressure group, PaO(2) was decreased in the high-pressure group. The high-pressure group also had greater neutrophil infiltration into alveolar spaces, upregulation of CD54 and CD11b on alveolar macrophages, and more transforming growth factor-beta 1 mRNA in lung tissues. Tumor necrosis factor-alpha was not involved in the pathogenesis of the severe VILI observed. Histologic findings also demonstrated more infiltrating neutrophils, destructive change of the alveolar wall, and deposition of matrix in the high-pressure group. These results suggest that a series of proinflammatory reactions and profibrogenetic process may be involved in the course of VILI.

Immediate and late clinical and angiographic outcomes after GFX coronary stenting: Is high-pressure balloon dilatation necessary?

The GFX stent is a balloon-expandable stent made of sinusoidal element of stainless steel. The adjunct high-pressure balloon dilatations were usually recommended in routine stenting procedure. The aim of this study was to evaluate the immediate and long-term clinical and angiographic outcomes and to investigate the necessity of high-pressure balloon dilatation during GFX stenting. In all, 172 consecutive patients underwent single 12 or 18 mm GFX stent implantation in 188 native coronary lesions. Two types of stenting technique were used: (1) stent size of a final stent-to-artery ratio of 1:1 (inflation pressure > 10 atm, high-pressure group), and (2) stent size of 0.5 mm bigger than reference vessel (inflation pressure < or = 10 atm, low-pressure group). The adjunct high-pressure balloon dilatations were performed only in cases of suboptimal results. The adjunct high-pressure balloon dilatation was required in 11 of 83 lesions (13%) in the high-pressure group and in 7 of 105 lesions (7%) in the low-pressure group (p = 0.203). Procedural success rate was 100%. There were no significant differences of in-hospital and long-term clinical events between the two groups. The overall angiographic restenosis rate was 17.7%; 18.4% in the high-pressure group and 17.1% in the low-pressure group (p = 0.991). The GFX stent is a safe and effective device with a high procedural success rate and favorable late clinical outcome for treatment of native coronary artery disease. Further randomized trials may be needed to compare stenting techniques in GFX stent implantation.